Myocardial Infarction (Heart Attack)

Content of This Page

Introduction

 1- Introduction

2- Causes

3- Pathophysiology

4- Signs & Symptoms

5- Risk Factors

6- ECG Changes

7- Investigations & Lab Results

8- Complications

9- Treatment

Myocardial infarction (MI), commonly known as a heart attack, occurs when there is sudden blockage of blood flow to a part of the heart muscle, leading to tissue death due to lack of oxygen. This usually happens because of a blood clot forming on a ruptured or eroded atherosclerotic plaque within a coronary artery. MI is extremely important in clinical practice because it is a major cause of death worldwide. Without urgent treatment, around 25% of patients die within minutes, and about 50% die within the first 24 hours. Even survivors face risks of serious complications such as heart failure, dangerous heart rhythms, and recurrent heart attacks. The condition places a huge burden on both healthcare systems and patients’ quality of life. Recognizing and treating MI quickly is crucial because timely intervention can restore blood flow, limit heart damage, and save lives. This is why the phrase “time is muscle” is often used in cardiology.
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Causes

  • Atherosclerotic plaque rupture or erosion (most common cause)

  • Coronary artery thrombosis (blood clot formation)

  • Coronary artery spasm (transient narrowing of the artery)

  • Severe coronary artery narrowing due to stable atherosclerosis

  • Imbalance between oxygen supply and demand :

    • Severe anaemia

    • Hypotension or shock

    • Sepsis

    • Tachyarrhythmias (e.g., atrial fibrillation)

    • Severe hypertension with or without left ventricular hypertrophy

  • Coronary artery dissection (tear in the artery wall)

  • Drug-induced vasospasm (e.g., cocaine, amphetamines)

  • Embolism to the coronary arteries (rare)

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Pathophysiology

  • Atherosclerotic plaque rupture or erosion → exposure of subendothelial collagen and lipid core → platelet adhesion, activation, and aggregation → formation of a thrombus (blood clot) → partial or complete blockage of a coronary artery → reduced blood flow to the myocardium (ischaemia) → shift to anaerobic metabolism and depletion of ATPaccumulation of lactate and hydrogen ions causing cellular injury → if the blockage persists beyond 20-30 minutesirreversible myocardial cell death (necrosis) begins → necrosis spreads from the subendocardium to the epicardium over several hours if not treated. the necrotic myocardium triggers inflammation and subsequent healing with scar formation.

Signs & Symptoms

  • Central chest pain (pressure, tightness, heaviness)

  • Pain radiating to left arm, jaw, neck, back

  • Pain duration >20 minutes

  • Not relieved by rest or nitroglycerin

  • Dyspnea (shortness of breath)

  • Diaphoresis (sweating)

  • Nausea and vomiting

  • Anxiety or a feeling of impending doom

  • Palpitations

  • Syncope or dizziness

  • Fatigue (especially in women, elderly, diabetics)

  • Atypical presentations (epigastric pain, indigestion-like symptoms)

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Risk Factors

  • Smoking

  • Hypertension

  • Diabetes mellitus

  • Hyperlipidemia (high LDL, low HDL)

  • Obesity

  • Sedentary lifestyle

  • Family history of premature coronary artery disease

  • Age (men >45 years, women >55 years)

  • Male sex

  • Stress and psychosocial factors

  • Excessive alcohol consumption

  • Chronic kidney disease

ECG Changes

  • ST-segment elevation (STEMI)

  • ST-segment depression (NSTEMI/Ischemia)

  • T-wave inversion

  • Pathological Q waves (indicate transmural infarction)

  • Hyperacute (peaked) T waves (early MI)

  • New left bundle branch block (LBBB)

  • Poor R wave progression

  • Arrhythmias (e.g., ventricular tachycardia, fibrillation)

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Complications

  • Arrhythmias (ventricular tachycardia, ventricular fibrillation)

  • Cardiogenic shock

  • Heart failure

  • Acute mitral regurgitation (papillary muscle rupture)

  • Ventricular septal rupture

  • Left ventricular free wall rupture → cardiac tamponade

  • Pericarditis (early or Dressler’s syndrome)

  • Left ventricular aneurysm

  • Thromboembolism (stroke, peripheral embolism)

  • Re-infarction

  • Dressler’s syndrome (post-MI pericarditis)

 

Investigations & Lab Results

-ECG

  • ST-segment elevation (STEMI)

  • ST-segment depression (NSTEMI/Ischemia)

  • T-wave inversion

  • Pathological Q waves (late finding)

-Cardiac Biomarkers

  • Troponin I/T – elevated (most sensitive and specific, rises within 3–6 hours)

  • CK-MB – elevated (useful for detecting reinfarction, rises within 3–6 hours)

  • Myoglobin – rises early but non-specific

-Blood Tests

  • Complete blood count (CBC) – may show leukocytosis

  • Renal function tests – for contrast use and overall assessment

  • Lipid profile – should be taken early (within 24 hours)

  • Blood glucose – often elevated in stress or diabetes

-Imaging

  • Chest X-ray – to exclude other causes (e.g., pneumothorax, heart failure)

  • Echocardiography – wall motion abnormalities, ejection fraction, complications

  • Coronary angiography – definitive for locating coronary artery blockages

-Other Tests

  • D-dimer – to rule out pulmonary embolism if indicated

  • BNP or NT-proBNP – assess for heart failure if suspected

Treatment

1. Initial Stabilization (MONA)

  • Morphine — for pain relief and anxiety

  • Oxygen — if O₂ saturation <90% or respiratory distress

  • Nitrates — to reduce preload and relieve chest pain (avoid if hypotension)

  • Aspirin — antiplatelet, chewable, immediately

2. Adjunct Medications

  • Beta-blockers — reduce myocardial oxygen demand, decrease arrhythmias (avoid in shock, bradycardia)

  • P2Y12 inhibitors — clopidogrel, ticagrelor, prasugrel to prevent platelet aggregation

  • Anticoagulants — unfractionated heparin or low molecular weight heparin

  • Statins — high intensity for plaque stabilization and lipid lowering

  • ACE inhibitors / ARBs — reduce remodeling and improve survival (especially with LV dysfunction, HTN)

3. Reperfusion Therapy

  • Primary PCI (Percutaneous Coronary Intervention) — preferred if within 90–120 minutes of first medical contact

  • Thrombolysis (Fibrinolytics) — if PCI unavailable within recommended timeframe

  • Coronary artery bypass grafting (CABG) — in multi-vessel disease or failed PCI

4. Management of Complications

  • Arrhythmias — antiarrhythmics, defibrillation if needed

  • Heart failure — diuretics, inotropes

  • Cardiogenic shock — inotropes, mechanical support if necessary

5. Secondary Prevention and Rehabilitation

    • Smoking cessation

    • Diet and exercise counseling

    • Control of diabetes, hypertension, lipids

    • Cardiac rehabilitation programs

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