Myocardial infarction

Necrosis of heart muscle due to prolonged ischemia from an acute loss of coronary blood flow (usually plaque rupture with thrombosis). A type of acute coronary syndrome, it is diagnosed by evidence of myocardial injury (troponin rise) in the setting of ischemia; it is subdivided into ST-elevation MI (STEMI) or non-ST-elevation MI (NSTEMI) based on ECG changes.

• MI ("heart attack") is extremely common and a leading cause of death worldwide. Rapid intervention is critical: untreated large MIs can lead to acute heart failure, shock, arrhythmias (e.g. ventricular fibrillation), or sudden cardiac arrest. Early reperfusion therapy significantly reduces mortality ("time is muscle").

• Classic presentation: crushing substernal chest pain or pressure (often with diaphoresis, nausea, anxiety) that may radiate to the left arm, shoulder, neck, or jaw. Patients often have CAD risk factors (e.g. older age, smoking, hypertension, diabetes).
• Atypical presentations: especially in women, elderly, or diabetic patients, MI may present as dyspnea, fatigue, epigastric pain, or syncope without chest pain. Some MIs are "silent" and detected only by ECG or troponins. On exam, patients may be pale, in distress, with an S4 gallop or signs of acute heart failure (e.g. jugular venous distension, crackles) if large infarct.

1. Initial approach: Obtain a 12-lead ECG within 10 minutes for any chest pain patient and give aspirin (chewed). If ECG shows STEMI (ST elevations in specific leads or new LBBB), activate emergency reperfusion (PCI preferred) immediately.
2. Biomarkers: If initial ECG is non-diagnostic, measure troponin at presentation and 3-6 hours later. A significant troponin rise confirms myocardial infarction (NSTEMI if no ST elevation). Persistent chest pain with initially normal ECG should prompt repeat ECGs or consider posterior leads (V7–V9) for hidden STEMI.
3. Stratify ACS type: Unstable angina has ischemic chest pain but no troponin elevation, whereas NSTEMI has elevated troponin (and often ST depressions/T-wave inversions) without ST elevations. STEMI presents with ST elevations (transmural injury pattern) on ECG plus troponin rise. STEMI warrants immediate reperfusion, NSTEMI urgent invasive management (within 24–48h), unstable angina similar to NSTEMI management but no fibrinolytics.
4. Risk assessment: Assess hemodynamics and risk (e.g. Killip class for heart failure severity). High-risk features (e.g. hypotension, Killip ≥II, large troponin rise, ventricular arrhythmias) merit ICU-level care and prompt intervention. Screen for contraindications to therapies (like fibrinolysis) if applicable.

1. Immediate (acute MI): Aspirin ASAP (plus P2Y₁₂ inhibitor like ticagrelor), and anticoagulation (e.g. heparin) to limit thrombus. For STEMI, urgent reperfusion by PCI is first-line (within 90 min ideally) or fibrinolytic therapy if PCI not available. Give nitroglycerin for pain and blood pressure control; add morphine for persistent pain or anxiety. Oxygen if O₂ saturation <90%.
2. NSTEMI/UA management: no immediate fibrinolysis needed, but start dual antiplatelet therapy (aspirin + P2Y₁₂ inhibitor for 12 months), anticoagulate (heparin), and consider early invasive angiography (within 1–2 days, sooner if high risk). High-risk patients may get adjuncts like IV nitroglycerin for persistent pain or GP IIb/IIIa inhibitors during PCI. Monitor in telemetry for arrhythmias.
3. Adjunct meds: Start a beta blocker within 24 hours if no contraindications (reduces arrhythmias and oxygen demand). Begin an ACE inhibitor especially if anterior MI or if the patient has heart failure, reduced LVEF, hypertension, or diabetes. These help limit adverse remodeling.
4. Secondary prevention: Long-term, all patients should be on high-intensity statin therapy, aspirin indefinitely, plus continue beta-blocker and ACEi (if indicated) long-term. Arrange cardiac rehabilitation and counsel on lifestyle changes (smoking cessation, diet, exercise) to address risk factors. Some post-MI patients may benefit from aldosterone antagonists (if LVEF < 40% and HF or diabetes) or ICD placement (if severe LV dysfunction persists >40 days post-MI).

• Mnemonic MONA: Morphine, Oxygen, Nitrates, Aspirin for initial management of MI (oxygen only if hypoxemic; morphine for severe pain).
• Door-to-balloon time: for STEMI, aim <90 minutes from arrival for PCI (or <30 minutes to needle for thrombolytics if PCI unavailable).
• Killip classification stratifies acute MI by heart failure: Class I = no HF signs; II = mild HF (rales or S3 gallop); III = acute pulmonary edema; IV = cardiogenic shock.
• Heart attack ≠ cardiac arrest: Myocardial infarction is a circulation problem (muscle dies from lack of blood) whereas cardiac arrest is an electrical problem (heart stops pumping effectively, often due to arrhythmia); an MI can trigger an arrest, but not all arrests are due to MI.

• Chest pain with unequal pulses or tearing back pain → think aortic dissection, not a classic MI (get immediate imaging).
• Post-MI mechanical complications: watch for acute mitral regurgitation (papillary muscle rupture) or ventricular septal rupture (new harsh murmur, heart failure, shock), and free wall rupture leading to tamponade (PEA arrest) – these often occur 2–7 days post-MI and require emergency surgical intervention.
• Cardiogenic shock (persistent hypotension, confusion, cold extremities, low urine output) in MI indicates massive infarction or complication – requires urgent reperfusion, inotropic support, and possibly mechanical circulatory support.

1. Chest pain patient → ABCs, 12-lead ECG within 10 min, give aspirin.
2. STEMI on ECG? → Activate cath lab for PCI (goal <90 min door-to-balloon); if PCI unavailable quickly, give thrombolytic within 30 min of arrival.
3. No ST elevation → get troponins at 0 and 3-6h. If positive → NSTEMI (manage with medications and timely angiography); if negative but high suspicion persists → possible unstable angina (admit for observation, repeat ECG/troponin, or stress test).
4. Acute management: All MI (STEMI or NSTEMI) get DAPT (aspirin + P2Y₁₂ inhibitor), anticoagulation, and supportive care (nitroglycerin, β-blocker if stable, oxygen if needed). Address complications (e.g. arrhythmias, heart failure) promptly (consider temporary pacing for heart block, mechanical support for shock, etc).
5. After acute phase → transition to oral meds (aspirin, beta-blocker, ACEi, high-intensity statin) and initiate cardiac rehab and risk factor modification for long-term care.

• Diaphoretic 60-year-old man with crushing chest pain radiating to left arm, ST elevations in V2–V4 and elevated troponin → acute anterior STEMI (left anterior descending artery occlusion).
• 68-year-old diabetic woman with only nausea, vomiting, and shortness of breath; ECG shows T-wave inversions, troponin is elevated → NSTEMI with atypical presentation.