Pharmacology  ·  Cardiovascular

Angina Overview & Hemodynamic Targets

Supply-demand framework, angina subtypes, classification, and the four pharmacological levers

• Angina pectoris results from myocardial ischemia whenever the heart muscle's oxygen demand exceeds the oxygen supply delivered by the coronary circulation — this single supply-demand relationship explains both why angina happens and how every antianginal drug works.
• Three distinct subtypes arise from different mechanisms: stable exertional angina is driven by a fixed atherosclerotic stenosis that limits supply during exertion; vasospastic angina results from transient coronary artery spasm at normal demand; and microvascular angina reflects impaired dilation of the small coronary resistance vessels despite normal epicardial arteries.
• Beta-blockers are contraindicated in vasospastic angina because blocking beta-2 receptors removes a normal coronary vasodilatory influence, leaving alpha-1-mediated vasoconstriction unopposed and potentially worsening spasm — a class effect applying to all beta-blockers.
• Every antianginal drug class works by pulling one or more of four hemodynamic levers: preload reduction (nitrates), afterload reduction (dihydropyridine calcium channel blockers), heart rate reduction (beta-blockers, non-dihydropyridine calcium channel blockers), or direct coronary vasodilation (nitrates, calcium channel blockers).
• The rate-pressure product — heart rate multiplied by systolic blood pressure — is a useful bedside estimate of myocardial oxygen demand; effective antianginal therapy lowers this product during everyday activity so ordinary exertion no longer reaches the ischemic threshold.