cardiac conditions, interventions & rehabilitation · cardiac conditions, interventions &...

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CARDIAC CONDITIONS,

INTERVENTIONS & REHABILITATION

Jassin M. Jouria, MD

Dr. Jassin M. Jouria is a medical doctor, professor of

academic medicine, and medical author. He graduated from

Ross University School of Medicine and has completed his

clinical clerkship training in various teaching hospitals

throughout New York, including King’s County Hospital

Center and Brookdale Medical Center, among others. Dr. Jouria has passed all

USMLE medical board exams, and has served as a test prep tutor and instructor for

Kaplan. He has developed several medical courses and curricula for a variety of

educational institutions. Dr. Jouria has also served on multiple levels in the academic

field including faculty member and Department Chair. Dr. Jouria continues to serves

as a Subject Matter Expert for several continuing education organizations covering

multiple basic medical sciences. He has also developed several continuing medical

education courses covering various topics in clinical medicine. Recently, Dr. Jouria

has been contracted by the University of Miami/Jackson Memorial Hospital’s

Department of Surgery to develop an e-module training series for trauma patient

management. Dr. Jouria is currently authoring an academic textbook on Human

Anatomy & Physiology.

Abstract

Just as a serious limb injury requires rehabilitation to return to optimal

performance, the heart also requires serious rehab in order to function

at its best after a trauma. When a cardiac event occurs, the patient

may suffer emotional difficulties and challenges to accept and

overcome events that caused the condition. Cardiac rehabilitation is a

whole-body approach to restore health that incorporates a multi-

dimensional methodology to address body, mind, and spirit. Exercise,

counseling, and physical therapy combine with medical management

to ensure that as much normal function as possible is restored, and

that every patient is able to adapt to lifestyle changes that reduce the

risk of a repeat occurrence. The cardiac rehabilitation team and

program goals for various cardiac diagnoses and interventions are

discussed to support further studies and to increase knowledge in

everyday practice.


Continuing Nursing Education Course Planners

William A. Cook, PhD, Director, Douglas Lawrence, MA, Webmaster,

Susan DePasquale, MSN, FPMHNP-BC, Lead Nurse Planner

Policy Statement

This activity has been planned and implemented in accordance with

the policies of NurseCe4Less.com and the continuing nursing education

requirements of the American Nurses Credentialing Center's

Commission on Accreditation for registered nurses. It is the policy of

NurseCe4Less.com to ensure objectivity, transparency, and best

practice in clinical education for all continuing nursing education (CNE)

activities.

Continuing Education Credit Designation

This educational activity is credited for 4 hours. Nurses may only claim

credit commensurate with the credit awarded for completion of this

course activity.

Statement of Learning Need

Assisting patients to lower their risk of heart disease following a new

cardiac diagnosis often involves specialized health professionals to

encourage and educate them on best practice exercise programs and

healthy lifestyle choices. Nurses are key partners within the health

team to support the patient with heart disease in their progress to heal

and to lead a healthy life.


Course Purpose

To provide nursing professionals with knowledge of a holistic approach

for cardiac rehabilitation to support the patient with heart disease to

recover and heal.

Target Audience

Advanced Practice Registered Nurses and Registered Nurses

(Interdisciplinary Health Team Members, including Vocational Nurses

and Medical Assistants may obtain a Certificate of Completion)

Course Author & Planning Team Conflict of Interest Disclosures

Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA,

Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures

Acknowledgement of Commercial Support

There is no commercial support for this course.

Activity Review Information

Reviewed by Susan DePasquale, MSN, FPMHNP-BC

Release Date: 3/1/2016 Termination Date: 3/17/2018

Please take time to complete a self-assessment of knowledge,

on page 4, sample questions before reading the article.

Opportunity to complete a self-assessment of knowledge learned will be provided at the end of the course.


1. Which of the following is a modifiable risk factor for

atherosclerosis:

a. Diabetes mellitus

b. Age

c. Family history of premature coronary heart disease

d. Male-pattern baldness

2. True or False: Angina is the term used to describe the pain

and discomfort that occurs when the heart is deprived of

blood.

a. True.

b. False.

3. Patients with typical myocardial infarction may have the

following prodromal symptoms in the days preceding the

event:

a. fatigue.

b. intense and unremitting for 30-60 minutes.

c. a feeling of indigestion or of fullness and gas.

d. All of the above.

4. There is evidence to show that comprehensive cardiac

rehabilitation programs, including exercise training, can do

the following:

a. Reduce smoking

b. Alter lipid profiles

c. Reduce blood pressure



Introduction

There are a number of conditions that require cardiac rehabilitation.

However, each patient must be assessed regardless of the condition to

ensure that he or she is a candidate for the program. If the patient

presents with a cardiac condition, and is determined to be a candidate,

cardiac rehabilitation will be initiated.

Cardiac Conditions And Rehabilitation

The conditions that require cardiac rehabilitation and program

selection are unique to the patient’s health history, health resources

and individual choices. Specific cardiac conditions in patients who

would benefit from enrollment in a cardiac rehabilitation program are

highlighted in this course. Its necessary for trained health

professionals to ensure that the patient with a cardiac condition, and

undergoing specific treatments and procedures, as well as their family

are educated on options for recovery and healing.

Myocardial Infarction (Heart Attack)

Myocardial infarction, commonly known as a heart attack, “is the

irreversible necrosis of heart muscle secondary to prolonged ischemia.

This usually results from an imbalance in oxygen supply and demand,

which is most often caused by plaque rupture with thrombus formation

in a coronary vessel, resulting in an acute reduction of blood supply to

a portion of the myocardium.”15

Myocardial infarctions occur when blood flow to a section of the heart

is blocked. This blockage prevents the heart from receiving the oxygen

that is required to function properly. Without sufficient oxygen, the


section of the heart will die. Myocardial infarctions are the leading

killer of men and women in the United States. However, with proper

treatment and long-term management, these effects can be

minimized. Cardiac rehabilitation is especially useful in treating

patients who have experienced myocardial infarctions.16

The following is a basic description of what occurs during a heart

attack:17

Heart attacks most often occur as a result of coronary heart

disease (CHD), also called coronary artery disease. CHD is a

condition in which a waxy substance called plaque builds up

inside the coronary arteries. The buildup of plaque occurs over

many years.

Eventually, an area of plaque can rupture (break open) inside of

an artery. This causes a blood clot to form on the plaque's

surface. If the clot becomes large enough, it can mostly or

completely block blood flow through a coronary artery.

If the blockage isn't treated quickly, the portion of heart muscle

fed by the artery begins to die. Healthy heart tissue is replaced

with scar tissue. This heart damage may not be obvious, or it

may cause severe or long-lasting problems.

A less common cause of heart attack is a severe spasm

(tightening) of a coronary artery. The spasm cuts off blood flow

through the artery. Spasms can occur in coronary arteries that

aren't hardened due to plaque buildup (“atherosclerosis”).


Heart attacks can be associated with or lead to severe health

problems, such as heart failure and life-threatening arrhythmias.

Heart failure is a condition in which the heart can't pump enough

blood to meet the body's needs. Arrhythmias are irregular

heartbeats. Ventricular fibrillation is a life-threatening

arrhythmia that can cause death if not treated right away.

Etiology

The primary cause of myocardial infarctions is atherosclerosis.

Approximately 90% of myocardial infarctions result from an acute

thrombus that obstructs an atherosclerotic coronary artery. Plaque

rupture and erosion are considered to be the major triggers for

coronary thrombosis. Following plaque erosion or rupture, platelet

activation and aggregation, coagulation pathway activation, and

endothelial vasoconstriction occur, leading to coronary thrombosis and

occlusion.18

Non-modifiable risk factors for atherosclerosis include the following:

Age

Sex

Family history of premature coronary heart disease

Male-pattern baldness

Modifiable risk factors for atherosclerosis include the following:19

Smoking or other tobacco use

Diabetes mellitus

Hypertension


Hypercholesterolemia and hypertriglyceridemia, including

inherited lipoprotein disorders

Dyslipidemia

Obesity

Sedentary lifestyle and/or lack of exercise

Psychosocial stress

Poor oral hygiene

Type A personality

Elevated homocysteine levels and the presence of peripheral

vascular disease are also risk factors for atherosclerosis.

Causes of myocardial infarction other than atherosclerosis

Non-atherosclerotic causes of myocardial infarction include the

following conditions:20

Coronary occlusion secondary to vasculitis

Ventricular hypertrophy (i.e., left ventricular hypertrophy,

idiopathic hypertrophic subaortic stenosis [IHSS], underlying

valve disease)

Coronary artery emboli, secondary to cholesterol, air, or the

products of sepsis

Congenital coronary anomalies

Coronary trauma

Primary coronary vasospasm (variant angina)

Drug use (i.e., cocaine, amphetamines, ephedrine)

Arteritis

Coronary anomalies, including aneurysms of coronary arteries

Factors that increase oxygen requirement, such as heavy

exertion, fever, or hyperthyroidism


Factors that decrease oxygen delivery, such as hypoxemia of

severe anemia

Aortic dissection, with retrograde involvement of the coronary

arteries

Infected cardiac valve through a patent foramen ovale (PFO)

Significant gastrointestinal bleed

In addition, myocardial infarction can result from hypoxia due to

carbon monoxide poisoning or acute pulmonary disorders.

Infarcts due to pulmonary disease usually occur when demand

on the myocardium dramatically increases relative to the

available blood supply.

Myocardial infarction induced by chest trauma has also been

reported, usually following severe chest trauma such as motor

vehicle accidents and sports injuries.

Coronary Artery Spasm - A less common cause of heart attack is

a severe spasm (tightening) of a coronary artery. The spasm

cuts off blood flow through the artery. Spasms can occur in

coronary arteries that aren't affected by atherosclerosis. What

causes a coronary artery to spasm isn't always clear. A spasm

may be related to:

Taking certain drugs, such as cocaine

Emotional stress or pain

Exposure to extreme cold

Cigarette smoking

Signs and Symptoms

Patients with typical myocardial infarction may have the following

prodromal symptoms in the days preceding the event (although typical


ST elevation myocardial infarction (STEMI) may occur suddenly,

without warning):

Fatigue

Chest discomfort

Malaise

Typical chest pain in acute myocardial infarction has the following

characteristics:15

Intense and unremitting for 30-60 minutes

Retrosternal and often radiates up to the neck, shoulder, and

jaw and down to the ulnar aspect of the left arm

Usually described as a substernal pressure sensation that also

may be characterized as squeezing, aching, burning, or even

sharp

In some patients, the symptom is epigastric, with a feeling of

indigestion or of fullness and gas

The patient’s vital signs may demonstrate the following in myocardial

infarction:17

The patient’s heart rate is often increased secondary to

sympathoadrenal discharge

The pulse may be irregular because of ventricular ectopy, an

accelerated idioventricular rhythm, ventricular tachycardia, atrial

fibrillation or flutter, or other supraventricular arrhythmias;

bradyarrhythmias may be present

In general, the patient's blood pressure is initially elevated

because of peripheral arterial vasoconstriction resulting from an

adrenergic response to pain and ventricular dysfunction


However, with right ventricular myocardial infarction or severe

left ventricular dysfunction, hypotension is seen

The respiratory rate may be increased in response to pulmonary

congestion or anxiety

Coughing, wheezing, and the production of frothy sputum may

occur

Fever is usually present within 24-48 hours, with the

temperature curve generally parallel to the time course of

elevations of creatine kinase (CK) levels in the blood. Body

temperature may occasionally exceed 102°F

Pathophysiology

The spectrum of myocardial injury depends not only on the intensity of

impaired myocardial perfusion but also on the duration and the level of

metabolic demand at the time of the event. “The damage in the

myocardium is essentially the result of a tissue response that includes

apoptosis (cell death) and inflammatory changes. Therefore, the

hearts of patients who suddenly die from an acute coronary event may

show little or no evidence of damage response to the myocardium at

autopsy. The typical myocardial infarction initially manifests as

coagulation necrosis that is ultimately followed by myocardial fibrosis.

Contraction-band necrosis is also seen in many patients with ischemia.

This is followed by reperfusion, or it is accompanied by massive

adrenergic stimulation, often with concomitant myocytolysis.”14

The following table provides an overview of the different outcomes

that can occur in the setting of a myocardial infarction.20


Arrhythmogenesis

In addition to the direct effects of ischemia and tissue

hypoxia, decreased removal of noxious metabolites,

including potassium, calcium, amphophilic lipids, and

oxygen-centered free radicals, also impair ventricular

performance. These abnormalities promote potentially

lethal arrhythmias.

Pericarditis

Epicardial inflammation may initiate pericarditis, which is

seen in more than 20% of patients presenting with Q-wave

infarctions.

Reduced systolic

function

Lack of adequate oxygen and insufficient metabolite

delivery to the myocardium diminish the force of muscular

contraction and decrease systolic wall motion in the

affected territory.

Abnormal regional

wall motion

Even brief deprivation of oxygen and the requisite

metabolites to the myocardium diminishes diastolic

relaxation and causes abnormal regional systolic contractile

function, wall thickening, and abnormal wall motion. If the

area affected is extensive, diminished stroke volume and

cardiac output may result.

Hypokinesis and

akinesis

In general, regions of hypokinesis and akinesis of the

ventricular myocardium reflect the location and extent of

myocardial injury.

Myocardial

infarction

expansion

In general, expansion of infarcted myocardium and

resultant ventricular dilatation (i.e., ventricular remodeling)

ensues within a few hours after the onset of a myocardial

infarction. An expanding myocardial infarction leads to

thinning of the infarct zone and realignment of layers of

tissue in and adjacent to it, causing ventricular dilatation.


Myocardial

rupture

Myocardial rupture was seen in as many as 10% of fatal

myocardial infarctions before the era of thrombolytics, but

it is now encountered much less often. When rupture

occurs, it may be associated with large infarctions;

indications include cardiogenic shock or hemodynamically

significant arrhythmia. Patients may have a history of

hypertension with ventricular hypertrophy.

Ventricular

aneurysm

A ventricular aneurysm is an outward bulging of a

noncontracting segment. In the early days of cardiac

imaging, ventricular aneurysms were seen in as many as

20% of patients with Q-wave myocardial infarction, but now

it is seen in less than 8%.

Cardiogenic shock

In patients with extensive myocardial injury, coronary blood

flow diminishes as cardiac output declines and heart rate

accelerates. Because coronary artery disease is usually

generalized or diffuse, ischemia that occurs at a distance

from the infracted segment may result in a vicious cycle in

which a stuttering and expanding myocardial infarction

ultimately leads to profound LV failure, hypotension, and

cardiogenic shock.

Effect on diastolic

function

Immediately after the onset of myocardial infarction, the

ability of ischemic myocardium to relax declines. Relaxation

is an active process that uses ATP. Impaired relaxation

increases LV end-diastolic volume (LVEDV) and LV end-

diastolic pressure (LVEDP).

The increased LVEDP results in ventricular dilation,

increased pulmonary venous pressure, decreased

pulmonary compliance, and interstitial and (ultimately)

alveolar pulmonary edema. These effects lead to increased

hypoxemia, which may worsen ischemic injury to the

myocardium.


Prognosis

Approximately thirty percent of patients who experience a myocardial

infarction die within twenty-four hours of onset. Those that survive the

initial event experience significant morbidity. An additional 5-10% of

survivors die within the first year after their myocardial infarction.

Approximately half of all patients with a myocardial infarction are

rehospitalized within 1 year of their index event.20

Better prognosis is associated with the following factors:

Successful early reperfusion (STEMI goals: patient arrival to

fibrinolysis infusion within 30 minutes or patient arrival to

percutaneous coronary intervention within 90 minutes)

Preserved left ventricular function

Short-term and long-term treatment with beta-blockers, aspirin,

and ACE inhibitors

Poorer prognosis is associated with the following factors:22

Increasing age

Diabetes

Previous vascular disease (i.e., cerebrovascular disease or

peripheral vascular disease)

Elevated Thrombolysis in Myocardial Infarction (TIMI) risk score

for unstable angina/NSTEMI (7 factors: Age ≥65 year, ≥3 risk

factors for cardiac disease, previous coronary disease, ST

segment deviation ≥0.5 mm, ≥2 episodes of angina in last 24


hours, aspirin use within prior week, and elevated cardiac

enzyme levels)

Delayed or unsuccessful reperfusion

Poorly preserved left ventricular function (the strongest predictor

of outcome)

Evidence of congestive heart failure (Killip classification ≥II) or

frank pulmonary edema (Killip classification ≥III)

Elevated B-type natriuretic peptide (BNP) levels

Elevated high sensitive C-reactive protein (hs-CRP), a

nonspecific inflammatory marker

Secretory-associated phospholipase A2 activity is related to

atherosclerosis and predicts all-cause mortality in elderly

patients; it also predicts mortality or MI in post-MI patients.

The presence of ST deviation in ECG lead aVR indicates an

increased mortality risk. Data from the APEX-AMI (Pexelizumab

in Conjunction With Angioplasty in Acute Myocardial Infarction)

trial were examined to determine the incidence and prognostic

value of aVR ST deviation in STEMI patients undergoing primary

percutaneous coronary intervention within 6 hours of symptom

onset; the investigators determined that aVR ST deviation was

associated with a 50% relative increase in the risk of death

within 90 days in patients with noninferior MI, while aVR ST


elevation in patients with inferior MI was associated with a

nearly 6-fold increase in such risk.

Blood glucose - elevated blood glucose level on admission is

associated with increased short-term mortality in nondiabetic

patients presenting with a first acute myocardial infarction.

Psychological depression - The combination of acute myocardial

infarction and psychological depression appears to worsen the

patient's prognosis. Acute myocardial infarction may precipitate

reactive depression whether or not beta-adrenergic blocking

agents or other CNS-active agents are administered.

Myocardial hibernation and stunning - After the occurrence of 1

or more ischemic insults, impaired wall motion is often transient

(myocardial stunning) or prolonged (myocardial hibernation).

These phenomena occur because of the loss of essential

metabolites such as adenosine, which is needed for adenosine

triphosphate (ATP)–dependent contraction. Hibernation, a

persisting wall-motion abnormality that is curable with

revascularization, must be differentiated from permanent,

irreversible damage or completed infarct.

Scar tissue and prognosis - Scars involving less than one third of

the thickness of the wall, as shown on contrast-enhanced MRI,

likely correspond to a recovery of myocardial function, whereas

with scars measuring more than one third the thickness of the

wall, the potential for recovery with therapy is limited (except in

cases involving research cell therapies or surgical scar revision).


Other findings associated with recovery are activity on 2-

[Fluorine 18]-fluoro-2-deoxy-D-glucose (FDG) positron emission

tomography (PET) scanning and a monophasic or biphasic

contractile response to dobutamine infusion, caused by the

induction of ischemia.

Heart Condition

Heart condition is a general term used to categorize a variety of

disorders that may occur within the cardiovascular system.

Coronary Artery Disease

Coronary artery disease (CAD) is a condition that is characterized by

the occurrence of atherosclerosis in the epicardial arteries. In this

condition, the plaque narrows the coronary artery lumen, thereby

impairing blood flow to the antegrade myocardial. Some patients may

exhibit symptoms of blood flow reduction, while others will be

asymptomatic. The reduction of coronary artery flow may occur during

instances of rest of exertion. There is no consistent presentation with

CAD. In many instances, the reduction in blood flow will culminate in a

myocardial infarction, but not in all instances. This will ultimately

depend on the severity of the obstruction and the rate or

progression.23

According to the American Heart Association:

“Patients with CAD can present with stable angina pectoris,

unstable angina pectoris, or an MI. They may seek medical

attention with their first symptomatic episode of chest

discomfort. Many of these patients suffer from unrecognized

CAD and may experience an acute plaque rupture or acute


myocardial infarction as their first coronary artery diagnostic

presentation. Electrical instability can ensue, including

potentially lethal cardiac dysrhythmias.

Identifying high-risk persons before their first myocardial event

is a multifaceted process that involves both patient and

physician education efforts. Screening for coronary artery

disease is not sufficient. Risk factor modification, from an early

age, initiates primary prevention efforts, forestalling the

development of symptomatic CAD. Severe CAD can be detected

before a patient develops symptoms, especially in a high-risk

patient subpopulation where pre-test probability of flow limiting

coronary artery disease is higher than average.

CAD is the most common type of heart disease and in 2008,

405,309 individuals died in the U.S. from this specific etiology.

Every year, approximately 785,000 Americans suffer a first

heart attack and another 470,000 will suffer an additional

myocardial infarction (MI). In 2010, CAD alone was projected to

cost the U.S. $108.9 billion including the cost of health care

services, medications, and lost productivity.”24

Coronary artery disease typically begins during adolescence and

progresses throughout the patient’s life. The rate of progression is

very slow, and most patients will be unaware of their medical status.

Although CAD typically progresses slowly, there are a number of risk

factors that can accelerate or modify the progression of the condition.


The most common risk factors include:25

Family history of premature CAD

Cigarette smoking

Diabetes mellitus

Hypertension

Hyperlipidemia

Sedentary lifestyle

Diagnosis

The diagnostic process for coronary artery disease includes a thorough

assessment and physical examination. Since the illness typically begins

in adolescence, the physician will need to conduct a thorough medical

history for the patient. In addition to the detailed medical history and

physical examination, the physician may also require an

electrocardiogram, laboratory blood tests, stress testing, and a cardiac

catheterization.26 These additional assessments are often required

when the initial examination produces results that indicate CAD.

The following table provides a detailed overview of the various

components of the patient assessment.27

History

The history should include any current symptoms and a

complete inventory of comorbid conditions. An inventory

of cardiac risk factors, and a complete family history are

essential components. The history should also include

information about the character and location of

discomfort, radiation of discomfort, associated

symptoms, and precipitating, exacerbating, or

alleviating factors.


The importance of the family history should not be

underestimated. A detailed assessment, particularly of

first-degree relatives for the presence of CAD and age of

diagnosis is imperative when evaluating a patient’s risk

factor profile.

Physical Examination

The results of the physical examination of a patient with

stable or unstable angina may be entirely normal. The

presence of multiple risk factors or atherosclerosis in

the carotid or peripheral arteries increases the likelihood

that a chest pain syndrome is related to myocardial

ischemia. Evaluation should include measurements of

blood pressure and the brachial index. Examination of

the carotid arteries should include auscultation for

bruits. Examination of the chest wall, neck, and

shoulders for deformities and tenderness may be helpful

in diagnosing musculoskeletal chest discomfort.

Cardiac auscultation may detect murmurs caused by

aortic stenosis or hypertrophic cardiomyopathy, either

of which can cause angina in the absence of epicardial

CAD.

Assessment of the abdominal aorta for an aneurysm or

bruits and palpation of lower extremity pulses is

necessary to evaluate for peripheral vascular disease.

Careful palpation of all peripheral pulses and

assessment of symmetry versus diminution are also

valuable noninvasive approaches for assessing the

integrity of the arterial circulation.

Finally, examination for xanthelasmas, tendon

xanthomas, retinal arterial abnormalities, and peripheral

neuropathy can be helpful.


Electrocardiography

A resting 12-lead electrocardiogram should be obtained

on all patients with suspected CAD. Electrocardiographic

results are normal in approximately 50% of patients

with chronic stable angina, and they can remain normal

during an episode of chest discomfort. Importantly, a

normal electrocardiogram does not exclude coronary

artery disease.

When abnormal, especially when Q waves are present in

a regional myocardial territory of diagnostic duration

can signify the presence of a past MI with high

accuracy.

Chest Radiography

The usefulness of a routine chest radiograph in a patient

with chest discomfort has not been established.

Calcification of the aortic knob is a common finding in

older patients and is a nonspecific indicator of flow-

limiting obstructive coronary disease. Coronary

calcification may also be present. A widened

mediastinum may signify an aortic aneurysm and

represent the first clue of unstable aortic disease as the

cause of chest discomfort.

Cardiac Computed

Tomography

Angiography

A noninvasive imaging assessment of coronary

atherosclerosis is now possible in the form of cardiac

computed tomography angiography. When negative,

this test possesses a high negative predictive value. The

positive predictive value is also high, but exact stenosis

quantification can be complicated. Associated

calcification can cause a blooming artifact, resulting in

an overestimation of stenosis severity. Additionally,

previous coronary artery intervention in the form of

coronary artery stent placement can create a blooming

shadowing artifact rendering stenosis severity

assessment within the stent challenging.


Echocardiography

Echocardiography is recommended for patients with

stable angina and physical findings suggesting

concomitant valvular heart disease. It is invaluable for

assessing the patient with suspected hypertrophic

cardiomyopathy. It is also recommended for the

assessment of global and regional left ventricular

systolic function in patients who have been diagnosed

with congestive heart failure, complex ventricular

arrhythmias, or a history of MI.

The echocardiogram is in many ways an ideal test when

assessing a patient with known CAD. It is painless,

carries no known risk, and the results are available

within approximately 30 minutes. An experienced

echocardiographer can identify 1 or more MIs, localize

the infarct to a coronary artery distribution, and assess

for associated ischemic structural complications such as

a left ventricular aneurysm, left ventricular

pseudoaneurysm, and ventricular thrombus.

Laboratory Studies

Routine laboratory measurements recommended, as a

part of the initial evaluation of patients with CAD,

should include determination of fasting glucose and

fasting lipid levels (total cholesterol, high-density

lipoprotein [HDL] cholesterol, triglycerides, and

calculated low-density lipoprotein [LDL] levels). Other

markers such as lipoprotein(a) (Lp[a]) and high-

sensitivity C-reactive protein may be useful in assessing

cardiac risk.

High-sensitivity C-reactive protein is gaining greater

prominence in assessing the inflammatory level of

vascular disease and predicting future risk of vascular

events, such as MIs and cerebrovascular accidents.


This was most recently highlighted in the Jupiter Trial

where patients with a LDL cholesterol level <130 mg/dL

and a high-sensitivity C-reactive protein >2.0 mg/L

were randomized to rosuvastatin 20 mg/d or placebo.

Those with a high-sensitivity C-reactive protein >2.0

were shown to derive benefit from rosuvastatin based

on a statistically significant reduction in myocardial

event rates, cardiovascular mortality, and rates of death

from any cause compared to those patients who were

administered placebo.

When working with patients who are diagnosed with coronary artery

disease, there are a number of key points to remember:28

The diagnostic and treatment options for CAD are changing

rapidly.

New pharmaceuticals are being developed and introduced into

the treatment armamentarium, particularly novel anti-platelet

agents.

Biologic markers are now used to track coronary artery disease

activity at the vascular level, guiding medication selection and

dose titration.

Procedures are less invasive and offer percutaneous treatment

options, such as drug-eluting stents, that were previously

unavailable.

Despite these advances, CAD and its deleterious manifestations

represent the primary cause of mortality in the U.S. This is

largely caused by poor dietary choices, sedentary lifestyles,

suboptimal control of serum triglyceride, cholesterol, and glucose


levels, inadequate prescription medication administration and

delayed dose titration, and ongoing tobacco use.

Efforts at primary and secondary prevention of obstructive CAD

among the general public are still lacking.

Public awareness campaigns are a partial success.

It is imperative for the physician to allocate time to address the

importance of lifestyle modification efforts.

The genetic basis of CAD is being unraveled at an accelerated

pace.

The future genetic assessment of a person’s lifetime risk for

developing atherosclerotic vascular disease, formerly an idea is

now emerging as a reality.

These findings can guide lifestyle modification prescription and

the choice and dosage of specific pharmaceuticals.

A preemptive approach is the best way to tackle the immensity

of CAD.

Medications, stenting, and bypass surgery are only curative

approaches. In addition to these methods, the patient must

meet the health care team at least halfway to achieve a

successful health outcome.

Angina

Angina is the term used to describe the pain and discomfort that

occurs when the heart is deprived of blood. Many patients describe the

feeling as a pressure or squeezing sensation in the chest. Some

patients will also experience discomfort in the shoulders, arm, neck,

jaw, or back. In some patients, the feeling will present as

indigestion.29 Angina is not a stand-alone heart condition. Instead, it is

a symptom of another heart problem. It is especially common in


instances of coronary heart disease. There are a number of different

types of angina, all producing a specific set of conditions.30 The

following section outlines the most common types of angina.

Stable Angina

Angina pectoris is said to be stable when its pattern of frequency,

intensity, ease of provocation, or duration does not change over a

period of several weeks. Identification of activities that provoke angina

and the amount of sublingual nitroglycerin required to relieve

symptoms are helpful indicators of stability versus progression. A

decrease in exercise tolerance or an increase in the need for

nitroglycerin suggests that the angina is progressing in severity or

transitioning to an accelerating pattern.

Symptoms of stable angina involves pain or discomfort that:31

Occurs when the heart must work harder, usually during physical

exertion

Doesn't come as a surprise, and episodes of pain tend to be alike

Usually lasts a short time (5 minutes or less)

Is relieved by rest or medicine

May feel like gas or indigestion

May feel like chest pain that spreads to the arms, back, or other

areas

Possible triggers of stable angina include:

Emotional stress – learn stress management

Exposure to very hot or cold temperatures – learn how cold and

hot weather affect the heart.

Heavy meals


Smoking – learn more about quitting smoking

Accelerating Angina

Angina pectoris is said to be accelerating when there is a change in the

pattern of stable angina. This may include a greater ease of

provocation, more prolonged episodes, and episodes of greater

severity, requiring a longer recovery period or more frequent use of

sublingual nitroglycerin. This suggests a transition and most likely

reflects a change in coronary artery blood flow and perfusion of the

myocardium. This frequently portends unstable angina or an acute

coronary syndrome, such as an acute MI; should a patient transition

from a stable to an accelerating pattern of angina then acute medical

attention is warranted.32

Unstable Angina

Unstable angina pectoris occurs when the pattern of chest discomfort

changes abruptly. Signs of unstable angina are: symptoms at rest, a

marked increase in the frequency of attacks, discomfort that occurs

with minimal activity, and new-onset angina of incapacitating severity.

Unstable angina usually is related to the rupture of an atherosclerotic

plaque and the abrupt narrowing or occlusion of a coronary artery,

representing a medical emergency with an incipient acute coronary

syndrome and an MI to follow. Immediate medical attention is

mandatory.

Unstable angina or sometimes referred to as acute coronary syndrome

causes unexpected chest pain, and usually occurs while resting. The

most common cause is reduced blood flow to the heart muscle

because the coronary arteries are narrowed by fatty buildups


(atherosclerosis) which can rupture causing injury to the coronary

blood vessel resulting in blood clotting which blocks the flow of blood

to the heart muscle. Unstable angina should be treated as an

emergency. If the patient has new, worsening or persistent chest

discomfort, he or she must receive care immediately. Symptoms of

unstable angina involves pain or discomfort that:33

Often occurs while the person may be resting, sleeping, or with

little physical exertion

Comes as a surprise

May last longer than stable angina

Rest or medicine usually do not help relieve it

May get worse over time

Can lead to a heart attack

Variant Angina

Unlike typical angina – which is often triggered by exertion or

emotional stress - variant angina almost always occurs when a person

is at rest, usually between midnight and early morning. These attacks

can be very painful.

Causes of Variant (Prinzmetal) Angina: The pain from variant angina is

caused by a spasm in the coronary arteries (which supply blood to the

heart muscle). The coronary arteries can spasm as a result of:

Exposure to cold weather

Stress

Medicines that tighten or narrow blood vessels

Smoking

Cocaine use


Symptoms of variant (Prinzmetal) angina include pain or discomfort

that:34

Usually occurs while resting and during the night or early

morning hours

Are usually severe

Can be relieved by taking medication

Microvascular Angina

This type of angina may be a symptom of coronary microvascular

disease (MVD). Coronary MVD is heart disease that affects the heart’s

smallest coronary artery blood vessels.

Causes of microvascular angina involve spasms within the walls of

these very small arterial blood vessels causes reduced blood flow to

the heart muscle leading to a type of chest pain referred to as

microvascular angina. The symptoms of microvascular angina involves

angina that occurs in coronary MVD, which may differ from the typical

angina that occurs in heart disease in that the chest pain usually lasts

longer than 10 minutes, and it can last longer than 30 minutes.

The pain or discomfort:35

May be more severe and last longer than other types of angina

pain;

May occur with shortness of breath, sleep problems, fatigue, and

lack of energy;

Often is first noticed during routine daily activities and times of

mental stress.


Heart Failure

Heart failure occurs when the heart is unable to pump blood at a rate

that is not adequate enough to maintain the requirements of tissue

metabolization, or at a rate that requires an elevated diastolic filling

pressure. According to the American Heart Association:

“heart failure affects nearly 5.7 million Americans of all ages and

is responsible for more hospitalizations than all forms of cancer

combined. It is the number 1 cause of hospitalization for

Medicare patients. With improved survival of patients with acute

myocardial infarction and with a population that continues to

age, heart failure will continue to increase in prominence as a

major health problem in the United States.”36

Heart failure statistics for the United States are as follows:

Heart failure is the fastest-growing clinical cardiac disease entity

in the United States, affecting 2% of the population

Heart failure accounts for 34% of cardiovascular-related deaths

Approximately 670,000 new cases of heart failure are diagnosed

each year

About 277,000 deaths are caused by heart failure each year

Heart failure is the most frequent cause of hospitalization in

patients older than 65 years, with an annual incidence of 10 per

1,000

Rehospitalization rates during the 6 months following discharge

are as much as 50%

Nearly 2% of all hospital admissions in the United States are for

decompensated heart failure, and the average duration of

hospitalization is about 6 days


In 2010, the estimated total cost of heart failure in the United

States was $39.2 billion, representing 1-2% of all health care

expenditures

The incidence and prevalence of heart failure are higher in

blacks, Hispanics, Native Americans, and recent immigrants from

developing nations, Russia, and the former Soviet republics. The

higher prevalence of heart failure in blacks, Hispanics, and

Native Americans is directly related to the higher incidence and

prevalence of hypertension and diabetes. This problem is

particularly exacerbated by a lack of access to health care and

by substandard preventive health care available to the most

indigent of individuals in these and other groups; in addition,

many persons in these groups do not have adequate health

insurance.

The higher incidence and prevalence of heart failure in recent

immigrants from developing nations are largely due to a lack of

prior preventive health care, a lack of treatment, or substandard

treatment for common conditions, such as hypertension,

diabetes, rheumatic fever, and ischemic heart disease.

Men and women have the same incidence and the same

prevalence of heart failure. However, there are still many

differences between men and women with heart failure, such as

the following:

o Women tend to develop heart failure later in life than

men

o Women are more likely than men to have preserved

systolic function

o Women develop depression more commonly than men


o Women have signs and symptoms of heart failure

similar to those of men, but they are more pronounced

in women

o Women survive longer with heart failure than men

The prevalence of heart failure increases with age. The

prevalence is 1-2% of the population younger than 55 years and

increases to a rate of 10% for persons older than 75 years.37

Causes

The causes of heart failure can be broken into four main categories:38

1) Underlying causes:

Underlying causes of heart failure include structural

abnormalities (congenital or acquired) that affect the peripheral

and coronary arterial circulation, pericardium, myocardium, or

cardiac valves, thus leading to increased hemodynamic burden

or myocardial or coronary insufficiency.

Underlying causes of systolic heart failure include the following:

Coronary artery disease

Diabetes mellitus

Hypertension

Valvular heart disease (stenosis or regurgitant lesions)

Arrhythmia (supraventricular or ventricular)

Infections and inflammation (myocarditis)

Peripartum cardiomyopathy

Congenital heart disease

Drugs (either recreational, such as alcohol and cocaine,

or therapeutic drugs with cardiac side effects, such as

doxorubicin)


Idiopathic cardiomyopathy

Rare conditions (endocrine abnormalities, rheumatologic

disease, neuromuscular conditions)

Underlying causes of diastolic heart failure include the following:

Coronary artery disease

Diabetes mellitus

Hypertension

Valvular heart disease (aortic stenosis)

Hypertrophic cardiomyopathy

Restrictive cardiomyopathy (amyloidosis, sarcoidosis)

Constrictive pericarditis

Underlying causes of acute heart failure include the following:

Acute valvular (mitral or aortic) regurgitation

Myocardial infarction

Myocarditis

Arrhythmia

Drugs (i.e., cocaine, calcium channel blockers, or beta-

blocker overdose)

Sepsis

Underlying causes of high-output heart failure include the

following:

Anemia

Systemic arteriovenous fistulas

Hyperthyroidism

Beriberi heart disease

Paget disease of bone


Albright syndrome (fibrous dysplasia)

Multiple myeloma

Pregnancy

Glomerulonephritis

Polycythemia vera

Carcinoid syndrome

Underlying causes of right heart failure include the following:

Left ventricular failure

Coronary artery disease (ischemia)

Pulmonary hypertension

Pulmonary valve stenosis

Pulmonary embolism

Chronic pulmonary disease

Neuromuscular disease

2) Fundamental causes

Fundamental causes include the biochemical and physiologic

mechanisms, through which either an increased hemodynamic

burden or a reduction in oxygen delivery to the myocardium

results in impairment of myocardial contraction.39

3) Precipitating causes

Overt heart failure may be precipitated by progression of the

underlying heart disease (i.e., further narrowing of a stenotic

aortic valve or mitral valve) or various conditions (fever, anemia,

infection) or medications (chemotherapy, NSAIDs) that alter the

homeostasis of heart failure patients.36


4) Genetics of cardiomyopathy

Dilated, arrhythmic right ventricular and restrictive

cardiomyopathies are known genetic causes of heart failure.40

Prognosis

In general, the mortality following hospitalization for patients with

heart failure is 10.4% at 30 days, 22% at 1 year, and 42.3% at 5

years, despite marked improvement in medical and device therapy.

Each rehospitalization increases mortality by about 20-22%.

Mortality is greater than 50% for patients with NYHA class IV,

ACC/AHA stage D heart failure. Heart failure associated with acute MI

has an inpatient mortality of 20-40%; mortality approaches 80% in

patients who are also hypotensive (i.e., cardiogenic shock).41

Pathophysiology

Heart failure can occur from a variety of conditions and will present

differently depending on the cause and severity of the condition. In

addition, the condition will have a different impact on the patient

depending on the causes and severity. The following table provides a

comprehensive overview of the different effects of heart failure.42

Systolic

dysfunction

In systolic dysfunction (also called heart failure (HF) with

reduced ejection fraction (EF)), the ventricle contracts poorly

and empties inadequately, leading initially to increased

diastolic volume and pressure and decreased EF. Many

defects in energy utilization, energy supply,

electrophysiologic functions, and contractile element

interaction occur, with abnormalities in intracellular Ca

modulation and cAMP production.


Predominant systolic dysfunction is common in HF due to MI,

myocarditis, and dilated cardiomyopathy. Systolic dysfunction

may affect primarily the left ventricle (LV) or the right

ventricle (RV); LV failure often leads to RV failure.

Diastolic

dysfunction

In diastolic dysfunction, also called HF with preserved EF,

ventricular filling is impaired, resulting in reduced ventricular

end-diastolic volume, increased end-diastolic pressure, or

both. Contractility and hence EF remain normal; EF may even

increase as the poorly filled LV empties more completely to

maintain cardiac output (CO). Markedly reduced LV filling can

cause low CO and systemic symptoms.

Elevated left atrial pressures can cause pulmonary

hypertension and pulmonary congestion. Diastolic dysfunction

usually results from impaired ventricular relaxation (an active

process), increased ventricular stiffness, valvular disease, or

constrictive pericarditis. Acute myocardial ischemia is also a

cause of diastolic dysfunction. Resistance to filling increases

with age, probably reflecting myocyte loss and increased

interstitial collagen deposition; thus, diastolic dysfunction is

particularly common among the elderly.

Diastolic dysfunction predominates in hypertrophic

cardiomyopathy, disorders with ventricular hypertrophy (i.e.,

hypertension, significant aortic stenosis), and amyloid

infiltration of the myocardium.

LV filling and function may also be impaired if marked

increases in RV pressure shift the interventricular septum to

the left. Diastolic dysfunction has increasingly been

recognized as a cause of HF. Estimates vary, but about 50%

of patients with HF have diastolic dysfunction and a normal

EF; the prevalence increases with age and with diabetes.


LV failure In failure due to LV dysfunction, CO decreases and pulmonary

venous pressure increases. When pulmonary capillary

pressure exceeds the oncotic pressure of plasma proteins

(about 24 mm Hg), fluid extravasates from the capillaries into

the interstitial space and alveoli, reducing pulmonary

compliance and increasing the work of breathing. Lymphatic

drainage increases but cannot compensate for the increase in

pulmonary fluid.

Marked fluid accumulation in alveoli (pulmonary edema)

significantly alters ventilation/perfusion (V/Q) relationships:

Deoxygenated pulmonary arterial blood passes through

poorly ventilated alveoli, decreasing systemic arterial

oxygenation (Pao2) and causing dyspnea. However, dyspnea

may occur before V/Q abnormalities, probably because of

elevated pulmonary venous pressure and increased work of

breathing; the precise mechanism is unclear.

In severe or chronic LV failure, pleural effusions

characteristically develop in the right hemithorax and later

bilaterally, further aggravating dyspnea. Minute ventilation

increases; thus, Paco2 decreases and blood pH increases

(respiratory alkalosis). Marked interstitial edema of the small

airways may interfere with ventilation, elevating Paco2 — a

sign of impending respiratory failure.

RV failure In failure due to RV dysfunction, systemic venous pressure

increases, causing fluid extravasation and consequent edema,

primarily in dependent tissues (feet and ankles of ambulatory

patients) and abdominal viscera. The liver is most severely

affected, but the stomach and intestine also become

congested; fluid accumulation in the peritoneal cavity

(ascites) can occur.


RV failure commonly causes moderate hepatic dysfunction,

with usually modest increases in conjugated and

unconjugated bilirubin, PT, and hepatic enzymes (i.e.,

alkaline phosphatase, AST, ALT, gamma-glutamyl

transpeptidase [GGT]). The impaired liver breaks down less

aldosterone, further contributing to fluid accumulation.

Chronic venous congestion in the viscera can cause anorexia,

malabsorption of nutrients and drugs, protein-losing

enteropathy (characterized by diarrhea and marked

hypoalbuminemia), chronic GI blood loss, and rarely ischemic

bowel infarction.

Cardiac

response

If ventricular function is impaired, a higher preload is

required to maintain CO. As a result, the ventricles are

remodeled over time: the LV becomes less ovoid and more

spherical, dilates, and hypertrophies; the RV dilates and may

hypertrophy. Initially compensatory, these changes

eventually increase diastolic stiffness and wall tension (i.e.,

diastolic dysfunction develops), compromising cardiac

performance, especially during physical stress. Increased wall

stress raises O2 demand and accelerates apoptosis

(programmed cell death) of myocardial cells. Dilation of the

ventricles can also cause mitral or tricuspid valve

regurgitation with further increases in end-diastolic volumes.

Hemodynamic

responses

With reduced CO, O2 delivery to the tissues is maintained by

increasing O2 extraction and sometimes shifting the

oxyhemoglobin dissociation curve to the right to favor O2

release. Reduced CO with lower systemic BP activates arterial

baroreflexes, increasing sympathetic tone and decreasing

parasympathetic tone. As a result, heart rate and myocardial

contractility increase, arterioles in selected vascular beds

constrict, venoconstriction occurs, and Na and water are

retained.


These changes compensate for reduced ventricular

performance and help maintain hemodynamic homeostasis in

the early stages of HF. However, these compensatory

changes increase cardiac work, preload, and afterload;

reduce coronary and renal perfusion; cause fluid

accumulation resulting in congestion; increase K excretion;

and may cause myocyte necrosis and arrhythmias.

Renal

responses

As cardiac function deteriorates, renal blood flow and GFR

decrease, and blood flow within the kidneys is redistributed.

The filtration fraction and filtered Na decrease, but tubular

resorption increases, leading to Na and water retention. Blood

flow is further redistributed away from the kidneys during

exercise, but renal blood flow improves during rest, possibly

contributing to nocturia.

Decreased perfusion of the kidneys (and possibly decreased

arterial systolic stretch secondary to declining ventricular

function) activates the renin-angiotensin-aldosterone system,

increasing Na and water retention and renal and peripheral

vascular tone. These effects are amplified by the intense

sympathetic activation accompanying HF.

The renin-angiotensin-aldosterone-vasopressin (antidiuretic

hormone [ADH]) system causes a cascade of potentially

deleterious long-term effects. Angiotensin II worsens HF by

causing vasoconstriction, including efferent renal

vasoconstriction, and by increasing aldosterone production,

which not only enhances Na reabsorption in the distal

nephron but also causes myocardial and vascular collagen

deposition and fibrosis.

Angiotensin II increases norepinephrine release, stimulates

release of vasopressin, and triggers apoptosis.


Angiotensin II may be involved in vascular and myocardial

hypertrophy, thus contributing to the remodeling of the heart

and peripheral vasculature, potentially worsening HF.

Aldosterone can be synthesized in the heart and vasculature

independently of angiotensin II (perhaps mediated by

corticotropin, nitric oxide, free radicals, and other stimuli)

and may have deleterious effects in these organs. HF that

causes progressive renal dysfunction (including that renal

dysfunction caused by drugs used to treat HF) contributes to

worsening HF and has been termed the cardiorenal

syndrome.

Neurohumoral

responses

In conditions of stress, neurohumoral responses help increase

heart function and maintain BP and organ perfusion, but

chronic activation of these responses is detrimental to the

normal balance between myocardial-stimulating and

vasoconstricting hormones and between myocardial-relaxing

and vasodilating hormones. The heart contains many

neurohumoral receptors (α1, β1, β2, β3, angiotensin II type 1

[AT1] and type 2 [AT2], muscarinic, endothelin, serotonin,

adenosine, cytokine, natriuretic peptides); the roles of all of

these receptors are not yet fully defined.

In patients with HF, β1 receptors (which constitute 70% of

cardiac β receptors) are downregulated, probably in response

to intense sympathetic activation. The result of

downregulation is impaired myocyte contractility and

increased heart rate. Plasma norepinephrine levels are

increased, largely reflecting sympathetic nerve stimulation, as

plasma epinephrine levels are not increased. Detrimental

effects include vasoconstriction with increased preload and

afterload, direct myocardial damage including apoptosis,

reduced renal blood flow, and activation of other

neurohumoral systems, including the renin-angiotensin-

aldosterone-vasopressin system.


Vasopressin is released in response to a fall in BP via various

neurohormonal stimuli. Increased vasopressin decreases

renal excretion of free water; possibly contributing to

hyponatremia in HF. Vasopressin levels in patients with HF

and normal BP vary.

Atrial natriuretic peptide is released in response to increased

atrial volume and pressure; brain (B-type) natriuretic peptide

(BNP) is released from the ventricle in response to ventricular

stretching. These peptides enhance renal excretion of Na, but

in patients with HF, the effect is blunted by decreased renal

perfusion pressure, receptor downregulation, and perhaps

enhanced enzymatic degradation. Because endothelial

dysfunction occurs in HF, fewer endogenous vasodilators

(i.e., nitric oxide, prostaglandins) are produced, and more

endogenous vasoconstrictors (i.e., endothelin) are produced,

thus increasing afterload.

The failing heart and other organs produce tumor necrosis

factor (TNF)-α. This cytokine increases catabolism and is

possibly responsible for cardiac cachexia (loss of lean tissue

≥ 10%), which may accompany severely symptomatic HF,

and for other detrimental changes.

The failing heart also undergoes metabolic changes with

increased free fatty acid utilization and decreased glucose

utilization; these changes may become therapeutic targets.

Changes with

aging

Age-related changes in the heart and cardiovascular system

lower the threshold for expression of HF. Interstitial collagen

within the myocardium increases, the myocardium stiffens,

and myocardial relaxation is prolonged. These changes lead

to a significant reduction in diastolic LV function, even in

healthy elderly people.


Modest decline in systolic function also occurs with aging. An

age-related decrease in myocardial and vascular

responsiveness to β-adrenergic stimulation further impairs

the ability of the cardiovascular system to respond to

increased work demands.

As a result of these changes, peak exercise capacity

decreases significantly (about 8%/decade after age 30), and

CO at peak exercise decreases more modestly. This decline

can be slowed by regular physical exercise. Thus, elderly

patients are more prone than are younger ones to develop HF

symptoms in response to the stress of systemic disorders or

relatively modest cardiovascular insults.

Stressors include infections (particularly pneumonia),

hyperthyroidism, anemia, hypertension, myocardial ischemia,

hypoxia, hyperthermia, renal failure, perioperative IV fluid

loads, nonadherence to drug regimens or to low-salt diets,

and use of certain drugs (including NSAIDs, β-blockers, and

certain Ca channel blockers).

Signs and Symptoms

Signs and symptoms of heart failure include the following:43

Exertional dyspnea and/or dyspnea at rest

Orthopnea

Acute pulmonary edema

Chest pain/pressure and palpitations

Tachycardia

Fatigue and weakness

Nocturia and oliguria


Anorexia, weight loss, nausea

Exophthalmos and/or visible pulsation of eyes

Distention of neck veins

Weak, rapid, and thready pulse

Rales, wheezing

S3 gallop and/or pulsus alternans

Increased intensity of P2 heart sound

Hepatojugular reflux

Ascites, hepatomegaly, and/or anasarca

Central or peripheral cyanosis, pallor

Diagnosis

Heart failure is diagnosed using a set of criteria and a classification and

staging process. There are a number of classification systems that can

be used to diagnose heart failure. The most widely used systems

include those outlined below.

Framingham:

The Framingham criteria for the diagnosis of heart failure consist of

the concurrent presence of either 2 major criteria or 1 major and 2

minor criteria. Major criteria include the following:44

Paroxysmal nocturnal dyspnea

Weight loss of 4.5 kg in 5 days in response to treatment

Neck vein distention

Rales

Acute pulmonary edema

Hepatojugular reflux

S3 gallop

Central venous pressure greater than 16 cm water


Circulation time of 25 seconds

Radiographic cardiomegaly

Pulmonary edema, visceral congestion, or cardiomegaly at

autopsy

Minor criteria are as follows:

Nocturnal cough

Dyspnea on ordinary exertion

A decrease in vital capacity by one third the maximal value

recorded

Pleural effusion

Tachycardia (rate of 120 bpm)

Bilateral ankle edema

The New York Heart Association (NYHA):

The New York Heart Association (NYHA) classification system

categorizes heart failure on a scale of I to IV are listed below.45

Class I: No limitation of physical activity

Class II: Slight limitation of physical activity

Class III: Marked limitation of physical activity

Class IV: Symptoms occur even at rest; discomfort with any

physical activity

The American College of Cardiology/American Heart Association

(ACC/AHA):

The American College of Cardiology/American Heart Association

(ACC/AHA) staging system is defined by the following 4 stages.46


Stage A: High risk of heart failure but no structural heart disease

or symptoms of heart failure

Stage B: Structural heart disease but no symptoms of heart

failure

Stage C: Structural heart disease and symptoms of heart failure

Stage D: Refractory heart failure requiring specialized

interventions

Testing

Diagnostic Testing

The following tests may be used as part of the initial evaluation for

suspected heart failure:47

Complete blood count (CBC)

Urinalysis

Electrolyte levels

Renal and liver function studies

Fasting blood glucose levels

Lipid profile

Thyroid stimulating hormone (TSH) levels

B-type natriuretic peptide levels

N-terminal pro-B-type natriuretic peptide

Electrocardiography

Chest radiography

2-dimensional (2-D) echocardiography

Nuclear imaging

Maximal exercise testing

Pulse oximetry or arterial blood gas


Heart Procedure or Surgery

Many patients who undergo heart procedures or surgery will benefit

from cardiac rehabilitation. In these instances, a rehabilitation

program will help the patient return to normal cardiac performance

levels. There are a number of cardiac procedures that can benefit from

post-procedure cardiac rehabilitation.

Coronary Artery Bypass Graft

Coronary artery bypass grafts are the most common cardiac surgeries

performed in the United States. The procedure is used to treat patients

who have significant narrowings and blockages of their coronary

arteries. It is most used to treat patients with coronary artery disease.

The buildup of fatty material in the arterial walls causes significant

narrowing which reduces blood flow. The procedure creates new,

unblocked routes around the blocked (narrowed) arteries. Once the

new routes are created, adequate blood flow will return to the heart,

thereby delivering the appropriate amounts of oxygen and nutrients to

the heart.48

One way to treat the blocked or narrowed arteries is to:

“bypass the blocked portion of the coronary artery with another

piece of blood vessel. Blood vessels, or grafts, used for the

bypass procedure may be pieces of a vein taken from the legs or

an artery in the chest. At times, an artery from the wrist may

also be used. One end of the graft is attached above the

blockage and the other end is attached below the blockage.

Thus, the blood is rerouted around, or bypasses, the blockage

through the new graft to reach the heart muscle. This bypass of


the blocked coronary artery can be done by performing coronary

artery bypass surgery.”49

The standard procedure for performing a bypass involves opening the

chest fully and stopping the heart. This requires an intensive

procedure in a standard hospital operating room.

“In order to open the chest, the breastbone (sternum) is cut in

half and spread apart. Once the heart is exposed, tubes are

inserted into the heart so that the blood can be pumped through

the body during the surgery by a cardiopulmonary bypass

machine (heart-lung machine). The bypass machine is necessary

to pump blood while the heart is stopped and kept still in order

for the surgeon to perform the bypass operation.”23

The following is a fact sheet that provides a thorough overview of the

standard bypass procedure, which the cardiac rehab team nurse may

share with patients and their families.48

When atherosclerosis develops in the coronary arteries, flow of blood through

these vessels is blocked, and the blood supply to heart muscle is jeopardized. If

the blockages are significant enough, the end result will be a heart attack or

sudden death. CABG is an operation that is designed to re-route the blood

around these blockages to prevent a heart attack or sudden death.

Conventionally an artery from behind the breastbone, and veins from the legs

are used to "bypass" the blood around the coronary artery blockages.

The operation takes 2-3 hours to perform, and begins after general anesthesia is

induced. Patients are completely asleep during the entire course of the operation.


The saphenous vein is removed through incisions in the legs. The length of the

incision is dependent upon the amount of vein required to complete the

necessary number of "bypasses" (i.e., 5 bypasses will require more vein than 2

bypasses). There are many "redundant" veins in the leg ... once some vein is

removed, the other veins in the leg take over for the missing vein. Once the vein

has been removed from the leg, it has the appearance of a long tube or

"conduit". The vein will be divided into separate shorter segments, each of which

will be used for individual bypasses. As vein is removed from the leg by a

physician assistant, the surgeon simultaneously opens the chest by dividing the

breast bone or sternum, affording excellent exposure of the heart. An artery

behind the sternum, the left internal mammary artery (LIMA) is taken down and

one end prepared for bypass grafting. Tubes or cannulae are inserted into the

heart and major blood vessels surrounding the heart in preparation for

cardiopulmonary bypass with the heart-lung machine.

At this point, the patient is placed on the heart-lung machine. Blood is re-

directed from the heart into the heart-lung machine. This permits the surgeon to

safely operate on the heart without blood pumping through it. The heart is then

stopped, and the heart-lung machine continues to pump freshly oxygenated

blood to the rest of the body, in effect, taking over the roles of the heart and

lungs. The diseased coronary arteries are now identified and opened beyond the

level of the blockages. The open ends of the saphenous veins and LIMA are now

sewn to the openings in the coronary arteries using very fine non-absorbable

suture material; these are called the "distal" anastamoses. Surgeons wear

special magnifying lenses in order to see the delicate suture and small vessels.

Because the "inflow" through the LIMA is left intact, as soon as the LIMA

anastamosis is completed, blood flow is established to that region of the heart. A

vein graft however, is harvested as a "free graft" and has no "inflow"; therefore,

after the "distal" vein graft anastamosis is constructed, the other end of the vein

graft is sewn to the aorta (the main artery leaving the heart) in order to

establish "inflow". These are called the "proximal" anastamoses. After this stage,

blood flow has now been established beyond all the blocked arteries, and the

heart has effectively been "bypassed"


The heart-lung machine is then gradually weaned off, and the patient's heart and

lungs resume their normal functions. The cannulae are removed from in and

around the heart, and the sternum and incisions are closed.

Drainage catheters are placed around the heart ... these are usually removed

after 24 hours. Temporary pacing wires to regulate the patient's heart rate are

sewn to the surface of the heart ... these are removed before the patient goes

home.

Following the operation, patients are transported to the Cardiac Post-Anesthesia

Care Unit, a specialized unit caring exclusively for open-heart surgery patients.

Patients generally awaken from anesthesia 4-6 hr after the operation. The

following morning all drainage catheters and monitoring lines are usually

removed, and patients are transferred to a standard hospital room in the cardiac

recovery wing of the hospital. Patients undergoing a CABG operation are usually

hospitalized for 4-5 days following the surgery.

Patients will receive the following detailed instructions prior to the

procedure(s):

You will be asked to empty your bladder prior to the procedure.

An intravenous (IV) line will be started in your arm or hand. Additional

catheters will be inserted in your neck and wrist to monitor the status of

your heart and blood pressure, as well as for obtaining blood samples.

Alternate sites for the additional catheters include the subclavian (under

the collarbone) area and the groin.

You will be positioned on the operating table, lying on your back.

The anesthesiologist will continuously monitor your heart rate, blood

pressure, breathing, and blood oxygen level during the surgery. Once you

are sedated, a breathing tube will be inserted into your throat and into

your trachea (breathing tube) to provide oxygen to your lungs, and you

will be connected to a ventilator, which will breathe for you during the

surgery.

A catheter will be inserted into your bladder to drain urine.

The skin over the surgical site will be cleansed with an antiseptic solution.


Once all the tubes and monitors are in place, incisions may be made in

one or both of your legs or one of your wrists to obtain a section of vein

to be used for grafts.

The doctor will make an incision (cut) down the center of the chest from

just below the Adam's apple to just above the navel.

The sternum (breastbone) will be divided in half with a special operating

instrument. The doctor will separate the two halves of the breastbone and

spread them apart to expose the heart.

Coronary artery bypass graft surgery--on-pump procedure:

In order to sew the grafts onto the very small coronary arteries, the heart

must be stopped to allow the doctor to perform the very delicate

procedure. Tubes will be inserted into the heart so that the blood can be

pumped through your body by a cardiopulmonary bypass machine.

Once the blood has been diverted into the bypass machine for pumping,

the heart will be stopped by injecting it with a cold solution.

When the heart has been stopped, the doctor will perform the bypass

graft procedure by sewing one end of a section of vein over a tiny opening

made in the aorta, and the other end over a tiny opening made in the

coronary artery just below the blockage. If the internal mammary artery

inside your chest is being used as a bypass graft, the lower end of the

artery will be cut from inside the chest and sewn over an opening made in

the coronary artery below the blockage.

You may have more than one bypass graft performed, depending on how

many blockages you have and where they are located. After all the grafts

have been completed, the doctor will examine them to make sure they

are working.

Once the bypass grafts have been completed, the blood circulating

through the bypass machine will be allowed back into your heart and the

tubes to the machine will be removed. Your heart will be restarted.

Temporary wires for pacing may be inserted into the heart. These wires

can be attached to a pacemaker and your heart can be paced, if needed,

during the initial recovery period.


Coronary artery bypass surgery--off-pump procedure:

Once the chest has been opened, the area around the artery to be

bypassed will be stabilized with a special type of instrument.

The rest of the heart will continue to function and pump blood through the

body.

The cardiopulmonary bypass machine and the perfusionist who runs it

may be kept on stand-by should the procedure need to be completed on

bypass.

The doctor will perform the bypass graft procedure by sewing one end of

a section of vein over a tiny opening made in the aorta, and the other end

over a tiny opening made in the coronary artery or internal mammary

artery just below the blockage.

You may have more than one bypass graft performed, depending on how

many blockages you have and where they are located.

Before the chest is closed, the doctor will examine the grafts to make sure

they are working.

Possible risks associated with coronary artery bypass graft surgery

include, but are not limited to, the following:50

Bleeding during or after the surgery

Blood clots that can cause heart attack, stroke, or lung problems

Infection at the incision site

Pneumonia

Breathing problems

Cardiac dysrhythmias/arrhythmias (abnormal heart rhythms)

Indications

Class I indications for CABG from the American College of Cardiology

(ACC) and the American Heart Association (AHA) are as follows:46

Left main coronary artery stenosis >50%


Stenosis of proximal LAD and proximal circumflex >70%

3-vessel disease in asymptomatic patients or those with mild or

stable angina

3-vessel disease with proximal LAD stenosis in patients with poor

left ventricular (LV) function

or 2-vessel disease and a large area of viable myocardium in

high-risk area in patients with stable angina

>70% proximal LAD stenosis with either ejection fraction < 50%

or demonstrable ischemia on noninvasive testing

Other indications for CABG include the following:51

Disabling angina (Class I)

Ongoing ischemia in the setting of a non–ST segment elevation

MI that is unresponsive to medical therapy (Class I)

Poor left ventricular function but with viable, nonfunctioning

myocardium above the anatomic defect that can be

revascularized

CABG may be performed as an emergency procedure in the

context of an ST-segment elevation MI (STEMI) in cases where it

has not been possible to perform percutaneous coronary

intervention (PCI) or where PCI has failed and there is persistent

pain and ischemia threatening a significant area of myocardium

despite medical therapy.

Contraindications

CABG is not considered appropriate in asymptomatic patients

who are at a low risk of MI or death. Patients who will experience

little benefit from coronary revascularization are also excluded.


Although advanced age is not a contraindication, CABG is less

commonly performed in the elderly. Because elderly patients

have a shorter life expectancy, CABG may not necessarily

prolong survival. These patients are also more likely to

experience perioperative complications after CABG.52

Many patients still undergo traditional bypass procedures. However, in

some instances, less invasive procedures may be used. "Off-pump"

procedures, in which the heart does not have to be stopped, were

developed in the 1990's. Other minimally-invasive procedures, such as

key-hole surgery (performed through very small incisions) and robotic

procedures (performed with the aid of a moving mechanical device),

increasingly are being used.53

The following table provides information on the different types of

bypass procedures:51, 54-60

Off-Pump

Coronary

Artery

Bypass

Grafting

Coronary artery bypass grafting (CABG) has conventionally been

an operation that requires the use of the heart lung machine. For

selected patients, surgeons have designed an innovative way to

bypass blocked arteries on the heart without the use of the heart-

lung machine ... this operation is called "off-pump coronary artery

bypass grafting" or "OPCAB". Although indications for performing

this procedure are more limited, and long-term results compared

with conventional CABG are unknown, there are some patients

who may benefit from this procedure.

The principals of OPCAB are in some ways similar to that of CABG,

namely, that an artery from behind the breast bone and/or veins

from the legs are used to "bypass" blood around coronary artery

blockages.


OPCAB is different from CABG in that the heart-lung machine is

not used. This means that the special catheters and "cannulae"

that are placed in and around the heart for a conventional CABG

operation are not used. The heart continues to pump blood to the

rest of the body, and surgeons must operate on a "beating heart".

An advantage of OPCAB over conventional CABG is that it may

eliminate some of the risks associated with using the heart-lung

machine. In most patients these risks are very, very small ... but

in some older patients with significant atherosclerotic disease of

their aorta, poor kidney function, or significant lung disease ...

these risks may be more considerable, and OPCAB might be a

reasonable and safer approach than conventional CABG. There are

many more variables that determine whether or not a patient

would be an acceptable candidate for OPCAB ... these issues are

best discussed with your surgeon.

A disadvantage of OPCAB is that because the heart is not stopped,

surgeons must perform delicate suturing on a "beating heart".

Consequently, stabilizing devices have been developed to help

limit the motion of the heart as surgeons operate. The operation

itself is similar to the CABG operation described above.

General anesthesia is induced, and the patient is asleep for the

entire course of the operation. The surgeon opens the chest by

dividing the breastbone or sternum. An artery behind the sternum,

the left internal mammary artery (LIMA), is taken down and one

end prepared for bypass grafting. If more than one coronary artery

will be bypassed, saphenous vein from the leg is removed and

prepared for the additional bypasses. A stabilizing device is now

placed on the surface of the heart, limiting the motion of the

beating heart. The coronary arteries are opened beyond the sites

of the blockage, and the open ends of the LIMA and vein grafts are

sewn to the openings in the coronary arteries. These are called the

"distal" anastamoses.


Because the "inflow" through the LIMA is left intact, as soon as the

LIMA anastamosis is completed, blood flow is established to that

region of the heart. A vein graft however, is harvested as a "free

graft" and has no "inflow" ... therefore, after the "distal" vein graft

anastamosis is constructed, the other end of the vein graft is sewn

to the aorta (the main artery leaving the heart) in order to

establish "inflow". These are called the "proximal" anastamoses.

At this point in the operation, blood flow has now been established

beyond all the blocked arteries, and the heart has effectively been

"bypassed".

Drainage catheters are placed around the heart ... these are

usually removed after 24hr. Temporary pacing wires to regulate

the patient's heart rate, are sewn to the surface of the heart ...

these are removed before the patient goes home.

The sternum and incisions are closed, and the patient is

transported to the Cardiac Post-Anesthesia Care Unit, a specialized

unit caring exclusively for open-heart surgery patients. Patients

generally awaken from anesthesia 4-6 hr after the operation. The

following morning all drainage catheters and monitoring lines are

usually removed, and patients are transferred to a standard

hospital room in the cardiac recovery wing of the hospital. Patients

undergoing an OPCAB are usually hospitalized for 3-4 days

following surgery. To see what to expect during the recovery of

this operation, please refer to our education section.

Robotic-

assisted

Coronary

Artery

Bypass

Grafting

The daVinci surgical robotic system is used to perform minimally

invasive heart surgery. Surgeons are pioneering new robotic

surgical approaches. Coronary Artery Bypass Grafting, or CABG, is

a surgical procedure to bypass the clogged coronary blood vessel,

and restore blood flow to the heart. The surgeon uses a section of

a healthy artery from the patient's left chest, known as the left

internal mammary artery (LIMA), to "bypass" the diseased section

of the patient's own coronary artery.


Traditional bypass surgery requires the chest to be cut open, the

patient's breastbone to be split, and the function of the heart to be

taken over by a heart-lung bypass machine. Skilled surgeons are

able to use the daVinci robot to carefully prepare the LIMA for use

as a single bypass to the heart without the use of the heart-lung

machine and with no incisions over the breastbone. With only

small incisions over the patient's left chest, smaller surgical

instruments, and greater precision in robotic surgery, patients

experience less pain and have more rapid recovery times.

Robotic-assisted coronary artery bypass grafting is a minimally

invasive procedure. The surgeon makes several small incisions

between the ribs, and then inserts a small camera and small

robotic arms through the incisions.

During the procedure, the surgeon sits at a console and controls

the robotic instruments. The camera that was inserted provides

images of the heart at a high magnification. Using robotic-assisted

coronary artery bypass grafting, patients can typically undergo a

single bypass using the LIMA to the main artery of the heart,

known as the left anterior descending artery, or LAD. If the patient

has disease in more than one vessel in the heart, this procedure

can at times be combined with coronary stents in the other

vessels, performed by cardiologists, to achieve repairs or bypasses

to each of the diseased vessels. In this way, for selected patients,

surgeons have designed an innovative way to bypass the main

blocked LAD artery with minimally invasive robotic surgery,

combined with stents to other vessels.

Although indications for performing this procedure are more

limited, and long-term results compared with conventional CABG

are unknown, there are some patients who may benefit from this

procedure.


Minimally

Invasive

Coronary

Artery

Bypass

Grafting

Coronary Artery Bypass Grafting, or CABG, is a surgical procedure

to bypass the clogged coronary blood vessel, and restore blood

flow to the heart. The surgeon uses a section of a healthy artery

from the patient's left chest, known as the left internal mammary

artery (LIMA), to "bypass" the diseased section of the patient's

own coronary artery.

Traditional bypass surgery required the chest to be cut open, the

patient's breastbone to be split, and the function of the heart to be

taken over by a heart-lung bypass machine. A minimally invasive

CABG is an "off-pump" procedure. Only a single 3-inch incision is

typically used over the patient's left chest between the ribs and no

incisions over the breastbone. The beating heart is held in place

with "stabilizers", which are instruments that immobilize the area

of the heart where the bypass is being done.

With only a single, small incision over the patient's left chest,

patients experience less pain and have more rapid recovery times.

Skilled surgeons are able to use a minimally invasive incision to

carefully prepare the LIMA for use as a single bypass to the heart

without the use of the heart-lung machine and with no incisions

over the breastbone. With a minimally invasive coronary artery

bypass procedure, the surgeon can typically perform a single

bypass using the LIMA to the main artery of the heart, known as

the left anterior descending artery, or LAD.

If the patient has disease in more than one vessel in the heart,

this procedure can at times be combined with coronary stents in

the other vessels, performed by cardiologists, to achieve repairs or

bypasses to each of the diseased vessels. In this way, for selected

patients, surgeons have designed an innovative way to bypass the

main blocked LAD artery with minimally coronary artery bypass

grafting, combined with stents to other vessels.


Although indications for performing this procedure are more

limited, and long-term results compared with conventional CABG

are unknown, there are some patients who may benefit from this

procedure.

Endoscopic

Vein

Harvesting

Standard incisions for harvesting saphenous vein for bypass

operations historically have been long incisions that run the length

of a patient’s leg. Alternatively several smaller “skip” incisions can

be made to provide a more cosmetic and less painful result.

Surgeons now utilize a new technology called Endoscopic Vein

Harvesting that permits them to harvest a complete leg’s length of

vein through a 1 or 2 small (1 cm) incisions. The incision can be

made anywhere along the leg, and vein is removed using specially

designed telescoping surgical and video equipment.

In addition to reducing the size of the surgical scar, Endoscopic

Vein Harvesting significantly reduces leg discomfort in the post-

operative period, and is associated with fewer complications such

as infection and hematoma formation.

Percutaneous Coronary Intervention

Percutaneous coronary intervention (PCI) is a non-surgical procedure

that is performed on patients who have narrowed arteries. The

procedure opens the narrowed arteries so that blood can flow more

easily to the heart.61 With this procedure, a catheter is inserted

through the skin in the groin or the arm. The catheter is inserted

directly into an artery. Once the catheter is secure in the artery,

several devices can be used to help expand the artery. The most

common devices include a balloon, stent, or an artherectomy device.


The catheter and its devices are threaded through the inside of the

artery back into an area of coronary artery narrowing or blockage.62

This procedure can be used on patients who are actively experiencing

a myocardial infarction. In these instances, the percutaneous coronary

intervention will be used as a method of intervening and stopping the

infarction by opening the blocked artery. This will reinstate blood flow

to the heart, thereby stopping the acute infarction. “Although

treatment of acute heart attack is a very important use of

percutaneous coronary intervention, it has several other uses.

Percutaneous coronary intervention can be used to relieve or reduce

angina, prevent heart attacks, alleviate congestive heart failure, and

allows some patients to avoid surgical treatment (coronary artery

bypass graft or CABG) that involves extensive surgery and often long

rehabilitation time.”63

Indications and Contraindications

Clinical indications for Percutaneous Coronary Intervention include the

following:

Acute ST-elevation myocardial infarction (STEMI)

Non–ST-elevation acute coronary syndrome (NSTE-ACS)

Unstable angina

Stable angina

Anginal equivalent (i.e., dyspnea, arrhythmia, or dizziness or

syncope)

High risk stress test findings

In an asymptomatic or mildly symptomatic patient, objective

evidence of a moderate to large area of viable myocardium or

moderate to severe ischemia on noninvasive testing is an


indication for PCI. Angiographic indications include

hemodynamically significant lesions in vessels serving viable

myocardium (vessel diameter >1.5 mm).64

Clinical contraindications for Percutaneous Coronary Intervention

include the following:65

Intolerance of long-term antiplatelet therapy or the presence of

any significant comorbid conditions that severely limit the

lifespan of the patient (this is a relative contraindication).

A Heart Team approach (involving interventional cardiologists

and cardiac surgeons) should be used in patients with diabetes

and multivessel coronary artery disease and in patients with

severe left main disease and a high Syntax score.

Relative angiographic contraindications include the following:66

Arteries < 1.5 mm in diameter

Diffusely diseased saphenous vein grafts

Other coronary anatomy not amenable to PCI

In patients with stable angina, medical therapy is recommended as

first-line therapy unless one or more of the following indications for

cardiac catheterization and PCI or coronary artery bypass grafting

(CABG) are present:67

Severe symptoms

A change in symptom severity

Failed medical therapy

High-risk coronary anatomy

Worsening left ventricular (LV) dysfunction


For patients with STEMI, immediate coronary angiography with

PCI is recommended (primary PCI).

For patients with NSTE-ACS, the American College of Cardiology

Foundation (ACCF)/American Heart Association (AHA) guidelines on

the management of NSTE-ACS (updated in 2014) recommend an early

invasive strategy in most cases, with timing as follows:68

Immediate (within 2 hours) - Patients with refractory or

recurrent angina with initial treatment, signs/symptoms of heart

failure, new/worsening mitral regurgitation, hemodynamic

instability, sustained ventricular tachycardia, or ventricular

fibrillation

Early (within 24 hours) - None of the immediate characteristics

but new ST-segment depression, a GRACE risk score >140, or

temporal change in troponin

Delayed invasive (within 25-72 hours) - None of the immediate

or early characteristics but renal insufficiency (glomerular

filtration rate [GFR] < 60 mL/min/1.73 m2), left ventricular

ejection fraction (LVEF) < 40%, early postinfarct angina, history

of PCI within the preceding 6 months, prior CABG, GRACE risk

score of 109-140, or TIMI score of 2 or higher

Ischemia-guided approach is recommended for patients with a

low-risk score (TIMI 0 or 1, GRACE < 1).

Equipment for a PCI Procedure

Balloon catheters for PCI have the following features:64

A steerable guide wire precedes the balloon into the artery and

permits navigation through the coronary tree


Inflation of the balloon compresses and axially redistributes

atheromatous plaque and stretches the vessel wall

The balloon catheter also serves as an adjunctive device for

many other interventional therapies

Atherectomy devices have the following features:69

These devices are designed to physically remove coronary

atheroma, calcium, and excess cellular material

Rotational or orbital atherectomy, which relies on plaque

abrasion and pulverization, is used mostly for fibrotic or heavily

calcified lesions that can be wired but not crossed or dilated by a

balloon catheter

Atherectomy devices may be used to facilitate stent delivery in

complex lesions

Directional coronary atherectomy (DCA) has been used to debulk

coronary plaques

Laser atherectomy is not widely used at present

Atherectomy is typically followed by balloon dilation and

stenting.

Intracoronary stents have the following features:67

Stents differ with respect to composition (i.e., cobalt chromium

or platinum chromium), architectural design, delivery system

and the drug delivered

Drug-eluting stents (DESs) have demonstrated significant

reductions in restenosis and target-lesion revascularization rates,

with further reduction with the second-generation DESs

(compared with first-generation DESs or bare-metal stents)


In the United States, the commercially available DESs are

second-generation models that elute everolimus and zotarolimus

The stents with bioabsorbable polymer, polymer-free systems or

fully bioresorbable scaffolds are still investigational and not

available for commercial use in the United States

Stents are conventionally placed after balloon predilation, but in

selected coronary lesions, direct stenting may lead to better

outcomes

Other devices used for PCI include the following:69

Thrombus aspiration is reasonable in selected patients

undergoing primary PCI; however, one trial showed no reduction

in the rate of death from any cause or the composite of death

from any cause, rehospitalization for myocardial infarction, or

stent thrombosis

Distal embolic protection during saphenous vein graft

intervention can be considered when technically feasible

Technique:

Intravascular ultrasonography (IVUS) and optical coherence

tomography (OCT) are used in PCI for the following purposes:64

Provision of information about atherosclerotic plaque

composition and burden, the vessel wall, vessel size, degree of

calcium, and degree of luminal narrowing

Assessment of indeterminate lesions

Evaluation of adequate stent deployment


Intracoronary Doppler pressure wires are used in PCI as follows:70

Characterization of coronary lesion physiology and estimation of

lesion severity

Comparison of pressure distal to a lesion with aortic pressure

enables determination of fractional flow reserve (FFR); FFR <

0.80 during maximal hyperemia (induced via administration of

adenosine) is consistent with a hemodynamically significant

lesion

Antithrombotic therapy includes the following:71

Aspirin 162-325 mg is given to all patients on the day of PCI

Unfractionated heparin, low-molecular-weight heparin (LMWHs)

or bivalirudin is used at the time of balloon angioplasty or PCI;

fondaparinux can be used but needs another agent along with it

to prevent catheter thrombosis and therefore is less commonly

preferred

Antiplatelet therapy:72

Patients receiving stents are treated with a combination of aspirin and

a P2Y12 receptor inhibitor (clopidogrel, prasugrel, or ticagrelor). The

minimum duration of P2Y12 receptor inhibitor therapy, according to

the current ACCF/AHA guidelines, is as follows:

Bare-metal stents - Minimum of 4 weeks

DESs - Minimum of 12 months

Use of proton pump inhibitors (PPIs) is appropriate in patients

with multiple risk factors for gastrointestinal bleeding who

require antiplatelet therapy.


Glycoprotein inhibitor therapy:73

Abciximab, tirofiban, and eptifibatide have all been shown to

reduce ischemic complications in patients undergoing balloon

angioplasty and coronary stenting; however, evidence

supporting their use was established largely before the use of

oral P2Y12 inhibitors

Several studies have failed to show the benefit of “upstream”

administration of GPIIb/IIIa inhibitors in the era of dual

antiplatelet therapy (DAPT); because GPIIb/IIIa inhibitors

increase the risk of bleeding, their routine use is no longer

recommended

GPIIb/IIIa inhibitors can be used as an adjunctive therapy at the

time of PCI, on an individual basis, for large thrombus burden or

inadequate P2Y12 receptor antagonist loading.

Coronary Angioplasty

Percutaneous coronary intervention (PCI) is performed to open blocked

coronary arteries caused by coronary artery disease (CAD) and to

restore arterial blood flow to the heart tissue without open-heart

surgery. Using a guidewire, a special catheter (long hollow tube) is

inserted into the coronary artery and past the blockage in the

blockage. The catheter contains a tiny balloon. When the catheter is in

place, the balloon is inflated.

The inflation of the balloon compresses the fatty tissue in the artery

and makes a larger opening inside the artery for improved blood

flow.74 The following procedural steps are involved during the PCI.


The use of fluoroscopy (a special type of X-ray, similar to an X-

ray "movie") assists the doctor in the location of blockages in the

coronary arteries as the contrast dye moves through the

arteries.

A technique called intravascular ultrasound (IVUS), a technique

that uses a computer and a transducer that sends out sound

waves to create images of the blood vessels, may be used during

PCI. The use of IVUS provides direct visualization and

measurement of the inside of the blood vessels and may assist

the doctor in selecting the appropriate size of balloons and/or

stents, to ensure that a stent, if used, is properly opened, or to

evaluate the use of other angioplasty instruments. A technique

called fractional flow reserve (FFR) assessment is often used

during a catheterization to assist in determining the significance

of a moderate coronary narrowing.

The technique involves placing a pressure-transducing wire

across the narrowing, and after a brief infusion of medication,

measuring the pressure change in the coronary artery. This may

assist the physician in deciding whether PCI or stenting is

appropriate.

The physician may determine that another type of procedure is

necessary. This may include the use of atherectomy (removal of

plaque) at the site of the narrowing of the artery. In

atherectomy, there may be tiny blades on a balloon or a rotating

tip at the end of the catheter. When the catheter reaches the


narrowed spot in the artery, the plaque is broken up or cut away

to open the artery.

Coronary Stenting

Coronary stents are now almost universally used in PCI procedures,

often following balloon angioplasty, which opens the narrowed artery

and facilitates stent placement. A stent is a tiny, expandable metal coil

that is inserted into the newly-opened area of the artery to help keep

the artery from narrowing or closing again.67 The following are

procedural steps used during stent placement.

Once the stent has been placed, tissue will begin to form over it

within a few days after the procedure. The stent will be

completely covered by tissue within a month or so. It is

necessary to take medications, such as aspirin, clopidogrel

(Plavix), prasugrel (Effient), or ticagrelor (Brilinta), which

decrease the "stickiness" of platelets (special blood cells that

clump together to stop bleeding), in order to prevent blood clots

from forming inside the stent. The physician will provide specific

instructions regarding which medications need to be taken and

for how long.

Newer stents (drug-eluting stents, or DES) are coated with

medication to prevent the formation of scar tissue inside the

stent. These drug-eluting stents release medication within the

blood vessel itself. This medication inhibits the overgrowth of

tissue that can occur within the stent. The effect of this

medication is to deter the narrowing of the newly stented blood

vessel. Because stents can become blocked, it is important for


the patient to talk with their physician about what is needed if

the patient experiences chest pain after a stent placement.

If scar tissue does form inside the stent, a repeat procedure may

be performed, either with balloon angioplasty or with a second

stent, or occasionally with local radiation therapy (called

brachytherapy) may be used to clear the scarred area and open

up the vessel.

Stents are most useful for:75

Short lesions in large native coronary arteries not previously

treated with PTCA

Focal lesions in saphenous vein grafts

Treatment of abrupt closure during PTCA

Other Procedures

Other related procedures that may be used to assess the heart

include:76

Resting or exercise electrocardiogram (ECG or EKG)

Holter monitor

Signal-averaged ECG

Cardiac catheterization

chest X-ray

Computed tomography (CT scan) of the chest

Echocardiography

Electrophysiological studies

magnetic resonance imaging (MRI) of the heart

Myocardial perfusion scans

Radionuclide angiography


Cardiac CT scan.

Rotational atherectomy - This is sometimes used to aid stent

placement when the plaque is hardened and calcified.

Valve Replacement

Heart valve replacement (or repair) is used to treat valvular heart

disease. It is especially common in patients with valvular stenosis and

valvular insufficiency.77 Heart valve repair or replacement surgery is a

treatment option for valvular heart disease. When heart valves

become damaged or diseased, they may not function properly.

Conditions which may cause heart valve dysfunction are valvular

stenosis and valvular insufficiency (regurgitation).78 When one (or

more) valve(s) becomes stenotic, it becomes more difficult for the

heart to pump blood through the valve. Valvular stenosis “may be the

result of infection or aging, and the effects on the patient will vary. In

some instances, such as when one or more valves become insufficient

(leaky), blood leaks backwards. Based on the symptoms and overall

condition of the heart, the physician may determine that the diseased

valve(s) needs to be surgically repaired or replaced.”79

The following describes the traditional procedure for repairing or

replacing a valve:

“Traditionally, repair or replacement of heart valves has

involved open-heart surgery, which means that the chest is

opened in the operating room and the heart stopped for a

time so that the surgeon may repair or replace the valve(s).

In order to open the chest, the breastbone, or sternum, is

cut in half and spread apart. Once the heart is exposed, large


tubes are inserted into the heart so that the blood can be

pumped through the body during the surgery by a

cardiopulmonary bypass machine (heart-lung machine). The

bypass machine is necessary to pump blood because the

heart is stopped and kept still while the surgeon performs the

valve repair or replacement procedure.”80

The detailed process is described below.81

An intravenous (IV) line will be started in the arm or hand.

Additional catheters will be inserted in the neck and wrist to

monitor the status of the heart and blood pressure, as well as for

obtaining blood samples. Alternate sites for the additional

catheters include the subclavian (under the collarbone) area and

the groin.

The patient will be positioned on the operating table, lying on his

or her back.

The anesthesiologist will continuously monitor heart rate, blood

pressure, breathing, and blood oxygen level during the surgery.

Once the patient is sedated, a breathing tube will be inserted

through the throat into the lungs. The patient will be connected

to a ventilator.

A catheter will be inserted into the bladder to drain urine.

The skin over the surgical site will be cleansed with an antiseptic

solution.


The physician will make an incision (cut) down the center of the

chest from just below the Adam's apple to just above the navel.

The sternum (breastbone) will be divided in half and spread

them apart to expose the heart.

In order to perform the valve repair or replacement, the heart

must be stopped to allow the doctor to perform the very delicate

procedure. Tubes will be inserted into the heart so that the blood

can be pumped through the body by a cardiopulmonary bypass

machine.

Once the blood has been completely diverted into the bypass

machine for pumping, injecting the heart with a cold solution will

stop it from beating.

When the heart has stopped, the doctor will perform the

procedure by removing the diseased valve and putting in the

artificial valve, in the case of a valve replacement. For a valve

repair, the procedure performed will depend on the type of valve

problem that exists, for example, separation of fused valve

leaflets, repair of torn leaflets, and/or the reshaping of valve

parts to ensure better function.

Once the procedure has been completed, the blood circulating

through the bypass machine will be allowed to reenter the heart,

and the heart will be shocked with small paddles to restart its

electrical activity.


Once the heart is beating again, the physician will observe the

heart to assess the function of the heart and the valves.

Temporary wires for pacing may be inserted into the heart.

These wires can be attached to a pacemaker and the heart can

be paced, if needed, during the initial recovery period.

The sternum will be rejoined and sewn together with small wires.

The skin over the sternum will be sewn back together. The

incision will be closed with sutures or surgical staples.

Tubes will be inserted into the chest to drain blood and other

fluids from around the heart. These tubes will be connected to a

suction device to drain fluids away from the heart.

A tube will be inserted through the mouth or nose into the

stomach to drain stomach fluids.

In recent years, more advanced techniques have been developed,

which require smaller incisions and less recovery time. One such

procedure is the transcatheter aortic valve replacement (TAVR).82 The

TAVR is a new alternative for some cases of aortic valve stenosis. A

cardiac surgeon and an interventional cardiologist typically do this

hybrid procedure. The diseased valve may be repaired using a ring to

support a person's own valve, or the entire valve may be removed and

replaced by an artificial valve. Artificial valves may be mechanical

(made of metal or plastic) or tissue (made from animal valves or

human valves taken from cadavers).


Cardiac Pacemakers

Artificial cardiac pacemakers are electronic devices that stimulate the

heart with electrical impulses to maintain or restore a normal rhythm

in people with slow heart rhythms. There are many situations in which

an artificial pacemaker may be recommended. Most commonly, a

pacemaker is used to treat arrhythmias.83 A pacemaker can relieve

some arrhythmia symptoms, such as fatigue and fainting. A

pacemaker also can help a person who has abnormal heart rhythms

resume a more active lifestyle. Faulty electrical signaling in the heart

causes arrhythmias.

Pacemakers use low-energy electrical pulses to overcome this faulty

electrical signaling. Pacemakers can:84

Speed up a slow heart rhythm.

Help control an abnormal or fast heart rhythm.

Make sure the ventricles contract normally if the atria are

quivering instead of beating with a normal rhythm (a condition

called atrial fibrillation).

Coordinate electrical signaling between the upper and lower

chambers of the heart.

Coordinate electrical signaling between the ventricles.

Pacemakers that do this are called cardiac resynchronization

therapy (CRT) devices. CRT devices are used to treat heart

failure.

Prevent dangerous arrhythmias caused by a disorder called long

QT syndrome.

Pacemakers also can monitor and record the heart's electrical

activity and heart rhythm. Newer pacemakers can monitor blood


temperature, breathing rate, and other factors. They also can

adjust the heart rate to changes in activity.

The decision to use such a device, as well as which specific type, will

depend upon multiple factors, including:85

The exact nature and underlying cause of the arrhythmia

Whether the condition is temporary or permanent

The presence or absence of symptoms as described above

The potential risk of complications from a pacemaker

An artificial pacemaker provides an electrical impulse (or "discharge")

that can stimulate the heart, thus restoring or maintaining a regular

heartbeat. Although various types of artificial pacemaker devices are

available, they generally include the following components:86

A thin metal box or case called a pulse generator, which contains

the power source producing the electrical impulses of the

pacemaker. In addition, the pulse generator contains a small

computer processor that can be programmed to set the rate of

the pacemaker, the pattern of pacing, the energy output, and

various other parameters. The pulse generator for most modern

permanent pacemakers weighs one to two ounces.

Flexible insulated wires or leads carry electrical impulses from

the generator to the heart muscle and relay information

concerning the heart's natural activities back to the pacemaker.

There may be several such wires, or leads, placed within the

heart, most commonly in the right atrium and right ventricle.


One or more electrodes at the tips of the leads transmit electrical

impulses to the heart muscle when needed and also sense the

heart's own electrical activity.

Arrhythmias

Pacemakers are used to treat arrhythmias, which are complications

with the rate or rhythm of the heartbeat. During an arrhythmia, the

heart can beat too fast, too slow, or with an irregular rhythm. “The

heart's conduction system must function normally for the heart to beat

properly and to pump blood effectively to meet the body's needs.

Problems with the flow of electrical impulses in the heart are called

arrhythmias, which is a general term meaning that there is an

abnormality in the pattern of electrical conduction or electrical

rhythm.”87

The decision to treat an arrhythmia with a pacemaker (or any other

treatment) depends in part upon whether the person has symptoms or

not as well as the severity of the symptoms. There are two primary

types of arrhythmias, bradyarrythmias and tachyarrythmias, which are

discussed below.

Bradyarrhythmias:

Bradyarrhythmias are heart rhythm abnormalities that cause an

abnormally slow heartbeat. Most bradyarrhythmias are due to one of

two kinds of problems: sinus bradycardia or heart block. Sinus

bradycardia occurs when the heartbeat is too slow because the heart's

"natural pacemaker" is operating too slowly. Although some people

(for example, competitive athletes) may have a slow heartbeat as a


result of good health, in others sinus bradycardia is an abnormal

condition that requires treatment.

Heart block is a term for a delay or interruption in the heart's

conduction system, causing the electrical impulses to travel too slowly

or to be stopped. There are several kinds of heart block, classified

according to location (where in the conduction system the block

occurs) and degree (whether the block is mild, causing delayed

conduction, or severe, causing conduction to stop).

In first-degree atrioventricular (AV) block, all electrical impulses reach

the ventricles from the atria, but are abnormally slowed as they pass

through the AV node. In second-degree AV block, some atrial impulses

fail to reach the ventricles ("dropped beats"), resulting in a slow or an

irregular heart rate. In third-degree AV block, the most serious form,

no atrial impulses are conducted to the ventricles. This condition is

sometimes called complete heart block. For the heart to continue to

beat, a separate electrical impulse (called an escape rhythm) may be

generated in the ventricles. Without an escape rhythm, the ventricles

(the chambers that pump blood throughout the body) stop beating.

In right bundle branch block (RBBB), the right bundle branch does not

conduct impulses; the electrical impulses reach the right ventricle only

by traveling through the heart muscle from the left ventricle. As a

result, activation of the right ventricle is delayed. In left bundle branch

block (LBBB), the left bundle branch does not conduct impulses;

electrical impulses reach the left ventricle only by traveling through

the heart muscle from the right ventricle. As a result, activation of the

left ventricle is delayed.87-90


Tachyarrhythmias:

Tachyarrhythmias are heart rhythm abnormalities that cause an

abnormally fast heartbeat. Two tachyarrhythmias that are sometimes

treated with a pacemaker are atrial fibrillation and ventricular

tachycardia.

Atrial fibrillation (AF) is a tachyarrhythmia originating in the atria.

Electrical impulses appear at random in the atria and spread through

the atrial muscle in an irregular, uncoordinated way. The atria "quiver"

rather than contract normally. As a result, blood is not pumped

effectively or regularly into the ventricles. Impulses to the ventricles

may be conducted very rapidly, resulting in a rapid and irregular heart

rate.

Ventricular tachycardia (VT) is a tachyarrhythmia originating in the

ventricles. A repetitive electrical impulse appears somewhere in the

ventricles and spreads through the ventricular muscle. Usually, VT

produces some effective ventricular contractions, but at a rapid rate.

With very rapid VT, blood may not be pumped effectively, and cardiac

arrest may result. Therefore, VT is a potentially dangerous

tachyarrhythmia.91-94

Arrhythmia Symptoms

The symptoms of arrhythmias vary, depending upon the specific

arrhythmia and other factors, especially if there is underlying heart

disease. While some people may have no symptoms, others may have

various symptoms and signs. Symptoms may include:88

Fainting episodes (syncope)

Dizziness or lightheadedness (presyncope)


Palpitations (a sensation of the heart pounding)

Confusion

Extreme fatigue

Shortness of breath

Impaired ability of the heart to pump enough blood to meet the

body's needs (heart failure)

Diagnostic Tests:

The following tests will be used to determine the type of arrhythmia:95

EKG (Electrocardiogram)

Holter and Event Monitors

Echocardiography

Electrophysiology Study

Stress Test

Underlying Causes:

A variety of conditions can lead to the development of cardiac

arrhythmias. Some of the more common causes are included below.96

Coronary artery disease, where there is a malfunction or damage

of the heart due to narrowing or blockage of arteries supplying

blood to heart muscle

Damage from a heart attack and the development of scar tissue

in the muscle of the heart

Certain structural heart malformations present at birth

(congenital heart defects)

Inherited genetic abnormalities that are not necessarily

associated with a structural problem of the heart, but may result

in an arrhythmia (such as the long QT syndrome)


Abnormalities in the control and regulation of the heartbeat by

the nervous system, leading to fainting (called neurocardiogenic

syncope)

Diseases of heart muscle tissue, called cardiomyopathies

Therapy with certain medications that may alter the heart's

normal rhythm

Normal aging of heart muscle

Types of Pacemakers

A variety of types of pacemakers have been developed to restore or

sustain a regular heartbeat in different ways.97

Demand pacemakers monitor the heart's natural electrical

activity and discharge only when the heart's own rate is too slow

or the heart misses a beat.

Fixed-rate pacemakers (which are rarely used today) discharge

impulses at a single, steady rate, regardless of the heart's own

electrical activity.

Rate-responsive pacemakers are designed to raise or lower the

heart rate to help meet the body's needs during physical activity

or rest. These devices also work on "demand."

Temporary pacemakers — Temporary pacemakers are intended

for short-term use during hospitalization. They are used because

the arrhythmia is expected to be temporary and eventually

resolve, or because the person requires temporary treatment

until a permanent pacemaker can be placed. The pulse generator

of a temporary pacemaker is located outside the body, and may

be taped to the skin or attached to a belt or to the patient's bed.

Patients with temporary pacemakers are hospitalized and

continuously monitored. Members of the healthcare team will


perform regular examinations to monitor for any possible

complications.

Permanent pacemakers — Permanent pacemakers are

pacemakers that are intended for long-term use.

Pacemakers may be single, dual, or triple chambered:98

Single-chamber pacemakers have one lead to carry impulses to

and from either the right atrium or right ventricle.

A dual-chamber pacemaker usually has two leads, one to the

right atrium and one to the right ventricle, which can allow a

heart rhythm that more naturally resembles the normal activities

of the heart.

Triple-chambered pacemakers typically have one lead in the

right atrium, one to stimulate the right ventricle, and one to

stimulate the left ventricle. These devices are inserted in

patients who have weakened heart muscle (which results in

heart failure). These pacemakers "resynchronize" the ventricles

and may improve the efficiency of the contraction of the heart,

improving its blood flow.

Indications for Permanent Pacemakers

The following is an explanation of the specific guidelines used when

determining if a permanent pacemaker is appropriate:

“Specific guidelines have been established concerning the

conditions when a permanent pacemaker is (1) definitely

beneficial, useful, and effective, (2) may be indicated, or (3)

is not useful or effective and, in some cases, may be harmful.

Patients should speak with their healthcare provider

concerning these guidelines and how they apply to their


specific case. As a general rule, permanent pacing is

recommended for certain conditions that are chronic or

recurrent and not due to a transient cause. Permanent pacing

may be considered necessary or appropriate for certain

people with symptomatic bradyarrhythmia or, less

commonly, to help prevent or terminate tachyarrhythmia.”83

Absolute indications for pacemaker placement include the following:99

Sick sinus syndrome

Symptomatic sinus bradycardia

Tachycardia-bradycardia syndrome

Atrial fibrillation with sinus node dysfunction

Complete atrioventricular block (third-degree block)

Chronotropic incompetence (inability to increase the heart rate

to match a level of exercise)

Prolonged QT syndrome

Cardiac resynchronization therapy with biventricular pacing

Relative indications include the following:100

Cardiomyopathy (hypertrophic or dilated)

Severe refractory neurocardiogenic syncope

Temporary emergency pacing is indicated for therapy of

significant and hemodynamically unstable bradydysrhythmias

and for prevention of bradycardia-dependent malignant

dysrhythmias.


Implantation Procedure/Guidelines:101

The pacemaker is most commonly implanted into soft tissue

beneath the skin in an area below the clavicle, which is known as

prepectoral implantation; this is located under the skin and fat

tissue but above the pectoral or breast muscle.

The pacemaker leads are typically inserted into a major vein

(transvenously) and advanced until the electrodes are secured

within the proper region(s) of heart muscle. The other ends of

the leads are attached to the pulse generator. Less commonly,

the pulse generator is placed under the skin of the upper

abdomen.

Generally the pacemaker is implanted in a sterile laboratory or

operating room by a specialist (cardiologist, surgeon, or cardiac

electrophysiologist) with experience in this procedure. Local

anesthesia is used to make the procedure as pain-free as

possible. In some cases, sedation or even general anesthesia

may be used. The position of the pacemaker leads is usually

checked using X-ray imaging (called fluoroscopy). The length of

the procedure depends upon the type of device being placed.

Recovery from the procedure is rapid, but there may be some

restrictions on arm movement and activities for the first few

weeks. Lead dislodgement is more common in the first few

weeks after implantation. The hospital stay is usually brief, and

in some cases the procedure can be done as a day surgery.

Uncommon but possible risks associated with permanent


pacemaker implantation include collapsed lung (pneumothorax),

infection, and bleeding.

Once implanted, pacemakers can be programmed to change the

baseline heart rate, the upper heart rate at which the pacemaker

will pace, and heart rate changes that should occur with

exercise.

Although pacemakers are most commonly used for arrhythmia, a

physician may also recommend a pacemaker in instances of:102

Atrial fibrillation – a common heart rhythm disorder in which the

upper chambers of the heart beat rapidly and chaotically.

Sometimes people with atrial fibrillation can also have slow

rhythms. Medicines used to control atrial fibrillation may result in

slow rhythms, which are treated by pacemakers.

Heart failure – a condition in which the heartbeat is not sufficient

to supply a normal volume of blood and oxygen to the brain and

other parts of the body. A special pacemaker can be carefully

programmed to increase the force of muscle contractions in the

heart. This is called “biventricular pacing” or “resynchronization”

therapy.

Syncope – a condition best known as the common faint, is

usually not serious. Some patients faint when their heart rhythm

becomes very slow. For a small percentage of people who

experience severe and frequent fainting spells, a pacemaker may

prevent the heart rate from slowing to the point of fainting.


Aging or heart disease damages the sinus node's ability to set

the correct pace for the heartbeat. Such damage can cause

slower than normal heartbeats or long pauses between

heartbeats. The damage also can cause the heart to switch

between slow and fast rhythms. This condition is called sick

sinus syndrome.

The patient has had an atrial fibrillation. A pacemaker can help

regulate the heartbeat after the procedure.

The patient is required to take certain heart medicines, such as

beta-blockers, which can slow the heartbeat too much.

The patient faints or has other symptoms of a slow heartbeat.

The patient has heart muscle problems that cause electrical

signals to travel too slowly through the heart muscle. The

pacemaker may provide cardiac resynchronization therapy (CRT)

for this problem. CRT devices coordinate electrical signaling

between the heart's lower chambers.

The patient has long QT syndrome, which puts him or her at risk

for dangerous arrhythmias.

Physicians also may recommend pacemakers for people who

have certain types of congenital heart disease or for people who

have had heart transplants. Children, teens, and adults can use

pacemakers.


Types of Pacemaker Programming

The two main types of programming for pacemakers are:103

Demand Pacing

A demand pacemaker monitors a person’s heart rhythm. It only

sends electrical pulses to the heart if the heart is beating too

slow or if it misses a beat.

Rate-responsive

A rate-responsive pacemaker will speed up or slow down the

heart rate depending on how active the patient may be. To do

this, the device monitors the sinus node rate, breathing, blood

temperature, and other factors to determine a person’s activity

level.

Procedure:

Placing a pacemaker requires minor surgery. The surgery usually is

done in a hospital or special heart treatment laboratory.99

Before the surgery, an intravenous (IV) line will be inserted into

one of the veins. The patient will receive medicine through the

IV line to help him or her relax.

The surgeon will numb the area where he or she will put the

pacemaker so the patient doesn’t feel any pain. The surgeon

may also give antibiotics to prevent infection.

A needle will be inserted into a large vein, usually near the

shoulder opposite the dominant hand. The needle will be used to

thread the pacemaker wires into the vein and to correctly place

them in the heart.

An x-ray will track the wires as they pass through the vein and

into the heart will so that they can be placed properly. Once the


wires are in place, the doctor will make a small cut into the skin

of the chest or abdomen.

The pacemaker's small metal box will be inserted through the

cut, placed just under the skin, and connected it to the wires

leading to the heart. The box contains the pacemaker's battery

and generator.

Three basic types exist to serve different purposes, which are

described below.101

Single-Chamber Pacemakers

In a single-chamber pacemaker, only one wire (pacing lead) is

placed into a chamber of the heart. Sometimes it is the upper

chamber, or atrium. Other times it is the lower chamber, or

ventricle.

Dual-Chamber Pacemakers

In dual chamber pacemakers, wires are placed in two chambers

of the heart. One lead paces the atrium and one paces the

ventricle. This approach more closely matches the natural pacing

of the heart. This type of pacemaker can coordinate function

between the atria and ventricles.

Rate-Responsive Pacemakers

These have sensors that automatically adjust to changes in a

person's physical activity.


Other devices

Some devices, such as implantable cardioverter defibrillators

(ICDs), designed primarily for other purposes, can function as

pacemakers in certain situations.

Guidelines for Pacemaker Use

Patients with pacemakers are advised to avoid electromagnetic

interference. Although contemporary pacemakers are less susceptible

to interference than older models, electromagnetic energy can

interfere in some cases. Thus, experts advise that individuals with

pacemakers be aware of the following:85

Household appliances

Pacemaker manufacturers do not recommend any special

precautions when using normally functioning common household

appliances such as microwave ovens, televisions, radios,

toasters, and electric blankets.

Cellular phones

Due to the growing use of hand-held cellular phones, patients

must be aware of their potential adverse effects. As examples,

evidence suggests that cellular phones do not cause interference

with permanent pacemakers. While some older generation

pacemakers and implantable cardioverter-defibrillators (ICDs)

did occasionally experience interference from cellular telephones,

clinical experience suggests that there is no significant

interference between pacemakers or ICDs and modern wireless

communication devices or portable media players.


Anti-theft systems

Electromagnetic anti-theft security systems are often found in or

near the workplace, at airports, in stores, at courthouses, or in

other high-security areas. Although interference with a

pacemaker is possible, it is unlikely that any clinically significant

interference would occur with the transient exposure associated

with walking through such a field. Based upon several studies

and observations, experts advise that patients with pacemakers

should:

o Be aware of the location of anti-theft systems and move

through them at a normal pace

o Avoid sitting or standing close to an anti-theft system

Metal detectors at airports

Similar to antitheft systems, metal detectors at airports can

potentially interfere with pacemakers, although this is unlikely.

Such exposure has been shown to cause interference in some

cases and may be related to the duration of exposure and/or

distance between the security system and the pacemaker. Metal

detectors will likely be triggered by the presence of a pacemaker

and therefore at places such as airports, it will be important for

individuals with pacemakers to carry an identification card for

their pacemaker, and airport personnel will likely prefer to do a

manual search.

External electrical equipment

External electrical fields do not seem to cause a problem for

most people with a pacemaker. However, in workplaces that


contain welding equipment or strong motor-generator systems,

because interference can inhibit pacing, it is recommended that

a person with an implanted cardiac device remain at least two

feet from external electrical equipment, verify that the

equipment is properly grounded, and leave the immediate locale

if lightheadedness or other symptoms develop.

Diagnostic or therapeutic procedures

Certain types of surgery and procedures may interfere with

pacemakers. Most importantly, the use of electrocautery can

inhibit pacemaker function. It is not uncommon therefore that a

pulse generator may require specific reprogramming before the

procedure and programming back to its baseline condition after

the procedure. In some instances, a magnet is all that is

required on the device to make sure that there is no problem

with the device during the procedure. Such procedures include:

o Magnetic resonance imaging (MRI), which uses a strong

magnetic field that is pulsed on and off at a rapid rate. For

most patients with a pacemaker, this procedure is

contraindicated.

o Transcutaneous electrical nerve/muscle stimulators

(TENS), which is a method of pain control.

o Diathermy, which heats body tissues with high-frequency

electromagnetic radiation or microwaves.

o Extracorporeal shock wave lithotripsy, the use of sound

waves to break up gallstones and kidney stones.

o Therapeutic radiation for cancer or tumors, which can

cause permanent pacemaker damage.


o Any surgery in which electrocautery is being used. The

risks are greatest when the electrocautery is being

performed close to the pulse generator.

Pacemaker complications include the following:104

Pneumothorax

Pericarditis

Infection

Skin erosion- Erosion of the pacer through the skin, while rare,

requires device replacement and systemic antibiotics.

Hematomas may be treated with direct pressure and

observation, rarely requiring surgical drainage.

Hematoma

Lead dislodgment - Lead dislodgment generally occurs within 2

days of device implantation pacer and may be seen on chest

radiography. Alternatively, fluctuating impedance may be a

subtle clue, as the patient may have normal impedance when

the lead is in contact with the endocardium, but infinite (or very

high) impedance when the lead is dislodged.

Venous thrombosis

Free-floating ventricular leads may trigger malignant

arrhythmias. Device-associated venous thrombosis is rare but

generally presents as unilateral arm edema. Treatment includes

extremity elevation and anticoagulation.

Major pacemaker malfunctions include the following:83

Failure to output

Failure to capture

Failure to sense


Pacemaker-mediated tachycardia

Runaway pacemaker

Pacemaker syndrome

Twiddler's syndrome

Cardiac monitor pseudomalfunction

Pacemaker pseudomalfunction

Implantable Cardioverter Defibrillator

An implantable cardioverter-defibrillator (ICD) is a device that is used

to treat a cardiac tachydysrhythmia. It is a type of permanent

pacemaker that is used to provide electrical stimuli, which causes

cardiac contraction when intrinsic myocardial electrical activity is

inappropriately slow or absent.105

Indications for Use

Indications for implantable cardioverter-defibrillator (ICD) implant can

be divided into two broad categories:106

Secondary prophylaxis against sudden cardiac death:

Multiple studies have shown the ICD to be superior to

antiarrhythmic drug therapy in patients with a history of life-

threatening VT and VF. Therefore, the indications for secondary

prophylaxis are well supported by clinical evidence gained from

randomized clinical trials. An ICD is recommended as initial

therapy in survivors of cardiac arrest due to VF or

hemodynamically unstable VT.

Published guidelines exclude cases in which there are

“completely reversible causes.” The exclusion for completely


reversible causes is somewhat controversial. As an example, an

acute MI predisposes to polymorphic VT, and the culprit lesion

may be reversed with intracoronary stenting. However, we know

that any patient who presents with an MI is at increased risk of

recurrent MI, which may again precipitate an unstable

ventricular arrhythmia.

One school of thought suggests that such patients should

undergo ICD implant, even though the cause of cardiac arrest is

completely reversible, because the risk of recurrence is

increased. In another example, consider cardiac arrest

secondary to transient prolongation of the QT interval, perhaps

secondary to drug therapy. QT interval prolongation increases

the risk of torsades de pointes, a potentially life-threatening

arrhythmia.

Withdrawal of the offending agent may normalize the QT

interval, thereby reversing the cause of cardiac arrest. However,

such a patient remains at risk of recurrent QT prolongation and

subsequent cardiac arrest, perhaps from an electrolyte

disturbance or as a result of ingestion of a different QT-

prolonging agent.

Primary prophylaxis:

Indications for primary prophylaxis account for most of ICD

implants, even though the evidence for such implants is often

less well established. Indications for an ICD implant as primary

prophylaxis against sudden cardiac death are listed below. The


indications are listed as Class I or Class IIa, as classified by the

ACC/AHA 2008 guidelines.

Class I means that the treatment is useful, that its benefit

greatly outweighs the risk, and that it should be administered.

Class IIa means that the benefit outweighs the risk and it is

reasonable to administer the treatment. Class IIb means that the

benefit probably outweighs the risk and that the treatment may

be considered. Class III means that the risk outweighs the

benefit, and the treatment should not be performed. Only Class I

and Class IIa indications are included in the table. For a

complete list, the reader is referred to the American College of

Cardiology (ACC)/American Heart Association (AHA) 2008

guidelines.

The greatest predictors of risk for sudden cardiac death include

left ventricular systolic function and heart failure symptoms. The

vast majority of investigational studies have quantified left

ventricular systolic function using the measure of left ventricular

ejection fraction (LVEF). The most widely used form of heart

failure symptom classification is the New York Heart Association

(NYHA) functional class classification system, which classifies

mild to no symptoms as Class I, and the most severe symptoms

as Class IV.107

Indications for ICD placement

Currently, indications for primary prophylaxis account for most of ICD

implants, even though the evidence for such implants is often less well

established. Class I indications (i.e., the benefit greatly outweighs the


risk, and the treatment should be administered) are listed below and

outlined in the following table:108,109

Structural heart disease, sustained VT

Syncope of undetermined origin, inducible VT or VF at

electrophysiologic study (EPS)

Left ventricular ejection fraction (LVEF) < 35% due to prior MI,

at least 40 days post-MI, NYHA class II or III

LVEF ≤35%, NYHA class II or III

LVEF ≤30% due to prior MI, at least 40 days post-MI

LVEF < 40% due to prior MI, inducible VT or VF at EPS

Class IIa indications (i.e., the benefit outweighs the risk and it is

reasonable to administer the treatment) are as follows:

Unexplained syncope, significant LV dysfunction, nonischemic

cardiomyopathy

Sustained VT, normal or near-normal ventricular function

Hypertrophic cardiomyopathy with 1 or more major risk factors

Arrhythmogenic right ventricular dysplasia/cardiomyopathy

(ARVD/C) with 1 or more risk factors for sudden cardiac death

(SCD)

Long QT syndrome, syncope or VT while receiving beta-blockers

Nonhospitalized patients awaiting heart transplant

Brugada syndrome, syncope or VT

Catecholaminergic polymorphic VT, syncope or VT while

receiving beta-blockers

Cardiac sarcoidosis, giant cell myocarditis, or Chagas disease


Indication Classification Supporting Studies

Structural heart disease, sustained VT Class I AVID, CASH, CIDS

Syncope of undetermined origin,

inducible VT or VF at EPS

Class I CIDS

LVEF < 35% due to prior MI, at least

40 days post-MI, NYHA Class II or III

Class I SCD-HeFT

LVEF ≤35%, NYHA Class II or III Class I SCD-HeFT

LVEF ≤30% due to prior MI, at least

40 days post-MI

Class I MADIT II

LVEF < 40% due to prior MI, inducible

VT or VF at EPS

Class I MADIT, MUSTT

Unexplained syncope, significant LV

dysfunction, nonischemic CM

Class IIa Expert opinion

Sustained VT, normal or near-normal

ventricular function


Hypertrophic CM with 1 or more major

risk factors


Arrhythmogenic right ventricular

dysplasia/cardiomyopathy (ARVD/C)

with 1 or more risk factors for sudden

cardiac death (SCD)


Long QT syndrome, syncope or VT

while receiving beta blockers

Class IIa Zareba et al, Viskin et

al., Goel et al., Monnig

et al., Goldenberg et al.,

Hobbs et al.


Nonhospitalized patients awaiting

heart transplant


Brugada syndrome, syncope Class IIa Expert opinion

Brugada syndrome, VT Class IIa Expert opinion

Catecholaminergic polymorphic VT,

syncope or VT while receiving beta

blockers


Cardiac sarcoidosis, giant cell

myocarditis, or Chagas disease


ICD Complications and Malfunctions:

Several complications of implantable cardioverter-defibrillators (ICD)

implant have been described, some of which are currently tracked in a

national database of ICD implants.

Acute surgical complications include the following:

Pain

Bleeding

Pneumothorax

Hemothorax

Cardiac perforation with or without pericardial effusion and

tamponade (sometimes requiring urgent drainage)

Pulseless electrical activity following intraoperative defibrillation

threshold testing111


An analysis of more than 350,000 ICD implantations included in the

National Cardiovascular Data Registry – ICD Registry revealed 3.1% of

patients experienced in-hospital adverse events, 1.2% experienced

major adverse events, and 0.4% died. Adverse events were lower

(1.9%) with single-chamber ICD implants than with dual-chamber ICD

implants (2.9%) or with biventricular ICD implants (4.1%). Specific

adverse event rates included lead dislodgement (1%), hematoma

(0.9%), pneumothorax (0.4%), and cardiac arrest (0.3%).112

Physician level of training and level of specialty certification have been

shown to affect the risk of adverse events associated with ICD implant.

An ICD Registry analysis found that physicians who implant more ICDs

have lower rates of procedural complications and in hospital mortality.

Implant volume may partially explain the difference in adverse events

among physicians with different specialty certifications. However, no

inverse relationship was found between procedure volume and adverse

event rate observed within the board certified category.105

Subacute and chronic complications

Subacute ICD complications include the following:

Pain

Infection

Pocket hematoma

Wound dehiscence

Lead dislodgment

Deep venous thrombosis

Upper extremity edema

Degradation of lead function


Chronic complications include the following:113

Device-related pain

Lead fracture

Inappropriate shocks

Erosion of device through skin

Immunologic rejection – Rare

Other complications include the following:

Infection - ICD infection rates are higher in patients undergoing

generator replacement compared with de novo implant. A

prospective study revealed an infection rate of 1.3% in patients

undergoing device replacement. In this study, postoperative

hematoma significantly increased the risk of infection (22.7% vs.

0.98%).108

Inappropriate shocks - One of the risks of ICD implant is that of

inappropriate ICD shocks. An inappropriate ICD shock is one that

is not precipitated by accurate detection of a malignant

ventricular arrhythmia, VT, or VF. Typically, inappropriate ICD

shocks result when atrial arrhythmias, such as atrial fibrillation,

atrial tachycardia, or atrial flutter, accelerate the ventricular rate

beyond the set limit for delivery of ICD shock therapy. However,

inappropriate shocks may also result from sinus tachycardia,

supraventricular tachycardia (SVT), illicit drug use (as with

cocaine and methamphetamine), and ventricular oversensing.

Ventricular oversensing may occur due to T-wave oversensing,

electromagnetic interference (EMI), a loose setscrew in the ICD

header, or ICD lead fracture. Analysis of the MADIT II trial data

revealed that 11.5% of the ICD patients received inappropriate


ICD shocks and that 31.2% of all ICD shocks were deemed

inappropriate.

Inappropriate ICD shocks were attributed to atrial fibrillation

(44%), supraventricular tachycardia (36%), and abnormal

sensing (20%). Patients with inappropriate shocks had greater

all-cause mortality. Drug therapy with hydroxymethylglutaryl-

coenzyme A reductase inhibitors, or so-called statins, has been

shown to reduce, by more than half, the frequency of

inappropriate ICD shocks secondary to occurrence of atrial

fibrillation and atrial flutter. There is some indirect evidence that

the incidence of inappropriate shocks may be lower in patients

with dual-chamber devices compared with patients who receive

single-chamber devices.114

Failure to shock and ineffective cardioversion - Failure to deliver

a shock may be caused by failure to sense, lead fracture, EMI,

and inadvertent ICD deactivation. Management includes external

defibrillation or cardioversion and antidysrhythmic medications.

Ineffective cardioversion may result from inadequate energy

output, rise in defibrillation threshold (possibly due to an

antiarrhythmic medication, such as amiodarone, flecainide, or

phenytoin), myocardial infarction at the lead site, lead fracture,

insulation breakage, scarring at the lead implantation site, and

lead dislodgment.

Many ICDs deliver a programmed set of therapies per

dysrhythmic episode. The number of therapies per episode is

programming specific. If a delivered therapy does not terminate


the arrhythmia, the device proceeds to the next programmed

therapy. For example, a total of 6 attempts at defibrillation are

attempted per episode of ventricular fibrillation. The device

attempts defibrillation and then reevaluates the cardiac rhythm.

If the arrhythmia persists, it delivers therapy number 2 and so

on until all 6 attempts have been delivered. Once this occurs,

the device does not deliver therapy until a new episode is

declared.

Initial therapy for ventricular tachycardia (VT) may be

antitachycardia pacing (also known as overdrive pacing) rather

than cardioversion. ICDs do not prevent all sudden deaths, and

acknowledging that cardiac arrest is not necessarily an ICD

malfunction is important. The device may have properly

delivered the required shocks for the triggering rhythm but still

have been ineffective in resolving it.106

Sprint Fidelis lead fracture - In July 2007, a higher than

expected rate of Sprint Fidelis model 6949 ICD lead fractures

were reported. Six patients presented with lead failure 4-23

months after implant. A subsequent database search for similar

reports revealed that 33% of affected patients had inappropriate

ICD shocks. Analysis of affected leads revealed 33% with high

lead impedance and a 35% rate of pace-sense and high-voltage

conductor fracture.110


Implantation risk evaluation

The acute risk of ICD implantation is small but is increased by multiple

factors. The following are risk factors established by an ICD registry

risk score model:108

Age greater than 70 years - 1 point

Female - 2 points

NYHA class III - 1 point

NYHA class IV - 3 points

Atrial fibrillation - 1 point

Prior valve surgery - 3 points

Chronic lung disease - 2 points

Blood urea nitrogen (BUN) > 30 mg/dL - 2 points

Reimplantation for reasons other than battery change - 6 points

Dual chamber ICD type - 2 points

Biventricular ICD type - 4 points

Nonelective ICD implant -3 points

The risk of any inhospital complication increases from 0.6%

among patients with a score of less than 5 to 8.4% among the

patients with greater than 19 risk points.

Goals Of Cardiac Rehabilitation

There are a number of different goals associated with cardiac

rehabilitation. The specific goals will depend on the cardiac condition,

the status of the patient, and the lifestyle goals of the patient (i.e.,

return to work). The rehabilitation team will work with each patient to

determine his or her goals and develop a concrete set of attainable

goals.


General Goals or Indications

The following bullets provide information regarding the main uses and

indications for cardiac rehabilitation. Cardiac rehabilitation is now a

Class I Indication in clinical guidelines for:7

Myocardial infarction (MI)

Percutaneous Coronary Intervention (PCI)

Coronary artery bypass grafting (CABG)

Angina

Heart failure

Valvular heart disease

Peripheral arterial disease (PAD)

The Performance Measures Set 1 (referral to CR from both an

inpatient and outpatient setting) has been endorsed by the

National Quality Forum (NQF).

The demonstrated evidence-based benefits of Cardiac Rehabilitation

include the following:10

20-30% reduction in all-cause mortality rates

Decreases mortality at up to 5 years post participation

Reduced symptoms (angina, dyspnea, fatigue)

Reduction in nonfatal recurrent myocardial infarction over

median follow-up of 12 months

Improves adherence with preventive medications

Increased exercise performance

Improved lipid panel (total cholesterol, HDL [good cholesterol],

LDL [bad cholesterol], and triglycerides)

Increased knowledge about cardiac disease and its management

Enhanced ability to perform activities of daily living

Improved health-related quality of life


Improved psychosocial symptoms (reversal of anxiety and

depression, increased self-efficacy)

Reduced hospitalizations and use of medical resources

Return to work or leisure activities

Increase Physical Fitness

An increase in physical fitness can benefit most individuals with

cardiovascular disease, including those who have been diagnosed with

heart failure. The specific exercise regimen will vary depending on the

needs and abilities of the individual, but all regimens will provide

additional benefits during the recovery or maintenance stage. One of

the primary benefits that occurs during an increase in physical fitness

is that the patient will experience an increased ability to use oxygen to

derive energy for work.115

Exercise training increases maximum ventilatory oxygen uptake by

increasing both maximum cardiac output (the volume of blood ejected

by the heart per minute, which determines the amount of blood

delivered to the exercising muscles) and the ability of muscles to

extract and use oxygen from blood. Beneficial changes in

hemodynamic, hormonal, metabolic, neurological, and respiratory

function also occur with increased exercise capacity. These changes

can also benefit persons with impaired left ventricular function, in

whom most adaptations to exercise training appear to be peripheral

and may occur with low-intensity exercise.116

An increase in physical fitness also produces decreased myocardial

oxygen demands for the same level of external work performed. This

is demonstrated by a decrease in the product of heart rate × systolic


arterial blood pressure (an index of myocardial oxygen demand).

These changes are also beneficial in persons with coronary artery

disease, who after exercise training may attain a higher level of

physical work before reaching the level of myocardial oxygen

requirement that results in myocardial ischemia.117

Another benefit that occurs when patients increase their physical

fitness through regular exercise training is a favorable alteration in

lipid and carbohydrate metabolism. The exercise-induced increase in

high-density lipoproteins is strongly associated with changes in body

weight, and greater increases in high-density lipoproteins have been

found in women who exercise at higher levels of recreational

running.118 Increased physical fitness in overweight women and men

enhances the beneficial effect of a low-saturated fat and low-

cholesterol diet on blood lipoprotein levels. Increased endurance

training in those who can tolerate it, will have a positive effect on

adipose tissue distribution.

This effect on adipose tissue distribution is likely to be important in

reducing cardiovascular risk. Exercise training and an increase in

general physical fitness is also shown to have a significant impact on

insulin sensitivity.12 In addition, intense endurance training has been

shown to initiate a highly significant salutary effect on fibrinogen levels

of healthy older men. Recent studies have shown that physical activity

plays an important role in the prevention and treatment of

osteoporosis and certain neoplastic diseases, especially colon cancer.

The following is a list of important points to consider regarding

physical fitness programs:119


Developing and maintaining aerobic endurance, joint flexibility,

and muscle strength is important in a comprehensive exercise

program, especially as people age.

Elderly women and men show comparable improvement in

exercise training, and adherence to training in the elderly is

high.

Resistance training exercise alone has only a modest effect on

risk factors compared with aerobic endurance training, but it

does aid carbohydrate metabolism through the development or

maintenance of muscle mass and effects on basal metabolism.

Furthermore, resistance training is currently recommended by

most health promotion organizations for its effects on

maintenance of strength, muscle mass, bone mineral density,

functional capacity, and prevention and/or rehabilitation of

musculoskeletal problems (i.e., low back pain).

In the elderly, resistance training is both safe and beneficial in

improving flexibility and quality of life. Persons with

cardiovascular disease are usually asked to refrain from heavy

lifting and forceful isometric exercises, but moderate-intensity

dynamic strength training is safe and beneficial in persons at low

risk.

Many activities of daily living require more arm work than leg

work. Therefore, persons with coronary artery disease are

advised to use their arms as well as their legs in exercise

training. The arms respond like the legs to exercise training both


quantitatively and qualitatively, although ventilatory oxygen

uptake is less with arm ergometry.

Although peak heart rates are similar with arm and leg exercise,

heart rate and blood pressure response during arm exercise is

higher than leg exercise at any submaximal work rate.

Therefore, target heart rates are designated 10 beats per minute

lower for arm training than for leg training. Dynamic arm

ergometry is usually well tolerated by persons with coronary

artery disease; however, there may be an increase in blood

pressure that may be of concern in certain persons.

Maximum ventilatory oxygen uptake drops 5% to 15% per

decade between the ages of 20 and 80, and a lifetime of

dynamic exercise maintains an individual's ventilatory oxygen

uptake at a level higher than that expected for any given age.

The rate of decline in oxygen uptake is directly related to

maintenance of physical activity level, emphasizing the

importance of physical activity.

Middle-aged men and women who work in physically demanding

jobs or perform moderate to strenuous recreational activities

have fewer manifestations of coronary artery disease than their

less active peers. Meta-analysis studies of clinical trials reveal

that medically prescribed and supervised exercise can reduce

mortality rates of persons with coronary artery disease.

In addition to the physical benefits of exercise, both short-term

exercise and long-term aerobic exercise training are associated


with improvements in various indexes of psychological

functioning. Cross-sectional studies reveal that, compared with

sedentary individuals, active persons are more likely to be better

adjusted, to perform better on tests of cognitive functioning, to

exhibit reduced cardiovascular responses to stress, and to report

fewer symptoms of anxiety and depression.

Exercise training reduces depression in healthy older men and in

persons with cardiac disease or major depression. Exercise also

improves self-confidence and self-esteem, attenuates

cardiovascular and neurohumoral responses to mental stress,

and reduces some type A behaviors.

Although exercise training generally has not been found to

improve cognitive performance, short bouts of exercise may

have short-term facilitative effects.

It is estimated that only 50% of all persons who initiate an

exercise program will continue the habit for more than 6

months. The issue of nonadherence is particularly important

because exercise is only beneficial if it is maintained for

extended periods of time. Thus, it is important to develop

strategies to improve exercise initiation and adherence,

especially for persons who are among the least active—some

African-American women, the less educated, the obese, and the

elderly.

Persons of all ages should include physical activity in a

comprehensive program of health promotion and disease


prevention and should increase their habitual physical activity to

a level appropriate to their capacities, needs, and interest.

Activities such as walking, hiking, stair-climbing, aerobic

exercise, calisthenics, resistance training, jogging, running,

bicycling, rowing, swimming, and sports such as tennis,

racquetball, soccer, basketball, and “touch” football are

especially beneficial when performed regularly. Brisk walking is

also an excellent choice. The training effect of such activities is

most apparent at exercise intensities exceeding 40% to 50% of

exercise capacity. (Exercise capacity is defined as the point of

maximum ventilatory oxygen uptake or the highest work

intensity that can be achieved).

Evidence supports that even low- to moderate-intensity activities

performed daily can have some long-term health benefits and

lower the risk of cardiovascular disease.

Low-intensity activities generally range from 40% to 60% of

maximum capacity. The 40% to 60% of maximum capacity

range is similar for young, middle-aged, and elderly persons.

Such activities include walking for pleasure, gardening, yard

work, housework, dancing, and prescribed home exercise.

For health promotion, dynamic exercise of the large muscles for

extended periods of time (30 to 60 minutes, three to six times

weekly) is recommended. This may include short periods of

moderate intensity (60% to 75% of maximal capacity) activity

(approximately 5 to 10 minutes) that total 30 minutes on most


days. Resistance training using eight to 10 different exercise sets

with 10 to 15 repetitions each (arms, shoulders, chest, trunk,

back, hips, and legs) performed at a moderate to high intensity

(for example, 10 to 15 pounds of free weight) for a minimum of

2 days per week is recommended.

Physical activity may have risks as well as benefits, although

risks are relatively infrequent. Estimates of sudden cardiac death

rates per 100 000 hours of exercise range from 0 to 2 per

100 000 in general populations and from 0.13 per 100 000 to

0.61 per 100 000 in cardiac rehabilitation programs. Studies

have also demonstrated the cardiovascular safety of maximum

strength testing and training in healthy adults and low-risk

cardiac patients. Falls and joint injuries are additional risks

associated with physical activity (especially in older women), but

most of these injuries do not require medical treatment. The

incidence of such complications is less in those participating in

low-impact activities such as walking.

Improve Physical and Mental Health

There is evidence to show that comprehensive cardiac rehabilitation

programs, including exercise training, can reduce smoking, alter lipid

profiles, reduce blood pressure, favorably alter body weight and

increase physical activity. Improvements in psychosocial outcomes

have also been shown. The following table provides an overview on the

goals and benefits in each of these areas:5.14.116.121-129


Smoking

Strong advice from physicians to stop smoking, especially in

hospital, has been shown to be important. In one uncontrolled

study, such physician recommendations, coupled with follow-up

advice from nurses, were associated with a one-year self-reported

quit rate of 62%.

In another study of patients who had undergone coronary bypass

surgery, reduced smoking rates were found at one year in the

group randomly allocated to a program of exercise training and

education, coupled with physician advice to stop smoking,

compared with the control group.

Spousal support has been shown to facilitate smoking cessation in

cardiac patients. In a randomized controlled study of inpatient

group education followed by weekly telephone calls for six weeks

after discharge from hospital, results showed a significantly

greater decrease in smoking and unhealthy eating habits, and a

significantly greater increase in physical activity, among patients

whose partners also participated in the program.

While there were no overall differences at 12 months between the

intervention and control groups, a greater rate of smoking

cessation was found in the intervention group among patients

whose partners had participated. In general, evidence suggests

that interventions to reduce smoking are more likely to be

effective if they are initiated in hospital when patients are more

highly motivated rather than after discharge from hospital.

Further, a meta-analysis of controlled trials of cardiac patient

education concluded that while interventions, on average, showed

no significant impact on smoking behavior, behaviorally oriented

interventions generally produced better outcomes. Behavioral

strategies, such as regular reinforcement of advice to stop

smoking and continuing support, appear necessary.


The positive studies described above indicate that follow-up

telephone contact by nurses is a convenient, inexpensive and

effective method of reinforcing physician advice to stop smoking.

Lapses tend to occur when interventions cease. Instructing

patients in relapse prevention methods before they lapse is

therefore of critical importance.

Lipids

Patients who participated in an educational program by mail and

telephone reported a significant decrease in dietary fat intake

after six months compared with a control group receiving usual

care, but no significant differences were found between groups in

cholesterol levels. Beneficial effects upon lipid levels have been

reported from interventions combining education and behavioral

strategies with the use of lipid lowering drugs. A large study of a

home-based multifactorial intervention combining education,

counseling and lipid lowering medication achieved a significant

mean reduction in total cholesterol and dietary fat intake in the

treatment group after four years, compared with the control

group.

Another multifactorial intervention, which included lipid-lowering

medication, also reported a significant reduction in serum

cholesterol levels in the intervention group compared with the

control group. A recent randomized controlled trial studied the

effects of diet alone, a combination of diet and exercise, exercise

alone and usual care in men and postmenopausal women with low

levels of HDL cholesterol and raised LDL cholesterol. This study

showed that the Step 2 diet of the US National Cholesterol

Education Program was ineffective in lowering LDL cholesterol

unless it was coupled with exercise training.

Similarly, a nonrandomized controlled study reported significant

improvements in lipid levels from a combination of education,

counseling and exercise compared with exercise alone.


Blood

pressure

The effectiveness of antihypertensive drugs in lowering blood

pressure is well established. Further, beneficial effects upon blood

pressure in cardiac patients have been reported from two

multifactorial interventions including exercise training. One

randomized controlled trial of a multifactorial intervention

including lifestyle advice, which was reinforced during the four

year follow-up, produced significant benefits in reduction of blood

pressure in cardiac patients in the intervention group compared

with the control group. A significant reduction in blood pressure

was also reported in a multifactorial intervention involving

exercise, education and support. However, in another randomized

controlled trial of exercise training and education, there was no

impact upon blood pressure levels.

A further multifactorial intervention of stress management,

exercise, intensive dietary restriction and support produced no

significant impact on blood pressure levels, with both the

intervention and control groups showing a decrease in blood

pressure at one year.

Education and behavioral interventions for weight reduction,

physical activity and moderation of dietary sodium and alcohol

consumption are recommended as definitive or adjunctive therapy

for hypertension. They are important components of a

multifactorial approach to reduce hypertension in cardiac patients.

Body weight

Dietary education, counseling and behavioral interventions

designed to reduce body weight can help patients lose weight and

should be provided as part of comprehensive cardiac

rehabilitation. Education as a sole intervention is unlikely to

achieve and maintain weight loss. Several studies have reported a

reduction in body weight as a result of comprehensive cardiac

rehabilitation programs which include exercise, education,

counseling and behavioral interventions.


A randomized controlled trial conducted over four years

demonstrated a statistically significant body weight reduction of 4

% in the intervention group compared with the control group.

Patients in the intervention group received individual advice

regarding lifestyle modification, which incorporated goal setting, a

monitored home exercise program, follow-up by mail, telephone

contact and regular visits to the clinic for follow-up.

Considerable weight loss occurred amongst the dedicated subjects

enrolled in a study of a one-year intervention including a low fat

vegetarian diet, group discussion for social support, stress

management and exercise. Significantly greater weight loss was

also reported in the treatment group in two further studies, and in

another study, a reduction in body fat was achieved in subjects

receiving the intervention.

In all three studies, however, the mean weight loss was less than

3 kg. A significant reduction in body mass index, percentage of

body fat and other measures was reported in one study and in

another, in percentage of body fat in women. Other studies

involving exercise reported no changes in body weight.

A randomized controlled study comparing exercise training alone,

exercise training plus group education and counseling, and a

control group found no significant differences between groups in

weight loss after three and six months. Positive results were

reported from three studies, which did not involve exercise.

Another randomized controlled trial reported a significant

reduction in mean body weight at one to 10 year follow-up in

patients in the intervention group receiving nutritional counseling

compared with the control group. In that study, the intervention

was intensive for the first three months, followed by a continued

intervention for three years.


Psychosocial

well-being

Education, counseling and behavioral interventions, either alone

or as part of multifactorial interventions, improve psychological

wellbeing and improve quality of life. They should therefore be

integral parts of comprehensive cardiac rehabilitation programs.

Psychological disability has long been recognized as a greater

barrier to recovery than physical impairment. Thus, an important

aim of cardiac rehabilitation programs should be to improve the

psychological wellbeing of patients.

The psychological benefits of exercise training are widely

acknowledged. An important issue is whether specific education,

counseling or behavioral interventions enhance psychological

wellbeing, additional to those benefits achieved through exercise

training.

Stress

The aims of stress management programs are to assist the

patient to identify stressors, to recognize characteristic emotional

and physical responses to stress, to decrease levels of general

arousal and to develop effective coping strategies. Through the

use of various techniques including relaxation therapy,

meditation, cognitive therapy, anxiety management and

biofeedback, the patient is taught how to reduce stressful

reactions by altering stress-inducing perceptions of situations.

By acquiring more effective coping skills, maladaptive responses

to stress may be reduced.

Several studies have reported benefits from relaxation therapy. In

one study, patients who received cognitive training early after

myocardial infarction had greater confidence in their ability to

control their stress than those who received relaxation therapy.

In another, relaxation training was found to enhance the

psychological effects of exercise training.


In a study involving monthly monitoring of stress levels of

patients and home nursing visits for those with high stress scores,

a significant reduction in stress scores was found as well as a

significantly reduced rate of long-term recurrence of acute

myocardial infarction and a marginal impact on cardiac mortality

during the first year after infarction. Little impact was observed

on those with low levels of stress in hospital. The authors

concluded that patients who can benefit from such an intervention

may be identified in hospital.

Summary

Patients with a cardiac condition must be assessed to ensure that he

or she is a candidate for a cardiac rehabilitation program. There are a

number of conditions require cardiac rehabilitation, and, likewise, a

number of different goals associated with cardiac rehabilitation. The

specific goals depend upon the cardiac condition, the status of and the

lifestyle goals of the patient. The cardiac rehabilitation team is trained

to work with each patient to determine his or her goals and to develop

a concrete set of individual attainable goals.

The primary goal of cardiac rehabilitation programs is to reduce

cardiac symptoms in patients. However, the specific goals will differ

depending on the type and severity of cardiac condition. In some

instances, the goal will be to eliminate the cardiac condition. In other

instances, the goal will be to maintain a level of health that prevents

further damage from the cardiac condition.116 Prior to initiating a

cardiac rehabilitation program, the medical provider will need to work

with the patient to determine the specific treatment goals. Throughout


the course of treatment, the patient is assessed and monitored to

ensure goals are being met.120 This course addressed the cardiac

conditions that would benefit from patient participation in a cardiac

rehabilitation program. The history and role of cardiac rehabilitation is

a lengthy topic recommended for further reading by the interested

learner.

There are a number of different goals associated with cardiac

rehabilitation. The specific goals will depend on the cardiac condition,

the status of the patient, and the lifestyle goals of the patient (i.e.,

return to work). The rehabilitation team will work with each patient to

determine his or her goals and develop a concrete set of attainable

goals.

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1. While men and women have the same incidence and the

same prevalence of heart failure, which of the following states a difference noted between men and women with

heart failure: a. Women tend to develop heart failure earlier in life than men

do.

b. Men are more likely than women to have preserved systolic

function.

c. Women develop depression more commonly than men do.

d. Women have signs and symptoms of heart failure similar to

those of men, but they are less pronounced in women.

2. Cardiac rehabilitation is useful in treating heart patients so long as the program is instituted before the patient has

experienced his or her first heart attack. a. True.

b. False.

3. Which of the following is a modifiable risk factor for

atherosclerosis: a. Diabetes mellitus

b. Age

c. Family history of premature coronary heart disease

d. Male-pattern baldness


4. There are a number of different goals associated with

cardiac rehabilitation. Which statement best describes the specific program for a patient?

a. the patient’s cardiac condition is not a factor because cardiac

rehabilitation is useful for patients with varied cardiac

conditions.

b. the lifestyle goals of the patient is not relevant because the

focus should be on cardiac rehabilitation.

c. The rehabilitation team will work with each patient to

determine his or her goals and develop a concrete set of

attainable goals.

d. None of the above.

5. Patients with pacemakers are advised to avoid electromagnetic interference. Which of the following

devices does the evidence suggest may interfere with permanent pacemakers?

a. Properly operating household appliances such as microwave

ovens, televisions, radios, toasters, and electric blankets.

b. Cellular phones.

c. Electromagnetic anti-theft security systems.

d. Diagnostic or therapeutic procedures used in certain types of

surgery and procedures.

6. True or False: Angina is the term used to describe the pain and discomfort that occurs when the heart is deprived of

blood. a. True.

b. False.


7. Patients with typical myocardial infarction may have the

following prodromal symptoms in the days preceding the event:

a. Fatigue.

b. Intense and unremitting for 30-60 minutes.

c. A feeling of indigestion or of fullness and gas.


8. The following is/are true when a patient increases his or

her physical fitness program: a. Most individuals with cardiovascular disease will benefit from

increased physical fitness so long as they have NOT been

diagnosed with heart failure.

b. One of the primary benefits that occurs during an increase in

physical fitness is that the patient will experience an

increased ability to use oxygen to derive energy for work.

c. Exercise training decreases maximum ventilatory oxygen

because the muscles extract and use oxygen from blood.

d. Physical fitness program do not benefit persons with impaired

left ventricular function.

9. There is evidence to show that comprehensive cardiac

rehabilitation programs, including exercise training, can do

the following: a. Reduce smoking

b. Alter lipid profiles

c. Reduce blood pressure



10. Intracoronary stents have the following features:

a. The commercially available second-generation DESs that elute

everolimus and zotarolimus are not approved for use in the

United States.

b. Bare-metal stents are used exclusively to target lesion

revascularization.

c. Drug-eluting stents (DESs) have demonstrated significant

reductions in restenosis.

d. Stents with bioabsorbable polymer, polymer-free systems or

fully bioresorbable scaffolds are approved and available for

commercial use in the United States.

11. Non-modifiable risk factors for atherosclerosis include the

following: a. A person’s age and gender

b. Family history of premature coronary heart disease

c. Male-pattern baldness

d. *All of the above.

12. Immediately after the onset of myocardial infarction, the ability of ischemic myocardium to relax declines. Impaired

relaxation ___________ LV end-diastolic volume (LVEDV) and LV end-diastolic pressure (LVEDP).

a. decreases

b. *increases

c. does not interfere with

d. may both increase or decrease


13. Studies have shown that _________________ helps to

reduce stress levels in patients after myocardial infarction. a. massage therapy

b. *cognitive behavioral therapy

c. group therapy

d. desensitization therapy

14. Aging or heart disease damages the ______________ ability to set the correct pace for the heartbeat.

a. *sinus node’s

b. atrial node’s

c. ventricle’s

d. heart’s atrioventricular

15. Beneficial effects upon lipid levels have been reported from interventions combining __________________________

with the use of lipid lowering drugs. a. low fat diet alone

b. exercise alone

c. *education and behavioral strategies

d. cognitive behavioral therapy

16. The greatest predictors of risk for sudden cardiac death include ________________and heart failure symptoms.

a. *left ventricular systolic function

b. right ventricular systolic and diastolic function

c. right ventricular filling pressure

d. answers b and c above


17. Rate-responsive pacemakers have sensors that

automatically adjust to changes in a person's __________. a. cardiac output

b. *physical activity

c. atrial rhythm

d. none of the above

18. Persons with cardiovascular disease may safely perform

a. heavy-lifting and forceful isometric exercises, under guidance

b. *moderate-intensity dynamic strength training, for person’s at

low risk

c. stretching and pilates exercises after completing cardiac rehab

d. hot yoga exercises, for no more than 30 minutes

19. A dual-chamber pacemaker usually has two leads, one to the ______________ and one to the ________________.

a. *right atrium and right ventricle

b. right atrium and left atrium

c. left atrium and left ventricle

d. both ventricles

20. The following tests may be used to determine type of an

arrhythmia, EXCEPT: a. EKG (Electrocardiogram)

b. Echocardiography

c. *Transesophageal electrocardiogram bubble study

d. Stress Test


21. Patients needing a temporary pacemaker would be

a. *hospitalized.

b. not requiring hospitalization.

c. sent home with a 24-hour ambulatory EKG.

d. not expected to need a permanent pacemaker.

22. _____________________________ is gaining greater

prominence in assessing the inflammatory level of vascular disease and predicting future risk of vascular events, such

as MIs and cerebrovascular accidents. a. High-sensitivity CPK

b. *High-sensitivity C-reactive protein

c. High-sensitivity CK

d. High-sensitivity LDL and LDH

23. Abciximab, tirofiban, and eptifibatide are examples of

a. *Glycoprotein inhibitor therapy

b. Antianginals

c. Antibiotics that specifically treat pericarditis

d. Anticoagulant therapy

24. Medications shown to reduce ischemic complications in patients undergoing balloon angioplasty and coronary

stenting belong to the following medication category:

a. Antianginals

b. Anticoagulants

c. *Glycoprotein inhibitor therapy

d. Antibiotic medication

25. True or False. Multiple studies have shown the ICD to be

superior to antiarrhythmic drug therapy in patients with a history of life-threatening VT and VF.

a. *True.

b. False.


26. While going through airports, individuals with pacemakers

should a. not be concerned of metal detectors being triggered

b. *carry their pacemaker ID card

c. not expect airport personnel to request a manual search.

d. Both and c above.

27. Diastolic dysfunction predominates in conditions of

a. hypertrophic cardiomyopathy.

b. disorders with ventricular hypertrophy.

c. amyloid infiltration of the myocardium.


28. For health promotion, dynamic exercise of the large muscles for extended periods of time is recommended,

such as a. a full hour seven days a week.

b. an hour every other day.

c. *30 to 60 minutes, three to six times weekly.

d. 15 to 20 minutes, every day of the week.

29. True or False. Increased physical fitness in overweight

women and men enhances the beneficial effect of a low-saturated fat and low-cholesterol diet on blood lipoprotein

levels. a. *True.

b. False.

30. Epicardial inflammation may initiate pericarditis, which is

seen in more than 20% of patients presenting with _________________.

a. *Q-wave infarctions.

b. ST depression.

c. prolonged QT interval.

d. sudden death.


31. Major pacemaker malfunctions include the following:

a. Failure to output.

b. Failure to capture.

c. Failure to sense.


32. The failing heart and other organs produce

a. *tumor necrosis factor.

b. tumor cells.

c. cytokines.

d. None of the above.

33. Each rehospitalization for heart failure increases mortality by about _________ percent.

a. 45 – 47

b. 33 – 35

c. *20 – 22

d. 15 - 17

34. The rate of decline in oxygen uptake is directly related to

a. geographic region.

b. *maintenance of physical activity level.

c. genetic factors.

d. Answers a and b above.

35. The TAVR is a new alternative for some cases of

a. coronary blockage.

b. pulmonary stenosis.

c. *aortic valve stenosis.

d. mitral valve prolapse.


36. Artificial heart valves may be

a. mechanical metal.

b. mechanical plastic.

c. tissue made from animal valves or human valves taken from

cadavers.


37. The demonstrated evidence-based benefits of Cardiac

Rehabilitation include all EXCEPT:

a. Reduced symptoms (angina, dyspnea, fatigue).

b. Increased exercise performance.

c. *Ability to no longer need to take heart medication and to

perform high intensity exercise and competitive sports.

d. Enhanced ability to perform activities of daily living.

Correct Answers:

1. c

2. b

3. a

4. c

5. d

6. a

7. d

8. b

9. d

10. c

11. d

12. b

13. b

14. a

15. c

16. a

17. b

18. b

19. a

20. c

21. a

22. b

23. a

24. c

25. a

26. b

27. d

28. c

29. a

30. a

31. d

32. a

33. c

34. b

35. c

36. d

37. c


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