Coronary artery disease Study Guide

📖 Core Concepts Coronary artery disease (CAD) – Atherosclerotic plaque narrows coronary arteries, reducing myocardial blood flow. Stable angina – Predictable chest discomfort on exertion; relieved by rest or nitroglycerin. Unstable angina / Acute coronary syndromes – New‑onset, worsening, or rest‑pain; heralds myocardial infarction (MI). Myocardial infarction – Prolonged ischemia → necrotic scar, no regeneration of heart muscle. Risk‑factor hierarchy – Modifiable (hypertension, smoking, diabetes, dyslipidemia, inactivity, obesity, diet, alcohol, depression) → Genetic/heritability (≈40‑60 %) → Environmental (air pollution, rheumatologic disease). Primary vs secondary prevention – Prevent first event vs prevent recurrence after an MI or revascularization. --- 📌 Must Remember Smoking ≈ 2× CAD risk even with 1 cigarette/day. Hypertension target: SBP < 140 mm Hg and DBP ≥ 60 mm Hg (beta‑blocker goal). Statins → ↓ LDL‑C, ↓ CAD events; high‑intensity for secondary prevention. Aspirin – primary‑prevention only in high‑risk, low‑bleeding‑risk patients; reduces first MI but not overall mortality. Dual antiplatelet therapy (aspirin + clopidogrel) – indicated after PCI or ST‑segment elevation MI; does not improve mortality in stable CAD. Nitroglycerin → NO → ↑ cGMP → vascular smooth‑muscle relaxation; sublingual for acute angina. Framingham Risk Score variables: age, sex, diabetes, total cholesterol, HDL‑C, smoking, SBP. 9p21 locus – strongest replicated genetic risk factor; adds to risk stratification. Women often present with dyspnea, fatigue, nausea, rather than classic chest pain; symptoms appear 10 years later. --- 🔄 Key Processes Atherosclerotic plaque formation Endothelial injury → chronic inflammation → LDL infiltration → foam‑cell & lipid core → calcium deposition → plaque growth. Ischemia → Angina ↑ myocardial O₂ demand (exercise) + ↓ supply (stenosis) → subendocardial ischemia → chest pressure. Myocardial infarction cascade Plaque rupture → thrombus → occlusion → >20 min severe flow ↓ → necrosis → scar formation. Nitroglycerin action Metabolized → NO → activates guanylate cyclase → ↑ cGMP → smooth‑muscle relaxation → ↓ preload & O₂ demand. Risk‑assessment workflow Collect demographics & labs → calculate Framingham (or polygenic) score → stratify (low/moderate/high) → tailor prevention plan. --- 🔍 Key Comparisons Stable vs Unstable Angina Stable: predictable, exertional, relieved by rest/nitroglycerin. Unstable: change in frequency/intensity, may occur at rest, heralds MI. Aspirin (primary) vs Aspirin (secondary) Primary: limited to high‑risk, low‑bleeding patients; modest MI reduction. Secondary: routine after MI/PCI; reduces recurrent events. PCI vs CABG PCI: quicker symptom relief, no survival advantage in stable CAD. CABG: preferred for multivessel disease, especially left‑main involvement; survival benefit. Exercise ECG vs Imaging Stress Test Exercise ECG: higher false‑positive/negative rates. Imaging (stress echo, PET, SPECT): better sensitivity & specificity. --- ⚠️ Common Misunderstandings “All chest pain = heart attack.” → Many non‑cardiac causes; pain pattern and context matter. “Aspirin always prevents death.” → In primary prevention it does not lower overall mortality; bleeding risk may outweigh benefit. “Normal coronary angiogram rules out CAD.” → Microvascular angina can cause symptoms despite normal large‑vessel anatomy. “Statins are only for high cholesterol numbers.” → Even with modest LDL‑C, statins reduce events in high‑risk patients. --- 🧠 Mental Models / Intuition “Supply‑Demand Balance” – Think of the heart like a car engine: when demand (speed, hill) exceeds fuel (blood flow) you feel “stalled” (angina). “Plaque as a Growing Tree” – Roots (inflammation) → trunk (lipid core) → branches (calcification) → eventually blocks the road (lumen). “Risk Stack” – Each risk factor adds a layer; the more layers, the higher the chance of a “collapse” (MI). --- 🚩 Exceptions & Edge Cases Silent CAD – Up to 20 % are asymptomatic; discovered incidentally or after MI. Women’s atypical presentation – Dyspnea, fatigue, nausea may be the only clues. Air‑pollution exposure – Contributes 28 % of CAD deaths worldwide; not captured in traditional risk scores. Genetic high risk – 9p21 carriers may develop CAD despite optimal lifestyle. --- 📍 When to Use Which Low pre‑test probability → No testing or coronary calcium scoring (optional). Intermediate probability → Exercise ECG or stress imaging (prefer imaging for higher accuracy). High probability / acute presentation → Immediate ECG, cardiac biomarkers, then urgent coronary angiography. Stable symptomatic CAD → Start lifestyle + antiplatelet + statin + β‑blocker; add nitroglycerin for breakthrough pain. Multivessel disease or left‑main stenosis → Consider CABG over PCI. --- 👀 Patterns to Recognize Chest pain triggered by exertion + relieved by rest → Stable angina. Pain at rest, worsening, or new pattern → Unstable angina / impending MI. Radiation to jaw/neck + diaphoresis + nausea → Classic MI presentation (especially in men). Dyspnea + fatigue without chest pain → Possible female or silent CAD. --- 🗂️ Exam Traps “Aspirin reduces overall mortality in all CAD patients.” – Incorrect for primary prevention; only secondary benefit. “PCI improves long‑term survival in stable CAD.” – Mortality is similar to optimal medical therapy; only symptom relief. “Normal ECG rules out acute coronary syndrome.” – Early or posterior MI may have a normal ECG; rely on biomarkers & clinical picture. “Statins are contraindicated in patients with low LDL.” – Even modest LDL‑C levels benefit from high‑intensity statins if high risk. “Microvascular angina is just anxiety.” – True ischemic mechanism in small vessels; requires targeted therapy. ---