Myocardial Infarction, Acute with ST-Segment Elevation

Essentials of Diagnosis

• Sudden but not instantaneous development of prolonged (> 30 minutes) anterior chest discomfort (sometimes felt as "gas" or pressure)

• Sometimes painless, masquerading as acute heart failure (HF), syncope, stroke, or shock

• ECG: ST-segment elevation myocardial infarction (STEMI) or left bundle branch block

• Immediate reperfusion treatment is warranted

  • Primary percutaneous coronary intervention (PCI) within 90 minutes of first medical contact is the goal and is superior to fibrinolytic therapy

  • Fibrinolytic therapy within 30 minutes of hospital presentation is the goal (if PCI is not possible) and reduces mortality if given within 12 hours of onset of symptoms

General Considerations

• Results, in most cases, from an occlusive coronary thrombus at the site of a preexisting (though not necessarily severe) atherosclerotic plaque

• More rarely, may result from prolonged vasospasm, inadequate myocardial blood flow (eg, hypotension), or excessive metabolic demand

• Very rarely, may be caused by embolic occlusion, vasculitis, aortic root or coronary artery dissection, or aortitis

• Cocaine use may cause infarction and should be considered in young individuals without risk factors

Symptoms and Signs

• Recent onset of angina or alteration in the pattern of angina or chest pressure, squeezing or "indigestion"

• Pain characteristics

  • Similar to angina in location and radiation but more severe

  • Usually occurs at rest, often in the early morning

  • Builds rapidly

  • Minimally responsive to sublingual nitroglycerin or oral opioids

• Associated symptoms

  • Diaphoresis

  • Weakness

  • Apprehensiveness

  • Aversion to lying quietly

  • Light-headedness

  • Syncope

  • Dyspnea

  • Orthopnea

  • Cough

  • Wheezing

  • Nausea and vomiting

  • Abdominal bloating

• 33% of patients do not experience chest pain, especially older patients, women, and patients with diabetes

• Of all deaths due to myocardial infarction, ~50% occur before patient reaches the hospital, usually of ventricular fibrillation

• Marked bradycardia (inferior infarction) to tachycardia (increased sympathetic activity, low cardiac output, or arrhythmia)

• Jugular venous distention indicates right atrial hypertension, often from RV infarction or elevated LV filling pressures

• Soft heart sounds may indicate LV dysfunction

• S₄ is common; S₃ indicates significant LV dysfunction

• Mitral regurgitation murmur usually indicates papillary muscle dysfunction or, rarely, rupture

• Pericardial friction rubs are uncommon in the first 24 hours but may appear later

• Edema is usually not present

• Cyanosis and cold temperature indicate low output

• Peripheral pulses should be noted, since later shock or emboli may alter the examination

Differential Diagnosis

• Acute coronary syndrome without ST-segment elevation

• Aortic dissection

• Pulmonary embolism

• Tension pneumothorax

• Pericarditis

• Esophageal rupture

• Stress cardiomyopathy (Tako-Tsubo cardiomyopathy or apical ballooning syndrome)

Laboratory Tests

• Quantitative CK-MB, troponin I, and troponin T elevations as early as 4–6 h after onset; almost always abnormal by 8–12 h

• Troponins

  • May remain elevated for ≤ 5–7 days

  • Therefore, not generally useful for evaluating suspected early reinfarction

• High-sensitivity troponin assays

  • When positive, help enable myocardial infarction to be detected earlier

  • Many conditions, including chronic HF are associated with elevated levels

  • When negative, may be useful in excluding myocardial infarction in patients with chest pain

Imaging Studies

• Chest radiograph: signs of HF, often lagging behind the clinical findings

• Echocardiography: assesses global and regional LV function, wall motion

• Doppler echocardiography: can diagnose postinfarction mitral regurgitation or ventricular septal defect

• Thallium-201 or technetium scintigraphy does not distinguish recent from old myocardial infarction

Diagnostic Procedures

• Angiography: can demonstrate akinesis or dyskinesis and measures ejection fraction

• Swan-Ganz hemodynamic measurements: can be invaluable in managing suspected cardiogenic shock

• ECG

  • Extent of abnormalities, especially the sum of the total amount of ST-segment deviation, is a good indicator of extent of acute infarction and risk of subsequent adverse events

  • The classic evolution of changes is from peaked ("hyperacute") T waves, to ST-segment elevation, to Q wave development, to T wave inversion; this may occur over a few hours to several days

  • The evolution of new Q waves (> 30 milliseconds in duration and 25% of the R wave amplitude) is diagnostic, but Q waves do not occur in 30–50% of acute infarctions (non-Q wave infarctions)

Medications

• Aspirin

  • All patients with definite or suspected acute myocardial infarction should receive aspirin at a dose of 162 mg or 325 mg at once regardless of whether fibrinolytic therapy is being considered or the patient has been taking aspirin

  • Chewable aspirin provides more rapid blood levels

• Fibrinolytic therapy (see Table 10–10)

  • Reduces mortality and limits infarct size in patients with acute myocardial infarction associated with ST-segment elevation (defined as ≥ 0.1 mV in two inferior or lateral leads or two contiguous precordial leads), or with left bundle branch block

  • Greatest benefit occurs if initiated within the first 3 hours, when up to a 50% reduction in mortality rate can be achieved

  • The magnitude of benefit declines rapidly thereafter, but a 10% relative mortality reduction can be achieved up to 12 hours after the onset of chest pain

• P2Y₁₂ inhibitors (eg, prasugrel, ticagrelor, or clopidogrel)

  • Given to patients with a definite aspirin allergy

  • P2Y₁₂ inhibitors, in combination with aspirin, have been shown to be beneficial to patients with acute STEMI

  • Guidelines call for a P2Y₁₂ inhibitor to be added to aspirin to all patients with STEMI, regardless of whether reperfusion is given, and continued for at least 14 days, and generally for 1 year

  • Prasugrel and ticagrelor are preferred; both have shown superior outcomes compared to clopidogrel

  • Prasugrel

    • Dose is 60 mg orally on day 1, then 10 mg daily

    • Contraindicated in patients with history of stroke or who are older than 75 years

  • Ticagrelor

    • Dose is 150 mg orally on day 1, then 90 mg twice daily

  • Clopidogrel

    • Loading dose of 600 mg orally (or 300 mg) results in faster onset of action than standard 75 mg maintenance dose

• Dual antiplatelet therapy (DAPT) (combination of aspirin and a P2Y₁₂ inhibitor)

  • Indicated for 1 year in patients with an acute coronary syndrome (ACS), including those with medical therapy and those patients undergoing revascularization

  • Recommended for at least 1 month for patients receiving bare metal stents

  • Recommended for at least 1 year for patients receiving drug-eluting stents

  • The DAPT study showed that up to 30 months of therapy in patients who had received drug-eluting stents resulted in fewer death, myocardial infarction, and stroke events but also more bleeding and a tendency for higher mortality

• Nitroglycerin

  • Agent of choice for continued or recurrent ischemic pain

  • Useful in lowering BP or relieving pulmonary congestion

• Morphine sulfate, 4–8 mg intravenously, or meperidine, 50–75 mg intravenously, if nitroglycerin alone does not relieve pain

• Enoxaparin reduced death and myocardial infarction at day 30 (compared with unfractionated heparin) at the expense of a modest increase in bleeding

  • Give as a 30-mg intravenous bolus and 1 mg/kg every 12 hours for patients aged < 75 years

  • Give with no bolus and 0.75 mg/kg intravenously every 12 hours for patients aged ≤ 75 years

• Fondaparinux reduced death and reinfarction (compared with unfractionated heparin when indicated, otherwise placebo) with less bleeding

  • Dose: 2.5 mg once daily subcutaneously

  • Not recommended as sole anticoagulant during PCI due to risk of catheter thrombosis

• Glycoprotein IIb/IIIa inhibitors, specifically abciximab, have been shown to reduce major thrombotic events, and possibly mortality, for patients undergoing primary PCI

• Triple therapy with aspirin, clopidogrel, and warfarin

  • Anticoagulation therapy in patients who have received a coronary stent presents particular challenge because triple therapy with aspirin, clopidogrel, and warfarin has a high risk of bleeding

  • Triple therapy should be

    • Limited to patients with a clear indication for warfarin (such as atrial fibrillation with a CHADS₂ score of 2 or more or a mechanical prosthetic valve)

    • Used for the shortest period of time (such as 1 month after placement of bare metal stent); drug-eluting stents that would require longer clopidogrel duration should be avoided if possible

    • Used with low-dose aspirin and with strategies to reduce risk of bleeding (eg, proton pump inhibitors for patients with a history of gastrointestinal bleeding)

    • Used with consideration of a lower target anticoagulation intensity (INR 2.0 to 2.5, at least for the indication of atrial fibrillation) during the period of concomitant treatment with aspirin and P2Y₁₂ therapy

  • The PIONEER trial

    • Evaluated rivaroxaban 2.5 mg twice daily plus clopidogrel, rivaroxaban 15 mg once daily plus clopidogrel, and warfarin plus aspirin plus clopidogrel, for patients with atrial fibrillation who had coronary stent placement, with a primary outcome of bleeding

    • There was less bleeding in the rivaroxaban plus clopidogrel arms than with "triple therapy," although the trial was not powered to assess efficacy, and thus the low dose of rivaroxaban may be inadequate

    • Consensus statements recommend that for patients with atrial fibrillation and coronary stents, oral anticoagulation (with either warfarin or direct-acting oral anticoagulation) be combined with clopidogrel with a relatively short duration of aspirin (from hospital discharge up to 3 months for the typical patient with atrial fibrillation and coronary stents)

  • Dabigatran, 110 mg and 150 mg, was also studied after PCI in patients with atrial fibrillation

    • Dual therapy with dabigatran and clopidogrel was shown to be beneficial for bleeding compared to triple therapy, with similar rates of thrombotic cardiovascular events

    • However, there were too few thrombotic events to be certain about efficacy of dropping the aspirin, and there was a suggestion of more MI and stent thrombosis with the 110 mg dose of dabigatran than with clopidogrel alone

Therapeutic Procedures

• ST elevation connotes an acute coronary occlusion and thus warrants immediate reperfusion therapy

• Primary PCI is the approach of choice in patients with absolute and many relative contraindications to fibrinolytic therapy

• In patients with cardiogenic shock, early catheterization and percutaneous or surgical revascularization are the preferred management and has been shown to reduce mortality

• For patients who have received fibrinolytic therapy but will undergo angiography in the first day or two, the early benefits of a P2Y₁₂ inhibitor need to be weighed against the necessary delay in bypass surgery for approximately 5 days for those patients found to require surgical revascularization

• See eTable 10–2

Follow-Up

• For nonhypotensive patients with low ejection fractions, large infarctions, or clinical evidence of HF, start ACE inhibitor on first postinfarction day; titrate and continue long-term

• Diltiazem appears to prevent reinfarction and ischemia in patients with non–Q-wave infarctions

• Patients with recurrent ischemic pain prior to discharge should undergo catheterization and, if indicated, revascularization

Complications

• Myocardial dysfunction, HF, and hypotension

• Postinfarction ischemia

• Sinus bradycardia, sinus tachycardia

• Supraventricular premature beats

• Atrial fibrillation, ventricular fibrillation

• Ventricular premature beats

• Ventricular tachycardia

• Accelerated idioventricular rhythm

• RBBB or LBBB or fascicular blocks

• Second- or third-degree AV block

• Rupture of a papillary muscle, interventricular septum, or LV free wall

• LV aneurysm

• Pericarditis, Dressler syndrome

• Mural thrombi

Prevention

• Control LDL cholesterol and BP

• Beta-blockers

• Antiplatelet agents

• Exercise training and cardiac rehabilitation programs

Prognosis

• Killip classification classifies HF in patients with acute myocardial infarction and has powerful prognostic value

  • Class I is absence of rales and S₃

  • Class II is rales that do not clear with coughing over one-third or less of the lung fields or presence of an S₃

  • Class III is rales that do not clear with coughing over more than one-third of the lung fields

  • Class IV is cardiogenic shock (rales, hypotension, and signs of hypoperfusion)

When to Refer

• All patients with acute myocardial infarction should be referred to a cardiologist

When to Admit

• All patients with possible myocardial infarction to the CCU