Acute Coronary Syndrome
Acute Coronary Syndrome is a heart attack or severe angina caused by a sudden blockage in a coronary artery, cutting off blood and oxygen to the heart muscle.
Emergency Management: Cardiac arrest due to Ventricular Fibrillation requires immediate CPR and rapid electrical defibrillation (unsynchronized shock at 200J biphasic).
A life-threatening spectrum of conditions encompassing ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina (UA). The core pathology is sudden, critical reduction in blood flow to the heart muscle, nearly always caused by the rupture or erosion of an atherosclerotic plaque in a coronary artery, followed by superimposed thrombosis.
Detailed Overview
Acute Coronary Syndrome represents a medical emergency where time is muscle. In STEMI, a totally occlusive thrombus causes full-thickness (transmural) myocardial necrosis, necessitating immediate reperfusion via primary PCI or fibrinolytics. NSTEMI and UA involve a partially occlusive thrombus causing subendocardial ischemia; NSTEMI shows biomarker evidence of necrosis (elevated troponins), while UA does not. If left untreated, ACS leads to fatal arrhythmias, cardiogenic shock, or irreversible heart failure.
Epidemiology & Demographics
Incidence: >1 million hospital admissions for ACS annually in the US. Average age of first heart attack is 65.6 years for males and 72.0 years for females. Males have a higher incidence at younger ages, but the gap closes post-menopause.
Etiological Mechanism
The primary cause is coronary artery atherosclerosis complicated by acute plaque rupture, fissuring, or erosion. Rare causes include coronary artery vasospasm (Prinzmetal angina), spontaneous coronary artery dissection (SCAD), or coronary embolism.
Primary Causes
Atherosclerotic plaque rupture with thrombosis
Coronary artery spasm
Coronary artery dissection
Demand ischemia (severe anemia, tachycardia)
An atherosclerotic plaque with a large lipid core and a thin fibrous cap becomes inflamed. Macrophages secrete metalloproteinases that degrade the fibrous cap, leading to its rupture. Highly thrombogenic core materials (tissue factor, collagen) are exposed to circulating blood. Platelets immediately adhere, activate, and aggregate (white thrombus). The coagulation cascade is activated, generating thrombin, which converts fibrinogen to a fibrin network that entraps red blood cells (red thrombus). This thrombus rapidly obstructs the coronary lumen. Within 20-30 minutes of total occlusion, irreversible ischemic necrosis of myocardial cells begins, spreading from the subendocardium to the epicardium.
Diagnostic Criteria & Guidelines
Diagnosis requires the presence of acute myocardial injury detected by abnormal cardiac biomarkers (High-Sensitivity Troponin > 99th percentile) in the setting of evidence of acute myocardial ischemia (symptoms of ischemia, new ischemic ECG changes like ST elevation/depression, or new wall motion abnormality on imaging).
Immediate dual antiplatelet therapy (Aspirin 324 mg chewed + Ticagrelor 180 mg or Clopidogrel 600 mg PO). Anticoagulation (Unfractionated Heparin drip or Enoxaparin 1mg/kg SC). For STEMI: Immediate Percutaneous Coronary Intervention (PCI) within 90 minutes. High-intensity statin (Atorvastatin 80 mg PO).
Second-Line & Adjunctive Therapy
If PCI is unavailable within 120 minutes for STEMI: IV Thrombolytics (Tenecteplase/TNKase 30-50 mg IV push based on weight). For NSTEMI/UA: Early invasive strategy (angiogram within 24 hours) vs ischemia-guided strategy depending on risk scores (TIMI/GRACE).
Surgical & Procedural Management
Coronary Artery Bypass Grafting (CABG) is indicated for left main coronary artery disease, severe 3-vessel disease, or in diabetic patients with multivessel disease.
Patient Counseling & Advice
Stress the absolute necessity of taking dual antiplatelet therapy exactly as prescribed to prevent potentially fatal stent thrombosis. Educate on the use of sublingual nitroglycerin for future chest pain and to call 911 if pain is unrelieved by 1 dose after 5 minutes.
Follow-Up & Monitoring Schedule
Follow-up with cardiology within 1-2 weeks post-discharge. Repeat echocardiogram in 4-12 weeks to assess recovery of Left Ventricular Ejection Fraction (LVEF). Routine monitoring of lipid panel to ensure LDL < 55 mg/dL on statin therapy.
Preventive Strategies
Primary: Aggressive management of hypertension, diabetes, and hyperlipidemia. Secondary: Lifelong Aspirin 81 mg, a P2Y12 inhibitor for 12 months, Beta-blocker (e.g., Metoprolol succinate 50 mg daily), ACE inhibitor/ARB (e.g., Lisinopril 10 mg daily), and a high-intensity statin.
In-hospital mortality for STEMI treated with primary PCI is ~5%. Prognosis heavily depends on the extent of myocardial damage, post-MI ejection fraction, and age. Post-MI heart failure significantly reduces long-term survival.