Left ventricular mechanical adaptation to chronic aortic regurgitation in intact dogs

Increased end-diastolic wall stress has been hypothesized to stimulate left ventricular (LV) hypertrophy following volume overload. We instrumented intact-chest dogs with radiopaque markers in both ventricles and created volume overload by puncturing one aortic valve cusp. End-diastolic stress increased immediately, then fell over 3 mo as the heart hypertrophied. End-systolic stress did not change significantly. Chamber contractility, quantified as Emax, the end-systolic pressure-volume line slope, increased. Emax normalized by multiplying by LV mass increased following the lesion before but not after beta-blockade with propranolol and did not change significantly over time, suggesting that chamber contractility changed because of increased mass and sympathetic tone rather than changed intrinsic muscle function. LV mass did not initially correlate with lesion size, but steady-state mass did. Over the range of lesions we produced, increased end-diastolic wall stress appears to stimulate hypertrophy at a fixed rate, which stops when end-diastolic wall stress has been reduced to an acceptable level.