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

A heart attack (acute myocardial infarction, AMI) occurs when blood flow through a coronary artery is suddenly and completely or severely blocked, causing ischaemic necrosis of the supplied myocardium. The underlying cause in over 90% of cases is acute plaque rupture or erosion in an atherosclerotic coronary artery, triggering platelet aggregation and thrombus formation. AMI is classified by ECG pattern: ST-elevation MI (STEMI) — complete coronary occlusion requiring emergency reperfusion within 90 minutes; and non-ST-elevation MI (NSTEMI) — partial occlusion with myocardial injury. Globally, ischaemic heart disease causes approximately 9 million deaths annually. In the USA, 805,000 heart attacks occur yearly, with one occurring every 40 seconds. Prompt recognition and treatment are life-saving — 'time is muscle.' Recognising the wide spectrum of heart attack presentations — including atypical presentations without classic chest pain that are more common in women, elderly patients, and those with diabetes — is critical for reducing the treatment delays that result in avoidable myocardial damage and preventable deaths.

Atherosclerosis — progressive lipid-rich plaque accumulation in coronary artery walls — is the underlying pathology in the vast majority of heart attacks. Plaque rupture exposes the subendothelial matrix to circulating platelets, triggering thrombus formation and coronary occlusion. Major modifiable risk factors: hypertension (systolic above 130 mmHg), hypercholesterolaemia (especially elevated LDL cholesterol), cigarette smoking (doubles cardiovascular risk), type 2 diabetes mellitus, obesity (BMI above 30), physical inactivity, and unhealthy diet (high saturated fat, trans fats, low fruits and vegetables). Non-modifiable risk factors: male sex, age (over 45 in men, over 55 in women), family history of premature coronary heart disease (first-degree relative below 55 years in males, below 65 in females), and genetic hyperlipidaemias. Rarer causes include coronary artery spasm (Prinzmetal's angina), cocaine use, coronary dissection (SCAD — affecting young women), and vasculitis.

Classic presentation: severe, crushing or squeezing central chest pain radiating to the left arm, jaw, neck, or back, lasting more than 15–20 minutes, not relieved by rest or nitrates. Diaphoresis (profuse sweating), pallor, nausea, vomiting, and a sense of impending doom are characteristic. Atypical presentations (common in women, elderly, and diabetics — who may have autonomic neuropathy blunting pain): epigastric pain, dyspnoea as the sole symptom, fatigue, syncope, jaw or arm pain without chest pain, or sudden-onset heart failure. Signs on examination: tachycardia, hypotension (cardiogenic shock — systolic below 90 mmHg), signs of cardiac failure (raised JVP, third heart sound, bilateral crepitations), and diaphoresis. Silent MI: entirely asymptomatic — detected retrospectively on ECG or imaging; more common in diabetics.

12-lead ECG: must be performed within 10 minutes of presentation — STEMI diagnosis requires ST elevation above 1 mm in at least 2 contiguous limb leads or above 2 mm in precordial leads (or new LBBB). Posterior MI: ST depression in V1–V4 (posterior leads V7–V9 confirm). NSTEMI shows ST depression, T-wave inversion, or new ECG changes without ST elevation. Cardiac troponin (high-sensitivity troponin T or I — hsTnT/hsTnI): the definitive biomarker of myocardial injury — elevated above the 99th percentile reference limit, with a rise and/or fall pattern. 0-hour/3-hour or 0-hour/1-hour rapid rule-out protocols (ESC 0/1h algorithm using hs-troponin) allow same-day diagnosis or exclusion. Echocardiogram: assesses left ventricular function, wall motion abnormalities, and complications (mitral regurgitation, VSD, pericardial effusion). Coronary angiography: defines coronary anatomy and identifies the culprit lesion for intervention.

STEMI — emergency reperfusion (time-critical): Primary percutaneous coronary intervention (primary PCI) — balloon angioplasty of the culprit coronary artery with drug-eluting stent implantation — within 90 minutes of first medical contact is the gold standard (reduced mortality from 30% to under 5%). Fibrinolysis (alteplase, tenecteplase) is used when primary PCI is not available within 120 minutes. Adjunctive pharmacotherapy: aspirin 300 mg loading dose immediately (then 75 mg daily lifelong); P2Y12 inhibitor — ticagrelor 180 mg loading (preferred) or prasugrel or clopidogrel; anticoagulation with unfractionated heparin or bivalirudin during PCI; IV beta-blocker (metoprolol) if no heart failure; glycoprotein IIb/IIIa inhibitor (tirofiban) for complex PCI. NSTEMI: dual antiplatelet therapy (aspirin + ticagrelor/clopidogrel); anticoagulation; risk stratification with GRACE or TIMI score; early invasive strategy within 24–72 hours for high-risk NSTEMI. Secondary prevention (all MI): high-intensity statin (atorvastatin 80 mg — target LDL below 1.4 mmol/L); ACE inhibitor (ramipril) or ARB; beta-blocker (bisoprolol or carvedilol — for at least 12 months or lifelong if reduced EF); mineralocorticoid antagonist (eplerenone) if EF below 35%; cardiac rehabilitation programme.

Without timely reperfusion, myocardial infarction causes numerous serious early and late complications. Early mechanical complications: cardiogenic shock — severe left ventricular dysfunction causing hypotension, impaired organ perfusion, and mortality of 40-60% despite treatment; ventricular free wall rupture (3-5 days post-MI) causing cardiac tamponade and sudden death; ventricular septal defect (VSD — from septal necrosis) causing acute left-to-right shunt requiring emergency surgical repair; papillary muscle rupture causing acute severe mitral regurgitation and pulmonary oedema. Arrhythmias: ventricular fibrillation (VF) causes sudden cardiac death in the first hours; complete heart block (from inferior MI); atrial fibrillation (associated with 1.5x increased 30-day mortality). Left ventricular dysfunction (reduced ejection fraction) leads to chronic heart failure in up to 40% of post-MI patients — causing breathlessness, reduced exercise tolerance, and fluid retention. Pericarditis (Dressler syndrome — 2-10 weeks post-MI) causes pleuritic chest pain requiring NSAIDs or colchicine. Left ventricular aneurysm (dyskinetic wall segment) may develop in anterior STEMI — a reservoir for mural thrombus causing cardioembolic stroke. Post-MI angina and reinfarction remain significant risks without optimal secondary prevention, highlighting the critical importance of cardiac rehabilitation and lifelong pharmacotherapy adherence.

Primary prevention targets modifiable cardiovascular risk factors: stop smoking (single most important intervention — within 1 year of quitting, heart attack risk halves); achieve blood pressure below 130/80 mmHg; lower LDL cholesterol (high-intensity statin for 10-year cardiovascular risk above 10% — use QRISK3 in the UK or Pooled Cohort Equation in the USA); manage diabetes with HbA1c below 53 mmol/mol; achieve and maintain healthy BMI (below 25); exercise 150 minutes of moderate-intensity aerobic activity weekly; adopt a Mediterranean-pattern diet (reduces cardiovascular events by 30% — PREDIMED trial). Low-dose aspirin (75 mg daily) is no longer recommended for primary prevention in most people (increased bleeding risk outweighs benefit). Secondary prevention after MI: dual antiplatelet therapy for 12 months (reduced to monotherapy thereafter), lifelong aspirin, statin, ACE inhibitor, and beta-blocker; attend cardiac rehabilitation (12-session supervised programme — reduces re-infarction risk by 25%).

A heart attack is a life-threatening emergency — call 999/112/911 immediately if you experience: central chest pain or pressure lasting more than 15 minutes, chest pain with radiation to the left arm, jaw, or back, sudden severe breathlessness at rest, or loss of consciousness. Do not drive yourself to hospital. While waiting for the ambulance: chew (not swallow whole) 300 mg aspirin if not allergic. Do not wait to see if symptoms resolve — every minute of delay leads to irreversible myocardial damage ('time is muscle'). If you survive a heart attack, ensure you attend all cardiac rehabilitation sessions, take all prescribed medications, and have regular follow-up with your cardiologist — secondary prevention significantly reduces the risk of a second event.