acute coronary syndrome 4

4/6/2014 Acute Coronary Syndrome

http://emedicine.medscape.com/article/1910735-overview#showall 1/14

Acute Coronary Syndrome

Author: David L Coven, MD, PhD; Chief Editor: Eric H Yang, MD more...

Updated: Mar 12, 2014

Practice Essentials

Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those for ST-segmentelevation myocardial infarction (STEMI) to presentations found in nonST-segment elevation myocardial infarction(NSTEMI) or in unstable angina. It is almost always associated with rupture of an atherosclerotic plaque andpartial or complete thrombosis of the infarct-related artery.

Signs and symptoms

Atherosclerosis is the primary cause of ACS, with most cases occurring from the disruption of a previouslynonsevere lesion. Complaints reported by patients with ACS include the following:

PalpitationsPain, which is usually described as pressure, squeezing, or a burning sensation across the precordium andmay radiate to the neck, shoulder, jaw, back, upper abdomen, or either armExertional dyspnea that resolves with pain or restDiaphoresis from sympathetic dischargeNausea from vagal stimulationDecreased exercise tolerance

Physical findings can range from normal to any of the following:

Hypotension: Indicates ventricular dysfunction due to myocardial ischemia, myocardial infarction (MI), oracute valvular dysfunctionHypertension: May precipitate angina or reflect elevated catecholamine levels due to anxiety or toexogenous sympathomimetic stimulationDiaphoresisPulmonary edema and other signs of left heart failureExtracardiac vascular diseaseJugular venous distentionCool, clammy skin and diaphoresis in patients with cardiogenic shockA third heart sound (S3) and, frequently, a fourth heart sound (S4)

A systolic murmur related to dynamic obstruction of the left ventricular outflow tractRales on pulmonary examination (suggestive of left ventricular dysfunction or mitral regurgitation)

Potential complications include the following:

Ischemia: Pulmonary edemaMyocardial infarction: Rupture of the papillary muscle, left ventricular free wall, and ventricular septum

See Clinical Presentation for more detail.

Diagnosis

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Guidelines for the management of non-ST-segment elevation ACS were released in 2011 by the European Society

of Cardiology (ESC).[1] The guidelines include the use of the CRUSADE risk score (Can Rapid risk stratification ofUnstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines).

In the emergency setting, electrocardiography (ECG) is the most important diagnostic test for angina. ECGchanges that may be seen during anginal episodes include the following:

Transient ST-segment elevationsDynamic T-wave changes: Inversions, normalizations, or hyperacute changesST depressions: These may be junctional, downsloping, or horizontal

Laboratory studies that may be helpful include the following:

Creatine kinase isoenzyme MB (CK-MB) levelsCardiac troponin levelsMyoglobin levelsComplete blood countBasic metabolic panel

Diagnostic imaging modalities that may be useful include the following:

Chest radiographyEchocardiographyMyocardial perfusion imagingCardiac angiographyComputed tomography, including CT coronary angiography and CT coronary artery calcium scoring

See Workup for more detail.

Management

Initial therapy focuses on the following:

Stabilizing the patients conditionRelieving ischemic painProviding antithrombotic therapy

Pharmacologic anti-ischemic therapy includes the following:

Nitrates (for symptomatic relief)Beta blockers (eg, metoprolol): These are indicated in all patients unless contraindicated

Pharmacologic antithrombotic therapy includes the following:

AspirinClopidogrelPrasugrelTicagrelorGlycoprotein IIb/IIIa receptor antagonists (abciximab, eptifibatide, tirofiban)

Pharmacologic anticoagulant therapy includes the following:

Unfractionated heparin (UFH)Low-molecular-weight heparin (LMWH; dalteparin, nadroparin, enoxaparin)Factor Xa inhibitors (rivaroxaban, fondaparinux)

Additional therapeutic measures that may be indicated include the following:

ThrombolysisPercutaneous coronary intervention (preferred treatment for ST-elevation MI)

Current guidelines for patients with moderate- or high-risk ACS include the following:

Early invasive approach



Concomitant antithrombotic therapy, including aspirin and clopidogrel, as well as UFH or LMWH

See Treatment and Medication for more detail.

Image library

A 62-year-old w oman w ith a history of chronic stable angina and a "valve problem" presents w ith new chest pain. She is symptomatic

on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure = 140/90 mm Hg

and heart rate = 98. Her electrocardiogram (ECG) is as show n. She is given nitroglycerin sublingually, and her pressure decreases to

80/palpation. Right ventricular ischemia should be considered in this patient.

Background

Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging from those for ST-segmentelevation myocardial infarction (STEMI) to presentations found in nonST-segment elevation myocardial infarction(NSTEMI) or in unstable angina. In terms of pathology, ACS is almost always associated with rupture of anatherosclerotic plaque and partial or complete thrombosis of the infarct-related artery. (See Etiology.)

In some instances, however, stable coronary artery disease (CAD) may result in ACS in the absence of plaquerupture and thrombosis, when physiologic stress (eg, trauma, blood loss, anemia, infection, tachyarrhythmia)increases demands on the heart. The diagnosis of acute myocardial infarction in this setting requires a finding of

the typical rise and fall of biochemical markers of myocardial necrosis in addition to at least 1 of the following[2]

(See Workup.):

Ischemic symptomsDevelopment of pathologic Q wavesIschemic ST-segment changes on electrocardiogram (ECG) or in the setting of a coronary intervention

The terms transmural and nontransmural (subendocardial) myocardial infarction are no longer used because ECGfindings in patients with this condition are not closely correlated with pathologic changes in the myocardium.Therefore, a transmural infarct may occur in the absence of Q waves on ECGs, and many Q-wave myocardialinfarctions may be subendocardial, as noted on pathologic examination. Because elevation of the ST segmentduring ACS is correlated with coronary occlusion and because it affects the choice of therapy (urgent reperfusiontherapy), ACS-related myocardial infarction should be designated STEMI or NSTEMI. (See Workup.)

Attention to the underlying mechanisms of ischemia is important when managing ACS. A simple predictor ofdemand is rate-pressure product, which can be lowered by beta blockers (eg, metoprolol or atenolol) andpain/stress relievers (eg, morphine), while supply may be improved by oxygen, adequate hematocrit, bloodthinners (eg, heparin, IIb/IIIa agents such as abciximab, eptifibatide, tirofiban, or thrombolytics), and/or vasodilators(eg, nitrates, amlodipine). (See Medications.)

In 2010, the American Heart Association (AHA) published new guideline recommendations for the diagnosis and

treatment of ACS.[3]

Etiology

Acute coronary syndrome (ACS) is caused primarily by atherosclerosis. Most cases of ACS occur from disruptionof a previously nonsevere lesion (an atherosclerotic lesion that was previously hemodynamically insignificant yetvulnerable to rupture). The vulnerable plaque is typified by a large lipid pool, numerous inflammatory cells, and athin, fibrous cap.

Elevated demand can produce ACS in the presence of a high-grade fixed coronary obstruction, due to increasedmyocardial oxygen and nutrition requirements, such as those resulting from exertion, emotional stress, orphysiologic stress (eg, from dehydration, blood loss, hypotension, infection, thyrotoxicosis, or surgery).



ACS without elevation in demand requires a new impairment in supply, typically due to thrombosis and/or plaquehemorrhage.

The major trigger for coronary thrombosis is considered to be plaque rupture caused by the dissolution of thefibrous cap, the dissolution itself being the result of the release of metalloproteinases (collagenases) from activatedinflammatory cells. This event is followed by platelet activation and aggregation, activation of the coagulationpathway, and vasoconstriction. This process culminates in coronary intraluminal thrombosis and variable degreesof vascular occlusion. Distal embolization may occur. The severity and duration of coronary arterial obstruction, thevolume of myocardium affected, the level of demand on the heart, and the ability of the rest of the heart tocompensate are major determinants of a patient's clinical presentation and outcome. (Anemia and hypoxemia canprecipitate myocardial ischemia in the absence of severe reduction in coronary artery blood flow.)

A syndrome consisting of chest pain, ischemic ST-segment and T-wave changes, elevated levels of biomarkers ofmyocyte injury, and transient left ventricular apical ballooning (takotsubo syndrome) has been shown to occur inthe absence of clinical CAD, after emotional or physical stress. The etiology of this syndrome is not wellunderstood but is thought to relate to a surge of catechol stress hormones and/or high sensitivity to thosehormones.

Prognosis

Six-month mortality rates in the Global Registry of Acute Coronary Events (GRACE) were 13% for patients withNSTEMI ACS and 8% for those with unstable angina.

An elevated level of troponin (a type of regulatory protein found in skeletal and cardiac muscle) permits riskstratification of patients with ACS and identifies patients at high risk for adverse cardiac events (ie, myocardial

infarction, death) up to 6 months after the index event.[4, 5] (See Workup.)

The PROVE IT-TIMI trial found that after ACS, a J-shaped or U-shaped curve association is observed between BP

and the risk of future cardiovascular events.[6]

LeLeiko et al determined that serum choline and free F(2)-isoprostane are also predictors of cardiac events inACS. The authors evaluated the prognostic value of vascular inflammation and oxidative stress biomarkers inpatients with ACS to determine their role in predicting 30-day clinical outcomes. Serum F(2)-isoprostane had anoptimal cutoff level of 124.5 pg/mL, and serum choline had a cutoff level of 30.5 mol/L. Choline and F(2)-isoprostane had a positive predictive value of 44% and 57% and a negative predictive value of 89% and 90%,

respectively.[7]

Testosterone deficiency is common in patients with coronary disease and has a significant negative impact on

mortality. Further study is needed to assess the effect of treatment on survival.[8]

A study by Sanchis et al suggests renal dysfunction, dementia, peripheral artery disease, previous heart failure,

and previous myocardial infarction are the comorbid conditions that predict mortality in NSTEMI ACS.[9] In patientswith comorbid conditions, the highest risk period was in the first weeks after NSTEMI ACS. In-hospitalmanagement of patients with comorbid conditions merits further investigation.

Patients with end-stage renal disease often develop ACS, and little is known about the natural history of ACS inpatients receiving dialysis. Gurm et al examined the presentation, management, and outcomes of patients withACS who received dialysis before presentation for an ACS. These patients were enrolled in the Global Registry ofAcute Coronary Events (GRACE) at 123 hospitals in 14 countries from 1999-2007.

NSTEMI ACS was the most common in patients receiving dialysis, occurring in 50% of patients (290 of 579)versus 33% (17,955 of 54,610) of those not receiving dialysis The in-hospital mortality rates were higher amongpatients receiving dialysis (12% vs 4.8%; p < 0.0001). Higher 6-month mortality rates (13% vs 4.2%; p < 0.0001),recurrent myocardial infarction incidence (7.6% vs 2.9%; p < 0.0001), and unplanned rehospitalizations (31% vs18%; p < 0.0001) were found among those who survived to discharge. Outcomes in patients who received dialysiswas worse than was predicted by the calculated GRACE risk score for in-hospital mortality (7.8% predicted vs12% observed; p < 0.05). This suggests that the GRACE risk score underestimated the risk of major events in

these patients.[10]

In a study that assessed the impact of prehospital time on STEMI outcome, Chughatai et al suggest that total

time to treatment should be used as a core measure instead of door-to-balloon time.[11] This is because on-scene time was the biggest fraction of "pre-hospital time. The study compared groups with total time to treatment



of more than 120 minutes compared with 120 minutes or less and found mortalities were 4 compared with 0 andtransfers to a tertiary care facility were 3 compared with 1, respectively.

Patient Education

Patient education of risk factors is important, but more attention is needed regarding delays in door-to-balloontime, and one major barrier to improving this delay is patient education regarding his or her symptoms. Lack ofrecognition of symptoms may cause tremendous delays in seeking medical attention.

Educate patients about the dangers of cigarette smoking, a major risk factor for coronary artery disease (CAD).The risk of recurrent coronary events decreases 50% at 1 year after smoking cessation. Provide all patients whosmoke with guidance, education, and support to avoid smoking. Smoking-cessation classes should be offered tohelp patients avoid smoking after a myocardial infarction. Bupropion increases the likelihood of successfulsmoking cessation.

Diet plays an important role in the development of CAD. Therefore, prior to hospital discharge, a patient who hashad a myocardial infarction should be evaluated by a dietitian. Patients should be informed about the benefits of alow-cholesterol, low-salt diet. In addition, educate patients about AHA dietary guidelines regarding a low-fat, low-cholesterol diet.

A cardiac rehabilitation program after discharge may reinforce education and enhance compliance.

The following mnemonic may useful in educating patients with CAD regarding treatments and lifestyle changesnecessitated by their condition:

A = Aspirin and antianginalsB = Beta blockers and blood pressure (BP)C = Cholesterol and cigarettesD = Diet and diabetesE = Exercise and education

For patients being discharged home, emphasize the following:

Timely follow-up with primary care providerCompliance with discharge medications, specifically aspirin and other medications used to controlsymptomsNeed to return to the ED for any change in frequency or severity of symptoms

Contributor Information and DisclosuresAuthorDavid L Coven, MD, PhD Assistant Professor of Clinical Medicine, Columbia University College of Physiciansand Surgeons; Director, Cardiology Outpatient Clinic, St Luke's Site, Attending Physician, Department ofMedicine, Division of Cardiology, St Luke's-Roosevelt Hospital Center

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians,American Medical Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)Arun Kalyanasundaram, MD, MPH Interventional Cardiology Fellow, Department of Cardiology, ClevelandClinic

Arun Kalyanasundaram, MD, MPH is a member of the following medical societies: American College ofCardiology, American College of Physicians, American Heart Association, Society for Cardiac Angiography andInterventions, Society of General Internal Medicine, Society of Hospital Medicine, and Southern MedicalAssociation


Jamshid Shirani, MD Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory,Director of Hypertrophic Cardiomyopathy Clinic, St Luke's University Health Network



Jamshid Shirani, MD is a member of the following medical societies: American Association for theAdvancement of Science, American College of Cardiology, American College of Physicians, AmericanFederation for Medical Research, American Heart Association, American Society of Echocardiography, andAssociation of Subspecialty Professors


Chief EditorEric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catheterization Laboratory andInterventional Cardiology, Mayo Clinic Arizona

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha


Additional ContributorsCraig T Basson, MD, PhD Gladys and Roland Harriman Professor of Medicine, Director of the Center forMolecular Cardiology, Director of Cardiovascular Research, Division of Cardiology, Department of Medicine,Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital

Craig T Basson, MD, PhD is a member of the following medical societies: American College of Cardiology andAmerican Heart Association


Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, JohnHopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns HopkinsUniversity School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of EmergencyMedicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine


David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; ViceChair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of EmergencyPhysicians and Society for Academic Emergency Medicine


Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute,Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State MedicalAssociation, American College of Cardiology, American College of Physicians, American Heart Association,American Medical Association, and Heart Rhythm Society


Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor,Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians,National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Managementposition; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical CenterCollege of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment



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