293. ischemic heart disease

Ischemic Heart DiseaseChapter 293. 294. 294

AcuteNon-ST Elevation Acute Coronary Syndrom- NSTE ACS

Unstable AnginaNon-ST elevation MI

ST Elevation Myocardial Infarct STMI

Stable AnginaClass1Class2Class3Class 4

Chronic

Oxigen Supply and demand

DefinitionsAcute coronary syndrome is defined as myocardial ischemia due to myocardial infarction (NSTEMI or STEMI) or unstable anginaUnstable angina is defined as angina at rest, new onset exertional angina (<2 months), recent acceleration of angina (<2 months), or post revascularization angina

CAUSES ACS

Thrombus formationDownstream embolizationDynamic Obstruction (Spasm –f.e. Prinzmetal ‘s Variant AnginaInvreased oxygen demand

DiagnosisDx of acute coronary syndrome is based on history, physical exam, ECG, cardiac enzymesPatients can then be divided into several groups

Non-cardiac chest pain (i.e., Gastrointestinal, musculoskeletal, pulmonary embolus) Stable angina Unstable angina Myocardial infarction (STEMI or NSTEMI) Other cardiac causes of chest pain (i.e., aortic dissection, pericarditis)

Diagnosis

Severe chest discomfortOccurs at restLasting >10 minRecent onset (up to 2 weeks)Crescendo pattern

Pathophysiology of ACSPlaque rupture and subsequent formation of thrombus – this can be either occlusive or non-occlusive (STEMI, NSTEMI, USA)Vasospasm such as that seen in Prinzmetal’s angina, cocaine use (STEMI, NSTEMI, USA)Progression of obstructive coronary atherosclerotic disease (USA)In-stent thrombosis (early post PCI)In-stent restenosis (late post PCIPoor surgical technique (post CABG)

Pathophysiology of ACS

Acute coronary syndromes can also be due to secondary causes

ThyrotoxicosisAnemiaTachycardiaHypotensionHypoxemiaAterial inflammation (infection, arteritis)

Diagnostic Tests

ECGEchocardiographyMyocardial SPECTBiomarkers – Troponin, CK-MB, MioglobinCCTA

Cardiac Biomarkers

Date of download: 9/30/2015

From: Diagnosis of Stable Ischemic Heart Disease: Summary of a Clinical Practice Guideline From the American College of Physicians/American College of Cardiology Foundation/American Heart Association/American Association for Thoracic Surgery/Preventive Cardiovascular Nurses Association/Society of Thoracic SurgeonsAnn Intern Med. 2012;157(10):729-734. doi:10.7326/0003-4819-157-10-201211200-00010

Clinical Classification of Chest Pain

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Pre-test ProbabilityIn the absence of abnormal findings on physical exam, ECG, or enzymes, the pre-test probability of acute coronary syndrome must be determined by the clinician A good history is crucial (is the chest pain typical or atypical; what are the associated symptoms) Determination of risk factors is also crucial (male, age >55, smoking, DM, HTN, FamHx, hyperlipidemia, known CAD)

Treatment of ACS; Aspirin

Aspirin is an antiplatelet agent that initiates the irreversible inhibition of cyclooxygenase, thereby preventing platelet production of thromboxane A2 and decreasing platelet aggregationAdministration of ASA in ACS reduces cardiac endpoints

ACC/AHA Guidelines for Aspirin Therapy

Aspirin should be given in a dose of 75-325 mg/day to all patients with ACS unless there is a contraindication (in which case, clopidogrel should be given)

Treatment of ACS; Clopidogrel

Clopidogrel is a potent antiplatelet agentIt should be administered to all patients who cannot take ASAThe CURE trial suggests a benefit to adding Clopidogrel to ASA/Heparin in patients going for PCIGive 300 mg loading dose followed by 75 mg/day

AHA/ACC Guidelines for ClopidogrelClopidogrel should be administered to patients who cannot take ASA because of hypersensitivity or gastrointestinal intoleranceIn hospitalized patients in whom an early, noninterventional approach is planned, clopidogrel should be added to ASA as soon as possible on admission and administered for at least 1 month and up to 9 months. Do not use clopidogrel if there is any possibility patient may be candidate for CABG

Treatment of ACS; NitratesNitroglycerin is considered a cornerstone of anti-anginal therapy, despite little objective evidence for its benefitBenefit is thought to occur via reduction in myocardial O2 demand secondary to venodilation induced reduction in preload as well as coronary vasodilation and afterload reductionTitrate to relief of chest pain; chest pain = death of myocardial cellsNo documented mortality benefit

Treatment of ACS; Beta Blockers

Beta Blockers reduce myocardial oxygen demand by reducing heart rate, contractility, and ventricular wall tensionAdministration of beta blockers in ACS reduces cardiac endpoints

AHA/ACC Guidelines for Beta Blocker Therapy

Intravenous beta blockers should be used initially in all patients (without contraindication) followed by oral beta blockers with the goal being decrease in heart rate to 60 beats per minuteA combination of beta blockers and nitrates can be viewed as first line therapy in all patients with ACS

Treatment of ACS; Heparin

Heparin (unfractionated heparin or UFH) has traditionally been the mainstay of therapy in acute coronary syndromes as its efficacy has been documented in several large, randomized trials

Treatment of ACS; LMWH

More recent studies indicate that low molecular weight heparin is also effective in the reduction of end points such as myocardial infarction or deathSome studies report that LMWH, when used in combination with ASA, may be superior to continuous infusion of Heparin

ACC/AHA Guidelines for Heparin Therapy

All patients with acute coronary syndromes should be treated with a combination of ASA (325 mg/day) and heparin (bolus followed by continuous infusion with goal of PTT 1-2.5X control) or ASA and low molecular weight heparin unless one of the drugs is contraindicated

Treatment of ACS; ACE-I

The best documented mechanism by which these agents act is to reduce ventricular remodeling over days to weeks after myocardial damage. However, there is data that a mortality benefit exists when these agents are used early in the course of ACSAdministration of ACE-I in ACS reduces cardiac endpoints

AHA/ACC Guidelines for ACE-I Therapy

ACE-I should be administered to all patients in the first 24 hours of ACS provided hypotension and other clear cut contraindications are absent

Treatment of ACS; Statins

Statins may be of benefit in ACSPossible mechanisms include plaque stabilization, reversal of endothelial dysfunction, decreased thrombogenicity, and reduction of inflammation

TIMI Risk Score

Age >65 yrsDaily ASA Therapy (>7 days prior to event)Symptoms of Unstable AnginaDocumented CAD (stenosis > 50%)3 or more traditional cardiac risk factorsElevated cardiac enzymesECG changes

TIMI Risk Score

Score of 3 or less = low riskScore of 4-5 = intermediate risk (use IIBIIIA)Score of 6-7 = high risk (use IIBIIIA)

Treatment of ACS; Emergent Revascularization

In the setting of STEMI primary PCI is associated with better outcomes than thrombolysisEmergent PCI is also indicated in the setting of a new LBBB

PCI Trials

PAMI (PTCA vs. thrombolysis)Netherlands Trials (PTCA vs. thrombolysis)GUSTO IIB (PTCA vs. thrombolysis)DANAMI-2 (stenting vs. thrombolysis)STAT (stenting vs. thrombolysis)

AHA/ACC Guidelines for Primary PCIPrimary PCI is indicated as an alternative to thrombolysis when the following criteria are met:

STEMI or new LBBBCan undergo PCI within 12 hours of the onset of symptomsThe MD doing the intervention does more than 75 PCI’s/yrThe procedure is done in a center that does more than 200 PCI’s/yr and has surgical backup

Conclusions; Approach to Chest Discomfort

Good History and Physical (note time and duration of symptoms)Careful evaluation of ECG (compare to previous when possible)Check Cardiac EnzymesMonitor on TelemetryOxygen

Conclusions; Treatment of NSTEMI/USA

ASANTG (consider MSO4 if pain not relieved)Beta BlockerHeparin/LMWHACE-I+/- Statin+/- Clopidogrel (don’t give if CABG is a possibility)+/- IIBIIIA inhibitors (based on TIMI risk score)

Conclusions; Treatment of STEMI ASANTG (consider MSO4 if pain not relieved)Beta BlockerHeparin/LMWHACE-I+/-Clopidogrel (based on possibility of CABG)IIBIIIA +/- StatinActivate the Cath Lab!!!

Medical Management of Acute Coronary Syndrome

Definition of MI - Acute Myocardial lnfarction

1. Evidence of myocardial necrosis: cardiac biomarker values (preferably cardiac troponin [cTn]) and with at least one of the following. Symptoms of ischemia. New or presumed new significant ST-T changes or new LBBB. Development of pathologic Q waves on ECG. Imaging evidence of new loss of viable myocardium or new regional wallmotion abnormality. Identification of an intracoronary thrombus by angiography or autopsy. Cardiac death with symptoms suggestive of myocardial ischemia andpresumed new ischemic ECG changes of new LBBB ， but death occurredbefore cardiac biomarkers were obtained or before cardiac biomarkervalues would be increased. Percutaneous coronary intervention (PCI)-related MI is arbitrarily de 有ned by elevation of cTn val ues (>5 x 99th percentile U RL) in patients with normal 七 as 巳 line val ues ( 王 99th percentile URL) or a rise of cTn val ues >20% ifthe baseline val ues are elevated and a re s 旧 ble or 句 I ling. In addition ， either(i) symptoms sugg 巳 stive of myoca rdial ischemia ， or (ii) new ischemic ECGchanges ， or (iii) angiographic 白 ndings consistent with a procedural complication ， or (iv) imaging demonstration of new loss of viabl 巳 myocardium ornew regional wall motion a bnormality a re required. Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischemia and with a rise and/or fal l of cardiac biomarker val ues with at least one value abo 、 e the 99thpercentile URL. Coronary artery bypass grafting (CAßG)-r 巳 lated MI is a rbitrarily definedby elevation of cardiac biomarker values (> 1 0 x 99th percentile U RL) inpatients with normal baseline cTn values ( 呈 99th percentile U RL). In addition ， either (i) new pathologic Q w 讥 es or new Lßßß ， or (ii) angiog日 phicdocumented new graft or new native coronary artery Occlu5ion ， or (iii)imaging evidence of n 巳 N 1055 of viable myocardium or new regional wallmotion abnorma

Criteria for Prior Myocardial l nfarctionAny one of the fol lowing criteria meets the diagnosis for prior MI. Pathologic Q waves with or without 5ym 仁 tom5 in the ab5 巳nce of nonischemlc caU5 巴 5. I maging evidence of a region of 1055 of viable myocardium that i5 thinnedand fails to contract ， in the absence of a noni5chemic cause.. Pathologic 有 ndings of a prior M

CLASSIFICATION OF MYOCARDIAL INFARCTlON

Type 1: Sponta neous Myocardial lnfarctionType 2: Myocardial l nfarction Secondary to an Ischemic ImbalanceType 3: Myocardial l nfarction Resulting in Death When Biomarker Values Are UnavailableType 4a: Myocardia 川 nfarction Related to Percutaneous Coronary Intervention (PCI)Type 4b: Myocardial lnfarction Related to Stent ThrombosisType 5: Myocardial l nfarction Related to Coronary Artery Bypass Grafting (CABG)

Primary PCI in STEMI



Pretest Likelihood of Coronary Artery Disease in Symptomatic Patients According to Age and Sex




Complications

Ventricular DisfunctionHemodinamic AssessmentHypovolemiaCardiogenic shockArrhythmias, conduction disturbancesPericarditisAneurism

Complications MIComplication Type Manifestations

Ischemic Angina, reinfarction, infarct extensionMechanical Heart failure, cardiogenic shock, mitral

valve dysfunction, aneurysms, cardiac rupture

Arrhythmic Atrial or ventricular arrhythmias, sinus or atrioventricular node dysfunction

Embolic Central nervous system or peripheral embolization

Inflammatory Pericarditis



Comparing Pretest Likelihoods of Coronary Artery Disease in Low-Risk Symptomatic Patients and High-Risk Symptomatic Patients

Table Title:




Follow-Up Noninvasive Testing in Patients With Known SIHD

Noninvasive Testing in Known SIHD: Asymptomatic (or Stable Symptoms)

Heart - Pathology

Heart - Pathology

Syndrome StenosesPlaque

Disruption Plaque-Associated ThrombusStable angina >75% No NoUnstable angina Variable Frequent Non-occlusiveTransmural MI Variable Frequent Occlusive

Subendocardial MI

Variable Variable Widely variable

Sudden death severe Frequent Often small

Heart - PathologyIschemic Heart Disease

Angina PectorisChest discomfort = prolonged, recurrent, different qualitiesCause = transient myocardial ischemia( seconds to minutes)Patterns

Stable = 75% vessel block, transient ( <15 minutes), aggravated by exertion, relived by rest & Nitroglycerin (VD)Prinzmetal = coronary spasm, episodic, Typical EKG change – ST elevation, Relived by VD but not restUnstable = 90% vessel block or Acute plaque change ( superimposed thrombus), prolonged ( >15 min.), not relived by rest, VD, Pre-infarction Angina

MI - Types

TransmuralFull thickness

Superimposed thrombus in atherosclerosis

Focal damage

Sub-endocardialInner 1/3 to half of ventricular wallDecreased circulating blood volume( shock, Hypotension, Lysed thrombus)Circumferential


MI= Also called Heart attackIncidence = disease of old

elderly (45% in 65 yrs. old) young ( 10% in 40yrs. Old),

Sex = Male > FemaleEthnic = same in African & AmericanRisk factors

Major modifiable- DM, HTN, Smoking, HypercholesterolemiaHRT for Postmenopausal females – will not protect the heart


MIPathogenesis

Coronary vessel occlusionAtherosclerosis with thrombus = MC cause ( 90% cases)Others = vasospasm (10%)

Most important mechanism = dynamic changes in the plaque (rather than plaque size), Plaque disruption PLTS aggregation thrombus and VC (happens in minutes)Irreversible changes = after 30 minutes of ischemia

ATP < 10% of normalMechanism of cell death = necrosis ( Coagulative)


TTC


MI -Morphologylight microscopy

First 12 hrs. after MI – no changeUp to 3 days = Coagulative necrosis, neutrophils1-2 weeks = Granulation tissue≥ 3 weeks = fine scar≥ 2 months = dense scar

EM – membrane disruption and Mitochondrial densitiesSpecial stain = TTC ( Triphenyl Tetrazolium chloride),

Detects and stains Mahogany brown with Lactate dehydrogenaseUnstained area = infarctionMahogany brown = viableWhite, glistening= scar

Most common and nonspecific change in ischemia = sub-endocardial myocyte vacuolization

MI- Microscopic features

One-day-old infarct

coagulative necrosis

wavy fibers

Up to 3 days duration

Neutrophilic infiltrate

1 -2 weeks

Granulation tissueScar

>3 weeks


MI –ReperfusionMechanisms

Intrinsic Extrinsic =

Thrombolytic drugs = < 1hr. After onset of MIPTCA/CABG = > 1hr. After onset of MI

Target = clot lysis and restoration of blood flowPost- reperfusion changes =

Contraction bands = hyper contracting myocytes, Stunned myocardium = transient, protective dysfunctionReperfusion damage = mostly apoptosis by free radicals ( unlike MI)


MI = ClinicalSilent MI = DM, Elderly, Cardiac transplantation recipients,Typical features = Rapid, weak pulse and sweating profusely (diaphoretic), Dyspnea, chest painLab=

Diagnostic Best markers = Troponins ( T & I), both sensitive and cardio – specificNext best – CK-MB

PredictiveCRP- >3mg/l – highest risk


MI –ComplicationsIn 75% of Patients with MIPoor prognosis in = elderly, females, DM, old case of MI, Anterior wall infarct – worst, posterior –worse, Inferior wall – best

1. Arrhythmia = Ventr. Fibrillation – MC arrhythmia lead to sudden death in MI patients, before they reach hospital2. pump failure – LVF, cariogenic shock, if >LV wall infarcts, lead to death ( 70% of hospitalized MI patients)3.Ventricular rupture = Free or lateral LV wall – MC site, later cause false aneurysm, 4.True aneurysm = rupture is very rare5.Pericarditis = Dressler’s syndrome ( Late MI complication)6.Recurrence


Sudden cardiac death = unexpected death in one hour due to cardiac causes with or without clinical symptomsCause – Atherosclerosis ( 90%), others (10%)

Romano- Ward syndrome – Long Q-T syndrome ( K+, Na+ channel defects)

Mechanism- Most likely due to arrhythmias ( VF)Patients – young athletes, with Pul. HTN, IHDMorphology

Prominent finding – increased heart massVacuolations in Sub – endocardial myocardium

Heart - Pathology

Ischemic Heart DiseaseChronic IHD = also called ischemic cardiomyopathyPatients = post heart transplant receipts, previous MI or CABG ptsCause =compromised ventricular functionMorphology =vacuoles, Myocyte HypertrophyDiagnosis= by exclusion

Heart - PathologyWhat is it?

Heart - PathologyWhat are these?



Alternative Diagnoses to Angina for Patients With Chest Pain

Table Title:




Date of download: 12/10/2015 Copyright © The American College of Cardiology. All rights reserved.

From: 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

J Am Coll Cardiol. 2014;64(24):e139-e228. doi:10.1016/j.jacc.2014.09.017




Global Registry of Acute Coronary Events Risk Calculator for In-Hospital Mortality for Acute Coronary Syndrome




Algorithm for Management of Patients With Definite or Likely NSTE-ACS**See corresponding full-sentence recommendations and their explanatory footnotes.†In patients who have been treated with fondaparinux (as upfront therapy) who are undergoing PCI, an additional anticoagulant with anti-IIa activity should be administered at the time of PCI because of the risk of catheter thrombosis.ASA indicates aspirin; CABG, coronary artery bypass graft; cath, catheter; COR, Class of Recommendation; DAPT, dual antiplatelet therapy; GPI, glycoprotein IIb/IIIa inhibitor; LOE, Level of Evidence; NSTE-ACS, non–ST-elevation acute coronary syndrome; PCI, percutaneous coronary intervention; pts, patients; and UFH, unfractionated heparin.

Figure Legend:




Stepped-Care Approach to Pharmacological Therapy for Musculoskeletal Symptoms in Patients With Known Cardiovascular Disease or Risk Factors for Ischemic Heart DiseaseASA indicates aspirin; COX-2, cyclooxygenase-2; GI, gastrointestinal; NSAIDs, nonsteroidal anti-inflammatory drugs; and PPI, proton-pump inhibitor.

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