Analysis of right and left ventricular performance of the XXXX heart with chronic myocardial infarction.

@entity308 @entity1184 @entity141 @entity1188 @entity35 @entity1284
1. The @entity35 heart develops a @entity1184 after @entity1188 which is secondary to @entity1284 in the left ventricle (LV) and to pressure overload in the right ventricle (RV). This study was undertaken to determine whether the reduced inotropic response to @entity141 presented by the LV of infarcted @entity35 extends to the RV and whether this hemodynamic profile in vivo affects the contractile performance of the ventricles assessed in vitro. 2. Male adult @entity35 were submitted to left coronary artery ligation to produce @entity1188 ( @entity1188 ) or to a sham surgery (SO) and used 4 to 5 weeks later. The hemodynamic data were recorded in the anesthetized animals and the systolic performance of both ventricles was evaluated in vitro in the hearts perfused by the Langendorff technique. The isovolumic systolic pressure (ISP) developed by both ventricles was measured at various diastolic pressures (0 to 30 mmHg) and @entity141 concentrations (0.62, 1.25, and 2.50 mM). 3. The RV systolic pressure was higher in @entity1188 (N = 12) than in SO (N = 12) @entity35 (42 +/- 5 vs 26 +/- 1 mmHg, P < 0.05). A positive and linear correlation (r = 0.86, P < 0.01) between RV systolic pressure and the RV weight to body weight ratio in @entity1188 @entity35 was observed. 4. Length-dependent activation, evaluated by using normalized ventricular function curves, was unchanged in the RV of @entity1188 hearts. In the @entity1188 LV, however, a slight improvement of the normalized systolic performance was observed in relation to SO hearts for diastolic pressures higher than 15 mmHg. 5. A similar @entity308 of the inotropic response to @entity141 was observed in both ventricles of @entity1188 hearts. Moreover, for @entity1188 hearts the increase of the ISP to @entity141 flattened at lower @entity141 concentrations in relation to the SO group. 6. The present results demonstrate that LV @entity1188 in @entity35 depresses the contractile performance of both ventricles. The reduced inotropic response to @entity141 presented by both ventricles may contribute to the reduced capacity of the @entity1188 heart to generate external work under conditions of higher metabolic demand.
