Heart Attack (Myocardial Infarction) — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

A heart attack — medically termed myocardial infarction (MI) — occurs when blood supply to a region of the heart muscle is abruptly interrupted, most often due to rupture of an atherosclerotic plaque in a coronary artery followed by thrombosis (clot formation). Without blood supply, heart muscle begins to die (infarct) within minutes. Cardiovascular disease causes approximately 18 million deaths annually, making MI the leading cause of death worldwide. Two main types exist: ST-elevation myocardial infarction (STEMI), where complete coronary occlusion causes full-thickness infarction requiring emergency reperfusion; and Non-STEMI (NSTEMI), where partial obstruction causes subendocardial damage — still serious but treated differently. Time from symptom onset to reperfusion (opening the artery) directly determines the amount of heart muscle saved: 'time is muscle'.

The underlying cause is coronary artery disease (CAD) — atherosclerosis, the build-up of lipid-rich plaques within coronary artery walls over decades. Plaque rupture exposes thrombogenic material, triggering platelet aggregation and coronary thrombus formation that occludes the vessel. Modifiable risk factors: hypertension (most important — doubles MI risk), smoking (2-4x risk), dyslipidaemia (elevated LDL cholesterol — direct cause of atherosclerosis), type 2 diabetes (2-4x risk), obesity, physical inactivity, unhealthy diet, alcohol excess, and psychological stress. Non-modifiable risk factors: male sex (risk 10-15 years earlier than females), increasing age, family history of premature CAD (first-degree relative under 55 male, under 65 female), and South Asian ethnicity (higher coronary risk). Less common causes of MI: coronary artery spasm (Prinzmetal's angina), coronary dissection (young women, peripartum), cocaine-induced vasospasm, and embolism.

Classic STEMI presentation: severe central crushing chest pain, often described as 'elephant sitting on the chest' — constant, not relieved by rest or nitrates, radiating to the left arm, jaw, neck, or back; accompanied by sweating (diaphoresis), nausea, vomiting, breathlessness, pallor, and sense of impending doom. Onset often at rest or with minimal exertion. Duration typically over 20 minutes (distinguishing from angina). Atypical presentations — more common in women, elderly, and diabetic patients — include epigastric pain, breathlessness alone, fatigue, arm or jaw pain, or sudden collapse. Silent MI (no symptoms) occurs in approximately 25% of cases. Signs: pallor, sweating, hypotension (cardiogenic shock), tachycardia or bradycardia, elevated JVP and lung crackles (acute pulmonary oedema), or new mitral regurgitation murmur (papillary muscle rupture).

12-lead ECG is the first and most critical investigation — performed within 10 minutes of hospital arrival. STEMI: ST-segment elevation in contiguous leads (>1mm limb leads; >2mm V1-V4), new LBBB, or posterior MI pattern. NSTEMI/Unstable Angina: ST-depression, T-wave inversion, or normal ECG. Cardiac biomarkers: high-sensitivity troponin I or T (hs-cTn) is the gold standard — rise in serum troponin confirms myocardial necrosis. ESC 0h/1h or 0h/2h algorithm using hs-cTn allows rapid rule-in or rule-out of NSTEMI. Serial ECGs every 30 minutes if initial ECG is non-diagnostic. Echocardiography: identifies regional wall motion abnormalities, left ventricular function (EF), complications (VSD, papillary muscle rupture, pericardial effusion). Coronary angiography defines the culprit lesion and guides revascularization. CT coronary angiography is used in low-to-intermediate risk NSTEMI for rapid assessment.

STEMI emergency treatment: Call emergency services immediately — 'Time is muscle.' Aspirin 300mg immediately (antiplatelet) plus P2Y12 inhibitor (ticagrelor 180mg or prasugrel) given at first medical contact. Primary Percutaneous Coronary Intervention (PPCI): emergency coronary angioplasty + stenting to re-open the blocked artery — target door-to-balloon time under 90 minutes. PPCI reduces 30-day mortality from approximately 9% (thrombolysis) to approximately 6-7% and is the preferred reperfusion strategy when available within 120 minutes. Thrombolysis (fibrinolytic therapy — tenecteplase, alteplase) is used when PPCI is not available within 120 minutes of diagnosis. Post-MI secondary prevention: dual antiplatelet therapy (aspirin + ticagrelor or clopidogrel) for 12 months; high-intensity statin (atorvastatin 40-80mg — target LDL <1.4 mmol/L); ACE inhibitor or ARB (reduces LV remodelling, prevents heart failure); beta-blocker (reduces arrhythmia risk, heart rate, and mortality). Aldosterone antagonist (eplerenone) added if EF under 40% with heart failure signs. Cardiac rehabilitation — supervised exercise and lifestyle program — improves survival after MI.

Acute in-hospital complications of myocardial infarction include cardiogenic shock (acute pump failure with hypotension requiring inotropes or IABP — mortality 40–50%), acute pulmonary oedema from left ventricular failure, and life-threatening arrhythmias (ventricular fibrillation — highest risk in first 24 hours; ventricular tachycardia; complete heart block in inferior MI from right coronary artery occlusion). Mechanical complications at 3–7 days post-STEMI include papillary muscle rupture causing acute severe mitral regurgitation, ventricular septal defect (VSD), and left ventricular free wall rupture — all require emergency surgical repair. Late complications: left ventricular remodelling and dilatation leading to heart failure (ischaemic cardiomyopathy — EF below 40%), left ventricular aneurysm formation (substrate for recurrent VT), and mural thrombus with systemic embolisation. Post-MI depression and anxiety affect 30–40% of survivors and independently increase recurrent event risk.

Primary prevention: control the major modifiable risk factors — treat hypertension to target below 130/80 mmHg, achieve LDL cholesterol under 2.5 mmol/L (statins for high-risk individuals), quit smoking (within 1 year of quitting, MI risk halves), control blood sugar in diabetes (HbA1c under 7%), achieve healthy weight, exercise 150+ minutes weekly, adopt Mediterranean-style diet. Aspirin is not recommended for primary prevention in most people due to bleeding risk exceeding benefit. Secondary prevention (after MI): all patients require lifelong aspirin, high-intensity statin, ACE inhibitor, and beta-blocker unless contraindicated. Annual cardiology review. Cardiac rehabilitation reduces recurrent MI risk and improves quality of life. Defibrillator training in public spaces (AEDs) improves out-of-hospital cardiac arrest survival.

CALL EMERGENCY SERVICES (999/911/112) IMMEDIATELY for: severe chest pain or tightness lasting over 15 minutes, chest pain radiating to the arm, jaw, or back, sudden breathlessness with chest discomfort, loss of consciousness, or collapse. Do not drive yourself to hospital — every minute of delay causes additional heart muscle death. Chew one aspirin (300mg) if available and not allergic, while waiting for the ambulance. For established heart disease patients, any new chest pain that is more severe, longer lasting, occurs at rest, or is not relieved by nitrates warrants immediate emergency review. Do not ignore atypical symptoms (jaw pain, back pain, severe indigestion) in known cardiac patients.