Coronary artery disease

Atherosclerotic narrowing of coronary arteries reduces blood flow to heart muscle (myocardial ischemia); umbrella term covering chronic stable angina and acute coronary syndromes (unstable angina, NSTEMI, STEMI), potentially leading to myocardial infarction or ischemic cardiomyopathy.

• Extremely common and the leading cause of death worldwide. CAD events like MI (heart attack) and heart failure are major causes of morbidity, making this a high-yield focus in exams. Early recognition and intervention (especially for acute coronary syndromes) can be life-saving.

• Chronic stable angina: Predictable chest pressure or tightness with exertion (e.g., climbing stairs), relieved by rest or nitroglycerin. Pain is typically substernal and may radiate to left arm or jaw; episodes last a few minutes and resolve with rest.
• Acute coronary syndromes (ACS): Chest pain occurs at rest or with minimal exertion (often >20 min, not relieved by rest). Pain is more intense and accompanied by autonomic signs: diaphoresis (sweating), nausea/vomiting, palpitations, and anxiety. Patients often appear ill and may have pale, cool skin. (Unstable angina presents similarly but without cardiac enzyme elevation; NSTEMI/STEMI have biomarker rise.)
• Atypical presentations: Women, elderly, and diabetic patients may not have classic chest pain. Instead, they can present with shortness of breath, extreme fatigue, indigestion, lightheadedness, or pain in atypical locations (back, epigastric) without chest pressure. Some MIs are even "silent," discovered only by ECG changes or later imaging.
• Ischemic cardiomyopathy: History of prior MIs or longstanding CAD can lead to a weakened heart muscle (low ejection fraction). Patients present with chronic heart failure symptoms: exertional dyspnea, exercise intolerance, lower extremity edema, and fatigue due to reduced cardiac output.

1. Evaluate chest pain characteristics and risk factors to estimate likelihood of CAD. Typical angina (substernal, exertional, relieved by rest) strongly suggests CAD, whereas pain that is pleuritic, positional, or reproducible by palpation points to non-cardiac causes (e.g., pericarditis, musculoskeletal pain, GERD).
2. If acute coronary syndrome (ACS) is suspected, obtain a 12-lead ECG immediately (within 10 minutes) and check cardiac troponin. ST-elevations on ECG indicate STEMI (activate emergency reperfusion protocol); elevated troponin without ST elevation indicates NSTEMI; angina at rest with normal troponin is unstable angina. Also promptly rule out other life-threatening causes of chest pain (aortic dissection, pulmonary embolism).
3. For stable angina (no acute MI), perform noninvasive testing to confirm CAD: an exercise stress test (or pharmacologic stress with imaging) can reveal inducible ischemia (ECG changes or perfusion deficits). A positive or high-risk stress test should be followed by coronary angiography for definitive diagnosis and to consider revascularization.
4. Always address modifiable factors: check blood pressure, glucose, and cholesterol levels. Managing risk factors (smoking cessation, BP control, statin therapy for LDL reduction, diabetes management) is key to slowing CAD progression and improving outcomes.

1. Lifestyle & risk factor management: Quit smoking (tobacco cessation), adopt a heart-healthy diet (e.g., Mediterranean diet, low in saturated fat and salt), exercise regularly, and maintain healthy weight. Control all modifiable risks: strict blood pressure control (<130/80), good glycemic control in diabetes, and treat hyperlipidemia (high-intensity statin for nearly all patients with CAD).
2. Chronic medical therapy: Antiplatelet therapy (daily low-dose aspirin indefinitely, plus a second antiplatelet like clopidogrel for 1 year if ACS or stent placement). β-blockers (e.g., metoprolol) are first-line to reduce angina symptoms and improve post-MI survival. ACE inhibitors/ARBs are recommended for CAD patients with diabetes, hypertension, or reduced EF for additional protective effects. Nitroglycerin (sublingual for acute relief; long-acting patches or isosorbide for chronic angina) helps symptom control; add calcium channel blockers or ranolazine if angina persists.
3. Acute ACS management: Aspirin (chewed) immediately. For STEMI, activate reperfusion therapy ASAP (preferably percutaneous coronary intervention within 90 minutes; if unavailable, administer fibrinolysis). Give heparin (anticoagulation) and a P2Y₁₂ inhibitor (e.g., clopidogrel). Administer oxygen if hypoxic and nitroglycerin for pain (and morphine for severe pain if needed). Start β-blocker within 24 hours if no contraindications (helps reduce infarct size and arrhythmias). After acute phase, continue dual antiplatelet therapy (usually 12 months for stents), high-intensity statin, and ACEi/β-blocker long-term.
4. Revascularization procedures: Improve coronary blood flow in appropriate patients. PCI (percutaneous coronary intervention with stenting) is used for accessible critical lesions, especially in ACS. CABG (coronary artery bypass graft surgery) is preferred for left main disease or multi-vessel CAD (e.g., 3-vessel disease with diabetes) or if lesions are not amenable to stenting. Revascularization relieves angina and, in certain high-risk cases, improves survival, but must be combined with optimal medical therapy.

• ~70% coronary stenosis typically causes angina with exertion; ~90% stenosis can cause angina even at rest.
• Plaque rupture with thrombus formation is the usual trigger for acute MI (ACS), not just gradual narrowing.
• A single normal troponin does not rule out MI—cardiac troponin can take 4–6 hours to rise after infarction, so serial enzymes are needed if suspicion remains high.

• Chest pain that is new, occurring at rest, or accelerating in frequency/severity (crescendo angina) → red flag for unstable angina/ACS. Requires immediate medical evaluation (ER visit) as it signifies an impending myocardial infarction risk.
• After an MI, watch for acute mechanical complications: sudden pulmonary edema, cardiogenic shock, or a new murmur in the 2–7 days post-MI period suggest papillary muscle rupture, septal rupture, or free wall rupture. These cause rapid hemodynamic collapse and require emergent surgical intervention.

1. Chest pain evaluation: If history is suggestive of angina (exertional, relieved by rest) or patient has CAD risk factors, consider coronary artery disease in the differential.
2. Immediate workup for suspected ACS: ECG within 10 minutes of arrival and troponin levels. Diagnose STEMI if ST elevations in a coronary artery territory (→ activate cath lab for urgent PCI). Diagnose NSTEMI if troponin is elevated without ST elevation. Unstable angina is suspected if ongoing rest angina with initially normal troponin.
3. Initial treatment for ACS: give aspirin immediately; stabilize with oxygen (if low O₂ sat), IV access, and nitroglycerin for pain. If STEMI, arrange immediate reperfusion (PCI or thrombolytics if PCI unavailable). For NSTEMI/unstable angina, begin anticoagulation and plan urgent cardiac catheterization (within 24–48 hours). Manage arrhythmias or hemodynamic issues in parallel (e.g., IV fluids for hypotension, antiarrhythmics for ventricular arrhythmias).
4. Nonemergent evaluation for CAD: If chest pain is stable (no acute MI) but CAD is suspected, perform an exercise stress test (or stress imaging). Positive test or high-risk findings should prompt invasive coronary angiography to confirm disease and allow for possible revascularization.
5. Long-term management: All patients with confirmed CAD should be on appropriate medical therapy (aspirin, statin, β-blocker, ± ACEi) and lifestyle modification. Ensure close follow-up for symptom control and risk factor optimization. Refer to cardiology for severe disease; consider elective PCI or CABG for symptoms refractory to medical therapy or high-risk anatomical lesions.

• A 55‑year‑old man with a history of hypertension and smoking develops substernal chest tightness when walking up stairs. The pain radiates to his left arm and resolves after 5 minutes of rest → stable angina (fixed atherosclerotic plaque causing predictable exercise-induced angina).
• A 64‑year‑old woman with diabetes experiences 30 minutes of severe chest pressure while at rest, with radiation to the jaw, nausea, and profuse sweating. Blood pressure is 90/60 and ECG shows ST elevations in V2–V4 → acute anterior STEMI (myocardial infarction due to occlusion of left anterior descending artery).
• A 72‑year‑old diabetic woman reports sudden extreme fatigue and shortness of breath, but no chest pain. She is diaphoretic. Cardiac enzymes are positive for infarction, though ECG changes are subtle → NSTEMI with atypical presentation (silent ischemia common in diabetic patients).