Acute coronary syndrome: an overview

ST-elevation myocardial infarction is acute transmural myocardial ischemia from complete coronary occlusion, diagnosed by ischemic symptoms with diagnostic ST-segment elevation and a rising troponin. It is a time-critical emergency in which immediate reperfusion, primary PCI within 90 minutes or fibrinolysis when PCI is unavailable, plus antiplatelet and anticoagulant therapy, determines survival.

Non-ST-elevation myocardial infarction is acute myocardial injury from partial or intermittent coronary occlusion, diagnosed by ischemic symptoms and a rising troponin without diagnostic ST elevation. Management is antiplatelet and anticoagulant therapy with risk stratification (TIMI or GRACE) guiding the timing of an invasive coronary strategy.

Unstable angina is acute myocardial ischemia from a non-occlusive coronary thrombus causing rest, new, or crescendo angina without a troponin rise, placing it on the acute coronary syndrome spectrum just short of NSTEMI. Diagnosis is clinical with ischemic ECG changes and negative serial troponins, and management mirrors NSTE-ACS with antithrombotic therapy and risk-guided angiography.

Chronic stable angina is reproducible, exertional chest discomfort from fixed coronary stenosis causing demand-related ischemia, relieved by rest or nitroglycerin. Diagnosis combines the typical anginal pattern with stress testing or coronary imaging, and treatment is antianginal and secondary-prevention medical therapy, with revascularization for refractory symptoms or high-risk anatomy.

Vasospastic (Prinzmetal) angina is angina from transient epicardial coronary artery spasm, causing rest chest pain with transient ST elevation, typically at night or in the early morning. Diagnosis rests on documenting spasm or reversible ST changes, and treatment is calcium channel blockers and nitrates while strictly avoiding non-selective beta-blockers and triggers.

Takotsubo (stress) cardiomyopathy is transient left ventricular systolic dysfunction, classically apical ballooning, triggered by emotional or physical stress and mimicking acute myocardial infarction, predominantly in postmenopausal women. Diagnosis requires the characteristic wall-motion pattern with nonobstructive coronaries and recovery over weeks, and treatment is supportive heart-failure care during the reversible phase.

MINOCA is myocardial infarction with nonobstructive coronary arteries, defined by infarction criteria but less than 50 percent stenosis on angiography, requiring a search for the underlying mechanism such as plaque disruption, coronary spasm, spontaneous dissection, microvascular dysfunction, or embolism. Diagnosis pairs the infarction criteria with angiography and often cardiac MRI and intracoronary imaging, and treatment targets the identified cause.

Cardiogenic shock is primary cardiac pump failure that produces sustained hypotension and end-organ hypoperfusion despite adequate filling, most often from a large acute myocardial infarction. Survival depends on emergently reversing the cause, usually by revascularization, while supporting perfusion with vasopressors, inotropes, and, when refractory, mechanical circulatory support.

Acute pericarditis is inflammation of the pericardium, most often viral or idiopathic, presenting with pleuritic chest pain relieved by sitting forward, a pericardial friction rub, and diffuse ST elevation with PR depression. Treatment is an NSAID plus colchicine, and the main hazards are effusion, tamponade, and recurrence.

Aortic dissection is a tear in the aortic intima allowing blood to split the media, creating a false lumen, and is a surgical emergency. Type A (ascending) dissection needs emergency surgery, while type B (descending) is usually managed medically with rapid heart-rate and blood-pressure control; the priority is impulse control with a beta-blocker first.

Cardiac tamponade is life-threatening compression of the heart by a pericardial effusion, impairing diastolic filling and cardiac output. It presents with hypotension, distended neck veins, and pulsus paradoxus, is confirmed by echocardiography, and is treated by urgent pericardiocentesis; avoid vasodilators and aggressive diuresis.

Pulmonary embolism is thrombus, usually from a lower-extremity deep vein thrombosis, obstructing the pulmonary arterial circulation and causing V/Q mismatch, right ventricular strain, and hypoxemia. Diagnosis follows Wells criteria (with PERC in low-risk patients) to sequence D-dimer, CT pulmonary angiography, and V/Q scanning, and management is risk-stratified anticoagulation escalating to thrombolysis or embolectomy for hemodynamic instability.