Heart attack

Definition

A heart attack, medically known as myocardial infarction (MI), occurs when there is a sudden blockage of blood flow in a coronary artery, leading to ischemia and necrosis of the heart muscle. It is most often caused by rupture of an atherosclerotic plaque with subsequent thrombus formation.

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Classification

1. ST-elevation myocardial infarction (STEMI)

   • Full-thickness (transmural) myocardial necrosis

   • Characterized by persistent ST-segment elevation on ECG and elevated cardiac biomarkers

2. Non–ST-elevation myocardial infarction (NSTEMI)

   • Subendocardial myocardial necrosis

   • No persistent ST elevation on ECG but positive cardiac biomarkers

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Causes and Risk Factors

Primary cause

• Atherosclerotic plaque rupture and thrombus formation in a coronary artery

Other causes

• Coronary artery spasm (e.g., variant or Prinzmetal angina)

• Spontaneous coronary artery dissection (SCAD)

• Coronary embolism (rare)

• Severe anemia or hypoxia in patients with significant coronary disease

Risk factors

• Modifiable: Smoking, hypertension, diabetes mellitus, dyslipidemia, obesity, sedentary lifestyle, poor diet

• Non-modifiable: Age, male sex, family history of premature cardiovascular disease

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Pathophysiology

• Plaque rupture exposes thrombogenic material → platelet aggregation → thrombus formation

• Occlusion of coronary artery → cessation or severe reduction of blood flow to myocardial tissue

• Ischemia lasting >20–30 minutes causes irreversible myocyte death

• Necrosis triggers inflammatory response and scar formation over weeks

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Clinical Features

Typical symptoms

• Central, heavy, or crushing chest pain, often radiating to left arm, neck, jaw, or back

• Pain lasts more than 20 minutes, not fully relieved by rest or nitroglycerin

• Associated symptoms: shortness of breath, diaphoresis, nausea, vomiting, syncope

Atypical presentations

• More common in elderly, women, and diabetics

• May present with dyspnea, fatigue, syncope, epigastric discomfort, or no pain

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Diagnosis

Immediate priority: Rapid identification and treatment

Investigations:

1. Electrocardiogram (ECG) – within 10 minutes of presentation

   • STEMI: ST-segment elevation in ≥2 contiguous leads or new left bundle branch block

   • NSTEMI: ST depression, T-wave inversion, or nonspecific changes

2. Cardiac biomarkers

   • Troponin I/T: Elevated within 3–12 hours, remain elevated for days

   • CK-MB: Rises within 4–6 hours, returns to normal in 48–72 hours

3. Blood tests: CBC, electrolytes, renal function, glucose, lipid profile

4. Chest X-ray: Rule out other causes of chest pain, assess complications

5. Echocardiography: Assess wall motion abnormalities, complications

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Emergency Management

Aims: Restore coronary blood flow, limit myocardial damage, relieve symptoms, prevent complications

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Immediate (Pre-hospital or Emergency Department)

1. Airway, breathing, circulation – ensure stability

2. Oxygen if saturation <90%

3. Aspirin 300 mg orally (chewed) as soon as possible

4. Nitroglycerin 0.3–0.6 mg sublingual every 5 minutes as needed for chest pain (if no hypotension, RV infarction, or recent PDE5 inhibitor use)

5. Morphine 2–4 mg IV slowly for persistent severe pain (caution in hypotension or RV infarction)

6. Cardiac monitoring – for arrhythmia detection

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Reperfusion Therapy (STEMI)

• Primary percutaneous coronary intervention (PCI)

  • Preferred if performed within 120 minutes of first medical contact

  • Balloon angioplasty ± stent placement

• Fibrinolytic therapy (if PCI unavailable within timeframe and no contraindications)

  • Tenecteplase, alteplase, or streptokinase

  • Best if started within 30 minutes of hospital arrival and within 12 hours of symptom onset

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Medical Therapy During Acute Phase

• Dual antiplatelet therapy (DAPT)

  • Aspirin 300 mg loading dose → 75–100 mg daily

  • Plus clopidogrel 300–600 mg loading dose → 75 mg daily
    or ticagrelor 180 mg loading dose → 90 mg twice daily
    or prasugrel 60 mg loading dose → 10 mg daily (only in PCI patients without prior stroke/TIA)

• Anticoagulation

  • Unfractionated heparin IV bolus 60 units/kg (max 4000 units) → infusion

  • or Enoxaparin 1 mg/kg SC every 12 hours (adjust for renal function)

• Beta-blockers (e.g., metoprolol tartrate 25–50 mg orally every 6–12 hours, start within 24 hours if no contraindications)

• ACE inhibitors (e.g., ramipril start at 2.5 mg orally twice daily, titrate up) within 24 hours, especially if LVEF ≤40%

• High-intensity statin (e.g., atorvastatin 80 mg orally once daily) regardless of baseline cholesterol

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Post-MI Long-Term Management

Lifestyle modifications

• Smoking cessation, healthy diet, regular exercise, weight management

Ongoing medications (unless contraindicated)

• Aspirin (lifelong)

• P2Y12 inhibitor (12 months post-PCI or post-MI)

• Beta-blocker

• ACE inhibitor or ARB

• Statin

• Aldosterone antagonist (e.g., eplerenone 25–50 mg daily) in patients with LVEF ≤40% and symptoms of HF or diabetes

Cardiac rehabilitation – structured exercise and education program

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Complications

• Arrhythmias (ventricular fibrillation, atrial fibrillation, heart block)

• Cardiogenic shock

• Heart failure

• Mechanical complications (papillary muscle rupture, ventricular septal rupture, free wall rupture)

• Pericarditis

• Left ventricular thrombus and embolism

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Prognosis

• Depends on infarct size, time to reperfusion, and post-MI complications

• Early reperfusion and evidence-based medications significantly improve survival