DESCRIPTION

• Acute coronary syndrome (ACS) includes a clinical spectrum of ischemic discomfort resulting from atheromatous plaque rupture in a coronary artery leading to thrombus formation. Its spectrum ranges from unstable angina (UA) to non-ST elevation MI (NSTEMI) to ST elevation MI (STEMI).
• STEMI is the most severe form of ACS. An occlusive thrombus results in transmural-MI with ST elevation on the ECG and elevated levels of biomarkers.
• NSTEMI requires elevated biomarkers, may have ECG changes, but no ST elevation.
• UA involves increasing or new chest pain (crescendo angina) with normal biomarkers.

EPIDEMIOLOGY

Incidence

In 2009, an estimated 785,000 people in the U.S. had an initial ACS presentation, and another 470,000 had a recurrent event.

Prevalence

Coronary heart disease in U.S.: Whites 6.1%, blacks 6.0%, American Indians 5.6%, Asians 4.3%

RISK FACTORS

• HTN
• Dyslipidemia
• DM and glucose intolerance
• Family history of premature coronary heart disease (age <55 in father, or <65 in mother)
• Cigarette smoking
• Metabolic syndrome and obesity
• Chronic kidney disease
• Sedentary lifestyle
• Cocaine use
• Major depressive disorder

PATHOPHYSIOLOGY

• Atheromatous plaque rupture in a coronary artery resulting in platelet activation, aggregation, and deposition. This forms a thrombus along with coagulation cascade. Blood flow to myocardium is compromised resulting in ischemia/infarction.
• Lipid-rich plaques with thin fibrous caps are more likely to rupture.

COMMONLY ASSOCIATED CONDITIONS

Atherosclerosis in other vascular beds (ie, carotid artery stenosis, intracranial atherosclerosis, aortic atherosclerosis/aneurysm, peripheral arterial disease)

Outline

• Description
• Epidemiology
  • Incidence
  • Prevalence
• Risk Factors
• Pathophysiology
• Commonly Associated Conditions

History

Typical symptoms include crushing substernal chest "tightness" or "pressure" radiating to neck or arms. Associated diaphoresis, dyspnea, and nausea/vomiting are common.

Physical Exam

Nonspecific, a 3rd heart sound (S3), distended neck veins, pulmonary edema, mitral regurgitation murmur

DIAGNOSTIC TESTS & INTERPRETATION

Lab

• Cardiac biomarkers: Creatine kinase (CK)-MB, troponin I (TnI) or T (TnT), and myoglobin:
  • TnI or TnT specific for cardiac injury, rise in 4–6 hr, takes up to 10 days to normalize
  • CK-MB rapid rise in 4–6 hr with rapid fall over 36–48 hr, best for evaluating infarct size
  • Perform serial evaluation every 6–8 hr.
• ECG:
  • STEMI: ST-elevation >1 mm in 2 contiguous leads or new left bundle branch block (LBBB):
    • Inferior: II, III, aVF
    • Anterior: V2–V4
    • Anteroseptal: V1–V2
    • Lateral: I, aVL, V5–V6
  • STEMI: ST-depression >1 mm in V1–V3 may be posterior STEMI.
  • NSTEMI: ST-depression or T-wave inversion

Imaging

• Echo: Regional wall-motion abnormalities suggest ischemic or infarcted myocardium; poor LV function portends worse prognosis.
• Nuclear myocardial perfusion imaging (MPI, SPECT, PET), dobutamine stress echo, and adenosine stress MRI all have diagnostic and prognostic utility in low-intermediate risk patients with chest pain.

Diagnostic Procedures/Surgery

• Invasive coronary angiography indicated in patients with CHF, depressed LV function, ventricular arrhythmias, persistent or recurrent ischemia, large perfusion defect on MPI, prior revascularization, and all ACS patients with STEMI or shock.
• Pulmonary artery catheter monitoring may be considered for hypotension or shock.
• Intra-aortic balloon pump for patients in cardiogenic shock, prior to or after coronary angiography

DIFFERENTIAL DIAGNOSIS

• Cardiac: Pericarditis, myocarditis, demand ischemia
• Aorta: Acute aortic dissection
• Lung: Pulmonary embolism
• GI: Esophageal disorders, acute cholecystitis

Outline

• History
• Physical Exam
• Diagnostic Tests & Interpretation
  • Lab
  • Imaging
  • Diagnostic Procedures/Surgery
• Differential Diagnosis

First Line

• Aspirin (ASA) 162–325 mg as soon as possible, and continued indefinitely for all ACS. (Class I)
• Clopidogrel at least 300 mg once, then 75 mg/d for (1) patients intolerant to ASA, (2) when early conservative approach planned, or (3) post-percutaneous intervention (PCI) for all ACS. Clopidogrel often held until nonsurgical approach decided upon (PCI or medical management), although not supported by guidelines:
  • Discontinue 5–7 days prior to CABG due to bleeding risk. (Class I)
  • Continue at least 1 mo and ideally 1 yr after bare metal stent implantation. After drug eluting stent, continue at least 3 (sirolimus) to 6 (paclitaxel) mo, ideally 1 yr.
• Nitrates for ongoing chest pain; but avoid when systolic blood pressure (SBP) <90 mm Hg, RV infarction, or recent phosphodiesterase (PDE) inhibitor use.
• Adrenergic -receptor blockers (-blockers) (oral) relieve myocardial ischemia by lowering oxygen demand. Indicated for all ACS where hemodynamics permit. Goals are resting heart rate 50–60 beats/min and SBP <120 mm Hg.
• Oxygen supplementation for all patients
• Add unfractionated heparin (UFH) or subcutaneous low-molecular-weight heparin (LMWH) to aspirin/clopidogrel in UA/NSTEMI. (Class I)
  • Enoxaparin preferable to UFH in absence of renal failure or planned coronary artery bypass grafting (CABG) within 24 hr in UA/NSTEMI. (Class IIa).
• Platelet glycoprotein (GP) IIb/IIIa antagonists are optional alternatives to clopidogrel (Class 1), or may be added to clopidogrel (Class IIa) in UA/NSTEMI if (1) early catheterization planned or (2) recurrent ischemia occurs:
  • Eptifibatide or tirofiban for UA/NSTEMI.
  • Abciximab for STEMI undergoing PCI.
• ACE inhibitors indicated when LV ejection fraction (EF) <40, anterior infarction, or pulmonary congestion. An ARB is acceptable alternative for ACE-intolerant individuals. Start within 48 hr.
• Lipid-lowering therapy with hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) for all ACS regardless of lipid levels. Goal LDL <100 mg/dL, optional <70 mg/dL
• Aldosterone blockade (with spironolactone/eplerenone) for post-MI patients with CHF in absence of renal dysfunction or hyperkalemia.
• Treat ventricular arrhythmias with amiodarone or lidocaine.
• Fibrinolytic agents [alteplase (tPA), reteplase, or tenecteplase (TNK)] are alternatives to immediate PCI for STEMI. Contraindications include recent surgery, history of intracranial hemorrhage or aneurysm, severe HTN (SBP >170) and debatably older age (>75):
  • Up to 12 hr after symptom onset, though PCI is preferred if available within 90 min of presentation. STEMI patients in cardiogenic shock, those at increased risk of bleeding, or presenting late should always be managed with immediate PCI.
  • No fibrinolytic therapy for UA/NSTEMI.
• Diuretics for signs and symptoms of CHF
• Dobutamine 2–20 mcg/kg/min IV and/or Dopamine 5–15 mcg/kg/min IV, for SBP 70–100 mm Hg if signs of acute pulmonary edema or low-output cardiogenic shock
• Administer IV fluids for RV infarction.
• Insulin infusion may be necessary for DM.

Second Line

• Morphine sulfate IV for chest pain refractory to nitrates. 2 mg q5–15min
• Nondihydropyridine calcium channel blockers when -blockers contraindicated or when -blockers and nitrates fail to relieve symptoms of ischemia. Preferred agents for variant angina or cocaine-induced vasospasm.
• Bivalirudin and fondaparinux acceptable alternatives to heparin, especially in setting of heparin-induced thrombocytopenia.
• All NSAIDs are contraindicated.

Outline

• First Line
• Second Line

ADDITIONAL TREATMENT

General Measures

• STEMI: Reperfusion therapy is primary goal with STEMI or new LBBB MI. Risk of death, nonfatal MI, and recurrent ischemia reduced with early invasive strategy with PCI:
  • Therefore, preferred method is immediate PCI with door-to-balloon time <90 min
• UA/NSTEMI: Medical therapy to inhibit clotting cascade and decrease myocardial oxygen demand, and possibly PCI
• UA/NSTEMI: Early invasive strategy (PCI) beneficial with high-risk features
• Risk scores such as Thrombolysis In Myocardial Infarction (TIMI), Global Utilization of Strategies To Open occluded coronary arteries (GUSTO), Global Registry of Acute Coronary Events (GRACE), and Braunwald classifications help risk-stratify patients with UA/NSTEMI:
  • Identify UA/NSTEMI patients where early invasive strategy may improve outcomes

Referral

Follow-up 2–4 wk after discharge to evaluate functional status, cardiopulmonary symptoms and for medication changes.

Additional Therapies

• Cardiac rehabilitation recommended, with proven morbidity and mortality benefits
• Continual smoking cessation counseling
• Weight control
• Risk factor modification

SURGERY/OTHER PROCEDURES

CABG may be indicated with obstructive left main stenoses, 3-vessel disease, 2-vessel disease involving proximal left anterior descending artery (especially in diabetics or patients with depressed LV function), or obstructive stenoses not amenable to PCI.

IN-PATIENT CONSIDERATIONS

Admission Criteria

All patients with diagnosis of ACS should be admitted and have ECG monitoring.

Nursing

Smoking cessation counseling as inpatient

Discharge Criteria

No formal criteria. Patient should ideally be without chest pain, initiated on appropriate medications, with favorable vital signs. Control comorbidities such as DM.

Outline

• Additional Treatment
  • General Measures
  • Referral
  • Additional Therapies
• Surgery/Other Procedures
• In-Patient Considerations
  • Admission Criteria
  • Nursing
  • Discharge Criteria

FOLLOW-UP RECOMMENDATIONS

Patient Monitoring

• Cardiac care unit (CCU) monitoring for high-risk UA/NSTEMI and all STEMI patients
• No serial labs or imaging, though echo for post-MI LV EF is reasonable (>4 wk post discharge)

DIET

Low-fat, low-cholesterol, ie, AHA Step II diet; low sodium with HTN and CHF

PATIENT EDUCATION

• Educate patients on use of sublingual nitroglycerin for recurrent chest pain
• Driving, work and sexual activity may resume after 1–2 wk. PDE inhibitors contraindicated with nitrates

PROGNOSIS

• High risk of recurrent ACS.
• Patients with LV EF <35 >1 mo post MI, or with ventricular arrhythmias >2 days post MI, merit implantable cardioverter-defibrillator (ICD) due to risk of sudden cardiac death

COMPLICATIONS

• VSD in 1–2% in prethrombolytic era, usually 2–5 days after MI.
• Mitral regurgitation due to papillary muscle dysfunction or remodeled ventricle
• Cardiac rupture in 3% post MI cardiogenic shock
• Ventricular aneurysm or pseudoaneurysm
• Pericarditis affects 10% early. Late pericarditis (Dressler syndrome) 8 wk post MI.

Outline

• Follow-Up Recommendations
  • Patient Monitoring
• Diet
• Patient Education
• Prognosis
• Complications

CODES

ICD9

• 410.90 Acute myocardial infarction of unspecified site, episode of care unspecified
• 411.1 Intermediate coronary syndrome
• 414.00 Coronary atherosclerosis of unspecified type of vessel, native or graft
• 410.70 Subendocardial infarction, episode of care unspecified

SNOMED

• 394659003 acute coronary syndrome (disorder)
• 53741008 coronary arteriosclerosis (disorder)
• 401303003 acute ST segment elevation myocardial infarction (disorder)
• 401314000 acute non-ST segment elevation myocardial infarction (disorder)

CLINICAL PEARLS

• STEMI must be diagnosed quickly and treated with immediate revascularization, preferably PCI if available within 90 min.
• Elevated troponin or CK–MB levels are sine quo non of MI.
• ST-depression of >1 mm in V1–V3 may represent an acute posterior STEMI.
• Profound hypotensive response to nitroglycerin may signify RV infarct and is treated with IV fluids

Outline

• Codes
  • ICD9
  • SNOMED
• Clinical Pearls

ADDITIONAL READING

• Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007 Guidelines for the Management of Patients With UA/NSTEMI: A Report of the ACC/AHA. J Am Coll Cadiol. 2007;50(7):e1–157.
• Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with STEMI. J Am Coll Cardiol. 2004;44:671–719.
• Lloyd-Jones D, Adams R, Carnethon M, et al. Heart Disease and Stroke Statistics 2009 Update: A Report From the AHA. Circulation. 2009;119:e21–e181.
• Sabatine MS, Antman EM. The thrombolysis in myocardial infarction risk score in UA/NSTEMI. J Am Coll Cardiol. 2003;41:89S–95S.

Matthew Janik

Nanette K. Wenger