A 45-year-old man with untreated essential hypertension (BP 180/110) develops progressive dyspnea on exertion. Echocardiogram shows concentric LV hypertrophy with LV ejection fraction 55%. Which hemodynamic principle best explains why LV hypertrophy developed?
- A Increased preload from fluid retention causing volume-overload eccentric hypertrophy
- B Sympathetic overstimulation causes beta-1 receptor-mediated protein synthesis leading to dilated cardiomyopathy
- C Chronically increased afterload (systemic vascular resistance) causes increased systolic wall stress, triggering parallel sarcomere addition and concentric hypertrophy ✓
- D Reduced coronary reserve causing repetitive ischemia stimulating cardiomyocyte hyperplasia
Explanation
According to the law of Laplace, systolic wall stress = (Pressure × Radius) / (2 × Wall thickness). Sustained hypertension increases systolic pressure, raising wall stress. To normalize wall stress (as per Laplace), cardiomyocytes add sarcomeres in parallel (perpendicular to the long axis), increasing wall thickness without chamber dilation — concentric hypertrophy. This is the classic pressure-overload (afterload excess) response. Volume overload (preload excess, as in regurgitant lesions) causes sarcomere addition in series → eccentric hypertrophy (chamber dilation with proportional wall thickening). Cardiomyocytes are terminally differentiated and undergo hypertrophy, not hyperplasia.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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