A 58-year-old man with chronic hypertension (BP 160/95 mmHg) presents with exertional chest pain. Echocardiography shows concentric left ventricular hypertrophy. During cardiac catheterization, the phase marked **A** in the Wiggers diagram is noted to have markedly elevated wall tension. According to the LaPlace law, which of the following best explains the pathophysiology of myocardial ischemia during this phase in this patient?

Explanation

## Why option 1 is correct During isovolumetric contraction (phase **A**), all four cardiac valves are closed and ventricular volume remains constant while pressure rises rapidly. This phase has the HIGHEST oxygen demand of the myocardium. According to the LaPlace law (wall tension = pressure × radius / 2 × wall thickness), in chronic hypertension with concentric LV hypertrophy, the increased ventricular radius (from volume overload effects) combined with increased wall thickness creates elevated wall tension. Although hypertrophy partially compensates by reducing wall stress per unit area, the absolute wall tension remains elevated, and this tension is the major determinant of myocardial oxygen consumption during isovolumetric contraction. The increased oxygen demand during this high-tension phase, combined with reduced coronary perfusion pressure (diastolic pressure is often normal or low relative to wall tension), predisposes to subendocardial ischemia in hypertensive patients. ## Why each distractor is wrong - **Option 0**: While wall thickness does reduce wall stress, this option incorrectly states that increased thickness reduces wall stress sufficiently to lower oxygen demand. In fact, the absolute wall tension remains high, and it is this tension—not duration—that drives oxygen consumption during isovolumetric contraction. The phase duration is not prolonged in simple hypertension. - **Option 2**: Decreased contractility would actually lower the rate of pressure rise and reduce oxygen demand, but this is not the mechanism of ischemia in hypertensive LVH. The problem is increased wall tension from hypertrophy, not decreased contractility. - **Option 3**: Aortic stenosis is a different pathology and would affect the ejection phase (B), not the isovolumetric contraction phase. This option confuses valve pathology with the normal physiology of phase A. **High-Yield:** Isovolumetric contraction (phase A, S1 to S2) is the period of highest myocardial oxygen demand and wall tension; LaPlace law explains why LVH from hypertension increases ischemia risk during this phase despite compensatory wall thickening. [cite: Guyton & Hall 14e Ch 9 — Cardiac Cycle and Wiggers Diagram; LaPlace Law and Myocardial Wall Stress]