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

A heart attack (myocardial infarction, MI) occurs when blood supply to part of the heart muscle is suddenly blocked, usually by a blood clot forming on a ruptured atherosclerotic plaque in a coronary artery. Without urgent treatment, the affected heart muscle dies within hours. Heart attacks are a leading cause of death and disability globally — in the United States, a heart attack occurs every 40 seconds. Survival and outcomes depend critically on the speed of diagnosis and reperfusion therapy, with the principle of 'time is muscle' guiding all modern emergency protocols. A heart attack demands the fastest possible clinical response: every 30 minutes of additional delay in restoring coronary blood flow results in approximately 7.5% additional mortality risk. Public awareness campaigns teaching chest pain recognition and the importance of calling emergency services immediately rather than waiting to see if symptoms resolve are vital public health interventions.

The most common underlying cause is coronary artery disease (atherosclerosis) — fatty plaques accumulate in coronary artery walls over decades. A heart attack occurs when a plaque ruptures, triggering platelet aggregation and thrombus formation that suddenly blocks coronary blood flow. Modifiable risk factors include smoking (doubles MI risk), hypertension, high LDL cholesterol, diabetes, obesity, physical inactivity, and excessive alcohol use. Non-modifiable risk factors include age, male sex, family history of early coronary artery disease, and post-menopausal status in women. Rarer but important causes of myocardial infarction include coronary artery spasm (Prinzmetal angina), spontaneous coronary artery dissection (SCAD — a primary cause of MI in young women with no atherosclerosis), cocaine and amphetamine misuse causing vasospasm, and type 2 MI from oxygen supply-demand mismatch in severe anaemia, hypotension, or tachyarrhythmia.

Classic symptoms include crushing chest pain or pressure described as a tight band or heavy weight on the chest, radiating to the left arm, jaw, neck, or back, lasting more than 20 minutes and not relieved by nitroglycerin or rest. Associated symptoms include profuse sweating, nausea, vomiting, severe breathlessness, dizziness, and sense of impending doom. Women, the elderly, and diabetics more often present atypically: jaw or arm pain alone, epigastric discomfort, unusual fatigue, or silent (asymptomatic) MI. Any suspected heart attack requires immediate emergency services activation — do not drive yourself to hospital. Women with MI more frequently present atypically — with jaw pain, back pain, nausea, unusual fatigue, and breathlessness rather than classic crushing chest pain — leading to under-recognition and significant treatment delays that contribute to worse outcomes in female MI patients.

The two cornerstones of acute MI diagnosis are the 12-lead ECG and cardiac troponin blood test. A STEMI (ST-elevation myocardial infarction) is diagnosed by ST-segment elevation in 2 or more contiguous leads on ECG and requires immediate primary PCI (door-to-balloon time target 90 minutes or less). NSTEMI (non-ST-elevation MI) is diagnosed by elevated high-sensitivity troponin T or I (reflecting myocyte death) without ST elevation. Serial troponin measurements at 0 and 1–3 hours confirm diagnosis. Echocardiography assesses left ventricular function and wall motion abnormalities. Coronary angiography localizes the culprit lesion before PCI. High-sensitivity cardiac troponin (hs-cTnT or hs-cTnI) assays now permit diagnosis or exclusion of NSTEMI within 0-1 hour using validated rapid rule-in/rule-out algorithms, substantially faster than conventional troponin protocols and enabling earlier definitive treatment decisions.

STEMI requires emergency primary percutaneous coronary intervention (PCI) — coronary angiography with balloon angioplasty and stent placement — ideally within 90 minutes of first medical contact. Dual antiplatelet therapy (aspirin 300 mg loading dose plus clopidogrel, ticagrelor, or prasugrel) and anticoagulation (heparin, bivalirudin) are given immediately. Thrombolysis (fibrinolytic drugs) is an alternative when primary PCI is not available within 120 minutes. NSTEMI is managed with early risk stratification and invasive coronary angiography within 24–72 hours for high-risk patients. All MI patients receive aspirin, beta-blockers, ACE inhibitors, high-intensity statins, and cardiac rehabilitation. After hospital discharge, cardiac rehabilitation — a structured programme of supervised exercise, cardiovascular education, dietary counselling, and psychological support — reduces all-cause mortality by 20-25% and is strongly recommended for all MI survivors, improving physical capacity, mental health, and long-term adherence to secondary prevention medications.

Immediate complications include cardiogenic shock (pump failure from massive MI), life-threatening ventricular arrhythmias (ventricular fibrillation — the most common cause of sudden cardiac death), complete heart block, and acute mitral regurgitation from papillary muscle rupture. Subacute complications include pericarditis (Dressler syndrome), left ventricular thrombus with stroke risk, and ventricular free wall rupture. Long-term complications include heart failure (left ventricular dysfunction from extensive myocardial scarring), recurrent MI, and arrhythmias. Cardiac rehabilitation significantly reduces mortality and reinfarction rates through supervised exercise, risk factor management, and psychological support.

Primary prevention: quit smoking, control blood pressure (target below 130/80 mmHg), achieve optimal lipid levels with statin therapy, treat diabetes, maintain healthy weight, and exercise 150 minutes of moderate-intensity activity per week. Secondary prevention after MI: lifelong aspirin, beta-blockers (at least 12 months, often longer), ACE inhibitors, high-intensity statins (atorvastatin 80 mg or rosuvastatin 40 mg), and SGLT2 inhibitors or GLP-1 agonists in diabetics with established CVD. Enroll in cardiac rehabilitation — it reduces mortality by 20–25%. Learn CPR and how to use an AED as bystander resuscitation triples survival from witnessed cardiac arrest.

Call 999 immediately (do not drive yourself) for: central crushing chest pain lasting more than 15 minutes, particularly radiating to the left arm, jaw, or back; breathlessness, sweating, nausea, or collapse with chest pain; any sudden-onset severe chest pain in a patient with known heart disease. Chew 300 mg aspirin while waiting if available and not allergic. Time is muscle — every minute of coronary artery occlusion destroys approximately 2 million cardiomyocytes; PCI within 90 minutes dramatically reduces mortality and heart failure. See a GP urgently for: exertional chest tightness or breathlessness that resolves at rest (possible stable angina requiring stress testing); and after any hospital admission for ACS — for cardiac rehabilitation, medication optimisation, and secondary prevention.