Cardiology · Acute Coronary Syndrome
The facts most likely to be tested
ST-elevation myocardial infarction (STEMI) requires immediate reperfusion therapy via primary percutaneous coronary intervention (PCI) within 90 minutes of first medical contact.
Fibrinolytic therapy is indicated for STEMI patients if primary PCI cannot be performed within 120 minutes of first medical contact and there are no absolute contraindications.
Dual antiplatelet therapy (DAPT) consisting of aspirin and a P2Y12 inhibitor (e.g., ticagrelor, prasugrel, or clopidogrel) is mandatory for all patients with ACS.
High-intensity statin therapy (e.g., atorvastatin 80 mg) must be initiated as soon as possible in all patients with ACS regardless of baseline LDL cholesterol levels.
Beta-blockers should be initiated within 24 hours in patients with ACS to reduce myocardial oxygen demand and prevent ventricular arrhythmias.
Nitroglycerin is contraindicated in patients with right ventricular infarction or concurrent use of phosphodiesterase-5 inhibitors due to the risk of severe hypotension.
Morphine is no longer routinely recommended in ACS management as it may interfere with the absorption and efficacy of P2Y12 inhibitors.
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A 62-year-old male presents to the emergency department with 90 minutes of crushing substernal chest pain radiating to the left jaw. His medical history is significant for hypertension and hyperlipidemia. An ECG reveals ST-segment elevation in leads V2-V6. The patient is hemodynamically stable, and the cardiac catheterization lab is available within 45 minutes.
What is the most appropriate next step in management?
Primary percutaneous coronary intervention (PCI)
The patient is presenting with an ST-elevation myocardial infarction (STEMI), and since primary PCI can be performed within the 90-minute window, it is the gold standard reperfusion strategy.
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Etiology / Epidemiology
Driven by atherosclerosis and plaque rupture. Primary risk factors: HTN, DM, smoking, dyslipidemia, and age.
Clinical Manifestations
Substernal chest pain, Levine sign, radiation to jaw/arm. ST-segment elevation or T-wave inversion on ECG.
Diagnosis
Coronary angiography is the gold standard. Troponin I/T elevation confirms myocardial necrosis.
Treatment
Aspirin 325mg immediately. PCI within 90 minutes for STEMI. Avoid nitrates in RV infarction.
Prognosis
Risk of ventricular arrhythmias and heart failure. LVEF < 35% indicates high mortality risk.
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Epidemiology & Etiology
ACS results from acute plaque rupture leading to thrombotic occlusion. Diabetes mellitus is a major risk factor, often presenting with atypical symptoms. Incidence increases significantly with age and male gender.
Pertinent Anatomy
The left anterior descending (LAD) artery is the most commonly occluded vessel. Occlusion of the right coronary artery (RCA) often affects the inferior wall and the SA/AV nodes.
Pathophysiology
Plaque rupture exposes subendothelial collagen, triggering platelet aggregation and the coagulation cascade. This creates a thrombus that limits myocardial perfusion, leading to ischemia and eventual necrosis. Prolonged ischemia results in myocardial stunning and loss of contractile function.
Clinical Manifestations
Patients present with crushing chest pain, diaphoresis, and nausea. ST-segment elevation >1mm in two contiguous leads is diagnostic for STEMI. New left bundle branch block is treated as a STEMI equivalent. Watch for S3 gallop indicating acute heart failure.
Diagnosis
The 12-lead ECG must be obtained within 10 minutes of arrival. Cardiac troponin is the most sensitive biomarker, rising within 2-4 hours. Coronary angiography provides definitive visualization of the culprit lesion.
Treatment
Initial management includes Aspirin, Nitroglycerin, and P2Y12 inhibitors (e.g., Clopidogrel). STEMI requires PCI (door-to-balloon <90 min) or fibrinolytics if PCI is unavailable. Nitrates are contraindicated in inferior MI with RV involvement due to severe hypotension.
Prognosis
Major complications include ventricular septal rupture, papillary muscle rupture, and Dressler syndrome. Patients require long-term beta-blockers and statins to reduce mortality and prevent remodeling.
Differential Diagnosis
Aortic dissection: tearing chest pain radiating to the back
Pulmonary embolism: sudden onset dyspnea and tachycardia
GERD: burning pain relieved by antacids
Pericarditis: pleuritic pain improved by leaning forward
Pneumothorax: sudden onset unilateral chest pain with absent breath sounds