Cardiac function, coronary flow and MO2hypertrophy induced by pressure and volume overloading1

Myocardial function, flow and O2 consumption were compared in cardiac hypertrophy induced by pressure-loading (P) and by volume overloading (V). Increases in LV-to-body weight ratios in P and V hypertrophied hearts were comparable. Indices of LV function such as cardiac output, stroke volume, stroke work, minute work, peak LV dP/dt, ratio of peak LV dP/dt-to-isovolumic pressure and -to-LVEDP, and Vmax were significantly reduced from normal only in hypertrophy induced by V. Left ventricular coronary flow was reduced from 167.1 +/- 27.2 in normal dogs to 146.2 +/- 17.1 cm3/min-100 g-1 in P hypertrophy, and was reduced further to 82.5 +/- 8.2 cm3/min-100 g-1 in V hypertrophy. Flows decreased similarly in epicardium and endocardium in both hypertrophied hearts. Cardiac O2 extraction in P and V hearts was greater than in control hearts. Myocardial O2 consumption was maintained at control values in P hypertrophy, and decreased by 54 +/- 3% in V hypertrophy. These findings indicate that LV function is impaired at rest in hypertrophy induced by V and is normal in hypertrophy induced by P.