Coronary artery disease is atherosclerotic narrowing of the coronary arteries that limits blood flow to the heart muscle. It ranges from stable angina to acute coronary syndromes, and boards emphasize risk-factor modification, how it is diagnosed, and the medical and revascularization strategies that reduce events.
Evidence-based · For exam prep, not medical advice
update Updated October 2026
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check_circleCAD is caused by atherosclerosis of the coronary arteries.
check_circleStable angina is predictable exertional chest pain relieved by rest or nitroglycerin.
check_circleAcute coronary syndrome reflects plaque rupture with unstable, often rest, symptoms.
check_circleDiagnosis uses stress testing and coronary angiography.
check_circleManagement combines lifestyle change, antiplatelets, statins, and revascularization when indicated.
Risk Factors and Pathophysiology
Coronary artery disease develops through atherosclerosis, the buildup of lipid-laden plaque in the coronary arteries. Major modifiable risk factors are hypertension, hyperlipidemia, diabetes, and smoking, while age, male sex, and family history are non-modifiable. As plaque enlarges it limits coronary flow, causing ischemia when demand exceeds supply; plaque rupture with thrombosis produces acute coronary syndromes.
Stable Angina vs Acute Coronary Syndrome
Stable angina is predictable, exertional chest pressure that is relieved within minutes by rest or nitroglycerin and reflects a fixed stenosis. Acute coronary syndrome — unstable angina, NSTEMI, or STEMI — results from acute plaque rupture and thrombosis, causing new, worsening, or rest pain. Distinguishing the two rests on the pattern of symptoms, the ECG, and cardiac troponin.
Diagnosis
In stable patients, diagnosis begins with risk assessment and stress testing (exercise or pharmacologic, with ECG or imaging) to detect inducible ischemia. Coronary CT angiography can assess for plaque non-invasively, while invasive coronary angiography defines the anatomy and enables revascularization. In suspected acute coronary syndrome, the ECG and serial troponins guide urgent management.
Management
Management targets both symptoms and prognosis. Lifestyle change and aggressive risk-factor control are foundational, with a high-intensity statin, antiplatelet therapy, and blood pressure and diabetes control. Antianginal drugs (beta blockers, nitrates, calcium channel blockers) relieve symptoms. Revascularization — percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) — is used for significant disease, with CABG often favored in complex multivessel or left main disease, particularly in diabetics.
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3 real questions on Coronary Artery Disease
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123
A child presents with fever, conjunctivitis, strawberry tongue, and desquamation of the hands. Echocardiography later shows coronary artery aneurysms. Which pathologic mechanism is most responsible for vascular injury?
Kawasaki_symptoms.jpg: Dong Soo Kimderivative work: Natr, CC BY 2.0 <https://creativecommons.org/licenses/by/2.0>, via Wikimedia Commons
Answer: C. Kawasaki disease is an acute medium-vessel vasculitis primarily mediated by T-cell activation and cytokine-driven endothelial injury. This leads to coronary artery inflammation and aneurysm formation. Immune complex deposition is more characteristic of type III hypersensitivity vasculitis. IgE-mediated processes are seen in allergic disease. Direct bacterial invasion is not the mechanism in Kawasaki disease.
Source: McCrindle, et al. (2017). Diagnosis, treatment, and long-term management of Kawasaki disease: a scientific statement for health professionals from the American Heart Association. Circulation.
A 64-year-old man dies suddenly from a transmural myocardial infarction. Gross autopsy examination of the left ventricle reveals a sharply demarcated tan-yellow region of tissue necrosis extending from the epicardium to the endocardium in the distribution of the left anterior descending coronary artery. Histologic examination of tissue is shown below. Tissue 1 cm away shows viable myocytes with early neutrophilic infiltration at the periphery. Which of the following best explains the relationship between the temporal evolution of myocardial necrosis and the spatial pattern of inflammation observed in acute myocardial infarction?
KGH, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons
Answer: B. Acute myocardial infarction exhibits a temporal-spatial relationship between necrosis and inflammation: ischemia triggers irreversible damage that progresses as a wavefront extending from the subendocardium (most ischemic region) toward the epicardium over 6–12 hours. The boundary zone between dead and dying tissue contains the advancing margin of ischemic necrosis, which is marked by early neutrophilic infiltration and represents the locus of ongoing cell death. The center shows complete coagulative necrosis (cardiomyocytes lysed, architecture destroyed), while the periphery shows viable myocytes being recruited into necrosis—this spatial pattern correlates with duration of ischemia and residual collateral perfusion. Option A incorrectly implies instantaneous injury; option C conflates ATP-dependent repair failure with DAMP signaling; options D and E overemphasize the role of inflammation in halting necrotic spread, when the wavefront is driven by ischemia duration rather than inflammatory containment.
Source: Thygesen, K., et al. (2018). Fourth universal definition of myocardial infarction. European Heart Journal, 40(3).
A 62-year-old man with hypertension and hyperlipidemia presents with crushing substernal chest pain and dyspnea. 12-lead ECG tracing is shown below. Troponin levels are elevated (troponin I 4.2 ng/mL, normal <0.04 ng/mL) and rise progressively over 6–12 hours. Coronary angiography reveals total occlusion of the right coronary artery (RCA) with TIMI 0 flow. Which of the following best explains the pathophysiologic sequence from coronary artery occlusion to myocardial infarction, and how the ECG and biomarker findings reflect the anatomic distribution and temporal evolution of myocardial necrosis in this patient?
Andrewmeyerson, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons
Answer: B. Acute coronary artery occlusion causes sudden interruption of blood flow to the myocardium supplied by that artery (in this case, the inferior wall supplied by the RCA). Ischemic myocytes rapidly deplete ATP from aerobic metabolism, leading to failure of sodium-potassium pumps and sodium-calcium exchangers. ATP depletion causes intracellular sodium accumulation and cellular depolarization, manifested on the ECG as ST-segment elevation in the leads overlying the ischemic region (inferior leads: II, III, aVF). ST-segment elevation indicates transmural ischemia (affecting the full thickness of the wall from endocardium to epicardium). Myocyte necrosis begins within minutes of ischemia onset and progresses as a wavefront from the subendocardium (most ischemic) to the subepicardium over 6–12 hours. Cardiac troponins (troponin I and T) are released into the circulation upon myocyte death and necrosis; the progressive rise in troponin over hours reflects the temporal progression of necrosis as the wavefront expands. Peak troponin occurs at 24–48 hours. Options A incorrectly implies immediate irreversibility; options C, D, and E invoke incorrect mechanisms (lactate acidosis, catecholamine-induced calcium overload, apoptosis-mediated ST elevation).
Source: Thygesen, K., et al. (2018). Fourth universal definition of myocardial infarction. European Heart Journal, 40(3).
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What is the difference between stable angina and a heart attack?expand_more
Stable angina is predictable, exertional chest pain from a fixed coronary narrowing that is relieved by rest or nitroglycerin. A heart attack (myocardial infarction) results from acute plaque rupture and clot formation, causing prolonged chest pain at rest with a rise in cardiac troponin and often ECG changes.
What are the risk factors for coronary artery disease?expand_more
Modifiable risk factors include hypertension, high cholesterol, diabetes, and smoking, while non-modifiable factors include increasing age, male sex, and a family history of early coronary disease. Controlling the modifiable factors substantially lowers risk.
How is coronary artery disease diagnosed?expand_more
In stable patients, stress testing detects inducible ischemia and coronary angiography (CT or invasive) defines the anatomy. In suspected acute coronary syndrome, the ECG and serial cardiac troponin measurements are used to diagnose and guide urgent treatment.
When is bypass surgery preferred over stenting?expand_more
Coronary artery bypass grafting (CABG) is often preferred over percutaneous coronary intervention (PCI) for complex multivessel disease or significant left main disease, and particularly in patients with diabetes, where it tends to offer better long-term outcomes. PCI is commonly used for less complex disease.
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