Patient A reports chest pain that occurs predictably when climbing two flights of stairs and resolves within 3 minutes of rest. Cardiac catheterization shows 75% stenosis in the LAD. Patient B reports chest pain at rest, usually between 2–5 AM, lasting 15 minutes, with complete resolution. Catheterization shows entirely normal coronary arteries. Which pairing best matches mechanism to patient?
ABoth have atherosclerosis; Patient B's plaque was missed by angiography
BPatient A has a fixed supply limitation (stable angina from stenosis); Patient B has dynamic vasospasm (Prinzmetal's angina) despite normal anatomy
CPatient A has vasospasm triggered by exertion; Patient B has microvascular disease causing ischemia at rest
DPatient B's symptoms are psychosomatic since ischemia cannot occur without obstructive anatomy
Stable angina follows the supply-demand logic of a fixed stenosis: the narrowed vessel delivers adequate flow at rest but fails under the increased demand of exertion, producing reproducible, effort-related symptoms. Vasospastic (Prinzmetal's) angina involves dynamic luminal narrowing from smooth muscle spasm — no fixed plaque is required. The nocturnal timing and angiographically normal arteries are classic features. Option B's second half is a real entity (coronary microvascular disease) but doesn't describe Patient B's scenario.
Question 2 Multiple Choice
A cardiologist considers prescribing a beta-blocker to a patient with documented vasospastic angina to reduce heart rate and myocardial oxygen demand. Why might this worsen the patient's condition?
ABeta-blockers reduce nitric oxide production by the endothelium, exacerbating the vasodilatory deficit
BBeta-blockers increase platelet aggregation, promoting thrombus formation over the spasming artery
CBeta-blockade leaves alpha-adrenergic vasoconstriction unopposed, which can intensify coronary artery spasm
DBeta-blockers are contraindicated in all forms of angina because they reduce cardiac output
Under normal circumstances, sympathetic stimulation activates both beta-receptors (causing vasodilation in coronary vessels) and alpha-receptors (causing vasoconstriction). In vasospasm, smooth muscle is already hyperreactive to vasoconstrictors. If beta-receptors are blocked but alpha-receptors remain active, catecholamine release shifts the balance entirely toward alpha-mediated vasoconstriction — potentially triggering or worsening spasm. This is why calcium channel blockers (which directly relax smooth muscle) are the preferred treatment for vasospastic angina.
Question 3 True / False
Vasospastic angina can produce ST-segment elevation on EKG — a finding typically associated with complete coronary artery occlusion — because the degree of spasm can cause transmural ischemia even without atherosclerotic plaque.
TTrue
FFalse
Answer: True
ST-elevation reflects transmural ischemia — injury current across the full thickness of the myocardium. In vasospastic angina, severe coronary spasm can reduce flow sufficiently to produce this pattern, even though the vessel's lumen is not permanently occluded. The elevation characteristically resolves when the spasm breaks (spontaneously or with nitrate administration). This is what distinguishes Prinzmetal's episodes from MI: the elevation is transient and typically associated with symptom resolution.
Question 4 True / False
Vasospastic angina mainly occurs in patients with underlying atherosclerosis, because endothelial damage from plaque formation is the source of reduced nitric oxide production that triggers spasm.
TTrue
FFalse
Answer: False
Vasospasm can occur in angiographically normal coronary arteries — this is a defining and clinically important feature. While atherosclerosis does cause endothelial dysfunction, other factors — including endothelial injury from smoking, cocaine use, or idiopathic mechanisms — can produce the same result: reduced NO production, smooth muscle hyperreactivity to circulating vasoconstrictors. The misidentification of vasospasm as exclusively atherosclerotic delays diagnosis in younger patients without traditional risk factors.
Question 5 Short Answer
Explain why nitroglycerin relieves vasospastic angina, and why this represents treatment of the consequence rather than the cause.
Think about your answer, then reveal below.
Model answer: Nitroglycerin is a nitrate that releases nitric oxide (NO) directly into smooth muscle cells, causing vasodilation by bypassing the damaged endothelium. In vasospasm, the endothelium cannot produce sufficient NO on its own because of dysfunction — so nitroglycerin compensates by providing an exogenous NO source. This relieves the spasm. But the underlying cause is the endothelial dysfunction and smooth muscle hyperreactivity to vasoconstrictors, which persist after the nitrate wears off. Nitroglycerin does not restore endothelial function; it substitutes for it.
This distinction matters clinically because patients with vasospastic angina need calcium channel blockers for long-term prevention (which address smooth muscle hyperreactivity directly) rather than just nitrates for acute episodes. Understanding the mechanism explains both why nitrates work and why they are insufficient as the sole therapy.