angina pectoris

**Definition:** Reversible myocardial ischemia causing chest discomfort (pressure, squeezing, tightness) often radiating to the left arm, jaw, neck, or back. Associated symptoms: dyspnea, diaphoresis, nausea. Women, diabetics, and the elderly may have atypical presentations.

**Pathophysiology:** Myocardial O2 demand exceeds supply. Determinants of demand: heart rate, contractility, wall stress (preload/afterload). Supply depends on coronary perfusion, which occurs mainly in diastole, and on O2-carrying capacity. Ischemia is reversible, so there is no necrosis and no troponin rise.

**Types:** - **Stable (typical/exertional) angina:** Fixed atherosclerotic stenosis (usually ≥70%). Brought on by exertion or stress, lasts <10-15 min, and is relieved by rest or nitroglycerin. ECG: ST depression during an episode (subendocardial ischemia). - **Unstable angina:** Rupture of an atherosclerotic plaque with a non-occlusive thrombus. Occurs at rest, is new-onset, or is crescendo (worsening in frequency, duration, or severity). Part of acute coronary syndrome. Troponin is negative, and ST depression or T-wave inversion may be present. - **Prinzmetal (variant/vasospastic) angina:** Coronary vasospasm, typically at rest and often at night or early morning. ECG shows transient ST elevation. Associated with smoking, cocaine, and triptans. Treat with calcium channel blockers and nitrates. Avoid nonselective beta-blockers and cocaine. - **Microvascular angina (cardiac syndrome X):** Chest pain with normal epicardial coronaries. Seen more often in women and caused by small-vessel dysfunction.

**Differentiation from MI:** STEMI and NSTEMI involve myocyte necrosis with troponin or CK-MB elevation. Pain in MI lasts >20-30 min and is not relieved by rest or nitroglycerin. Stable angina has no troponin rise. Unstable angina has a negative troponin.

**Diagnosis:** Clinical history and ECG. Exercise stress test with ECG (ST depression ≥1 mm). Pharmacologic stress (dobutamine, adenosine, or dipyridamole) with echo or nuclear imaging if the patient cannot exercise. Coronary CT angiography. Coronary angiography is the gold standard for defining anatomy.

**Management:** - Lifestyle modification and risk factor control (statin, BP and glucose control, smoking cessation). - Antiplatelet: aspirin (or clopidogrel if intolerant). - Anti-anginal: beta-blockers are first line (reduce HR and contractility, and improve survival post-MI). Nitrates (venodilation reduces preload; avoid with PDE-5 inhibitors because of severe hypotension). Calcium channel blockers (amlodipine, or verapamil/diltiazem). Ranolazine (late Na current inhibitor, no HR or BP effect; prolongs QT). - Sublingual nitroglycerin for acute relief. - Revascularization (PCI or CABG) for refractory symptoms, left main disease, or multivessel disease with diabetes or reduced EF. CABG improves survival in these groups. - Unstable angina: manage as ACS with antiplatelets, anticoagulation (heparin), beta-blocker, nitrates, statin, and early invasive strategy.

**High-yield pearls:** - Nitrates reduce preload, which reduces wall stress and O2 demand. They also dilate epicardial coronaries. - Beta-blockers are contraindicated in cocaine-induced chest pain and vasospastic angina. - Pain with exertion that resolves with rest = stable angina. Pain at rest or with increasing frequency = unstable angina. - Reversible ischemia means no necrosis, which is why troponin is normal in stable angina. - Subendocardium is most vulnerable to ischemia because it has the highest wall stress and is most distal to the epicardial supply, so it gives ST depression. Transmural ischemia gives ST elevation (Prinzmetal, STEMI). - Aortic stenosis can cause angina through increased demand (LVH) and reduced coronary perfusion even with normal coronaries. - Coronary steal: vasodilators (dipyridamole, adenosine) can precipitate ischemia in fixed stenosis, which is the basis of pharmacologic stress testing.