Introduction

Myocardial infarction (MI), commonly referred to as a heart attack, occurs when there is an abrupt reduction or cessation of blood flow to a part of the myocardium, leading to ischemia and necrosis. The most common cause is atherosclerotic plaque rupture, followed by thrombus formation in a coronary artery. Without oxygen and nutrients, irreversible myocardial cell death begins within 20–40 minutes.

• MI is a time-dependent emergency.

• The condition is central to ischemic heart disease (IHD), which is the leading cause of cardiovascular morbidity and mortality worldwide.

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Statistics

• According to WHO (2023), cardiovascular diseases account for 17.9 million deaths annually, with MI and stroke representing the largest share.

• In the U.S., ~805,000 MIs occur yearly, of which ~75% are first events and 25% are recurrent.

• Mortality rates:

  • In-hospital mortality for STEMI ≈ 7–10% (higher in elderly & women).

  • 30-day mortality ≈ 15%, but can be significantly reduced with rapid reperfusion therapy.

• Global burden: Developing countries now face rising MI incidence due to urbanization, sedentary lifestyles, and dietary changes.

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 Risk Factors

MI risk factors are broadly classified as modifiable and non-modifiable.

• Modifiable:

  • Hypertension: causes endothelial injury, accelerates atherosclerosis.

  • Dyslipidemia: high LDL and low HDL promote plaque formation.

  • Smoking: increases platelet aggregation, vasoconstriction, and oxidative stress.

  • Diabetes mellitus: accelerates atherosclerosis via glycation of end-products and endothelial dysfunction.

  • Obesity and metabolic syndrome: linked to insulin resistance and hypertension.

  • Sedentary lifestyle & diet: diets high in trans fats, salt, and sugar increase risk.

  • Alcohol & stress: contribute to arrhythmias, hypertension, and metabolic imbalance.

• Non-modifiable:

  • Age: risk increases sharply after 45 in men, 55 in women.

  • Sex: men more prone at younger ages; postmenopausal women approach similar risk.

  • Genetics/family history: first-degree relative with early CAD significantly increases risk.

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 Signs and Symptoms

• Typical presentation (classic angina equivalent):

  • Central chest pain or discomfort, often described as pressure, squeezing, or heaviness.

  • Pain radiates to the left arm, neck, jaw, shoulder, or back.

  • Associated symptoms: dyspnea, diaphoresis, nausea, vomiting, palpitations, and anxiety (“impending doom”).

  • Pain usually lasts >20 minutes and is not fully relieved by rest or nitroglycerin.

• Atypical presentations:

  • Epigastric discomfort, indigestion-like pain.

  • Syncope, confusion (common in elderly).

  • Silent MI: particularly in diabetics due to autonomic neuropathy.

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Classifications and Sub-classes

By Pathophysiology (Universal Definition of MI):

• Type 1: Spontaneous MI due to primary coronary event (plaque rupture/erosion, dissection).

• Type 2: Secondary MI due to imbalance in oxygen supply and demand (e.g., anemia, hypoxia, hypotension, arrhythmias).

• Type 3: Sudden unexpected cardiac death with symptoms suggestive of MI, before biomarkers are available.

• Type 4a: MI related to percutaneous coronary intervention (PCI).

• Type 4b: MI caused by stent thrombosis.

• Type 5: MI associated with coronary artery bypass grafting (CABG).

By ECG changes:

• ST-Elevation MI (STEMI):

  • Complete coronary occlusion.

  • Characterized by persistent ST elevation in ≥2 contiguous leads or new LBBB.

• Non-ST Elevation MI (NSTEMI):

  • Partial coronary occlusion.

  • ECG shows ST depression, T-wave inversion, or non-specific changes.

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 Diagnostic Procedures & Tests

1. Electrocardiogram (ECG):

   • Gold standard first-line test.

   • STEMI: ST elevation, pathological Q waves, new LBBB.

   • NSTEMI: ST depression, T-wave inversion.

2. Biomarkers:

   • Cardiac troponins (I, T): rise within 3–6 hours, peak at 12–24 hours, remain elevated 7–14 days.

   • CK-MB: rises in 3–12 hours, peaks at 24 hours, normalizes within 48–72 hours → useful for detecting reinfarction.

3. Imaging:

   • Echocardiography: assesses wall motion abnormalities, ejection fraction.

   • Coronary angiography: definitive test for coronary anatomy and blockages.

   • Cardiac MRI: identifies infarct size, viability, and complications.

4. Additional labs: Lipid profile, glucose, renal function, electrolytes.

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Treatment and Management

Acute/Emergency Management (first hours):

• MONA-B: Morphine, Oxygen, Nitrates, Aspirin, Beta-blockers.

• Dual antiplatelet therapy (DAPT): Aspirin + clopidogrel/ticagrelor.

• Anticoagulants: unfractionated heparin, LMWH, or bivalirudin.

• Reperfusion therapy:

  • Primary PCI (preferred if available within 90 minutes).

  • Fibrinolysis (e.g., alteplase, streptokinase, tenecteplase): if PCI not available within 120 minutes.

• Adjunct therapies: high-dose statins, ACE inhibitors, aldosterone antagonists (in select patients).

Long-term/Secondary Prevention:

• Continue Aspirin + P2Y12 inhibitor (DAPT for 6–12 months, then lifelong aspirin).

• Beta-blockers: reduce arrhythmias and myocardial oxygen demand.

• Statins: high-intensity to lower LDL <70 mg/dL.

• ACE inhibitors/ARBs: reduce remodeling, mortality.

• Lifestyle changes: diet, exercise, smoking cessation, cardiac rehab.

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Complications

Early (within 24–72 hrs):

• Arrhythmias: Ventricular tachycardia, Ventricular fibrillation, Atrio-ventricular block.

• Cardiogenic shock: severe LV dysfunction.

• Acute heart failure: pulmonary edema.

• Pericarditis: inflammation due to necrosis (fibrinous).

Late (days to weeks):

• Ventricular septal rupture → acute heart failure.

• Papillary muscle rupture → severe mitral regurgitation.

• Free wall rupture → cardiac tamponade, sudden death.

• LV aneurysm (weeks to months) → risk of thrombus and embolism.

• Dressler’s syndrome: autoimmune pericarditis (2–6 weeks post-MI).

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 Prevention

Primary prevention (before MI):

• Control risk factors: blood pressure, diabetes, lipids.

• Promote healthy diet (Mediterranean-style diet), physical activity, and weight control.

• Smoking cessation and moderation of alcohol.

• Low-dose aspirin for select high-risk patients.

Secondary prevention (after MI):

• Strict adherence to DAPT, statins, ACE inhibitors, beta-blockers.

• Lifestyle modifications.

• Participation in cardiac rehabilitation programs.

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Conclusion

Myocardial infarction remains a leading global health burden. With advances in reperfusion strategies, antiplatelet therapy, and secondary prevention, survival rates have improved significantly. Nevertheless, early recognition, rapid treatment, and strict control of risk factors are crucial for improving outcomes. Preventive strategies focusing on lifestyle and medical management remain the cornerstone of reducing incidence and recurrence of MI.