Diastolic Left Ventricular Pressure-Volume Relationship before and after Chronic Right Ventricular Pressure Overload in Dogs without Pericardia

We studied the effect of chronic right ventricular pressure overload on diastolic ventricular interdependence in dogs without pericardia, instrumented to measure left ventricular pressure, right ventricular pressure, and 3 left ventricular dimensions. We studied 12 dogs before (control) and nine dogs after 6 weeks of pulmonary artery constriction producing systolic right ventricular pressure 270 mm Hg. Compared to control, following pulmonary artery band there was greater (P < 0.01) interventricular septal mass (53 ± 15 vs. 35 ± 7 mg, mean ± SD), thickness (15 ± 2 vs. 10 ± 1 mm), and ratio of the surface area of the interventricular septal to total left ventricular surface area (0.38 ± 0.03 vs. 0.33 ± 0.02), but unchanged left ventricular free wall mass (81 ± 12 vs. 84 ± 14 mg) and thickness (11 ± 2 vs. 11 ± 2 mm). End-diastolic right and left ventricular pressures and left ventricular volume were varied by vena cava and pulmonary artery occlusions and releases. Volume was calculated as an ellipsoid and the data in each dog fit to: left ventricular pressure = a0 + a]V + a2V 2 + a3V 3 + a4V 4 + bPRV, r > 0.91 in each dog. During control, b was similar, whether calculated from both pulmonary artery and vena cava occlusions (0.47 ± 0.09) or from vena cava occlusions alone (0.43 ± 0.11), and was greater than the ratio of the interventricular septal surface area to left ventricular surface area (0.33 ± 0.02, P < 0.05). Following the pulmonary artery band, b decreased to 0.21 ± 0.10 (P < 0.05) and was less than the ratio of interventricular septal surface area to the left ventricular surface area which increased to 0.38 ± 0.03 (P < 0.05). We conclude that the effect of alterations in right ventricular pressure on the end-diastolic left ventricular pressure volume relationship, independent of the pericardium, is reduced following the pulmonary artery band that produces interventricular septal hypertrophy. These results are consistent with the hypothesis that the effect of alterations of right ventricular pressure on the diastolic left ventricular pressure-volume relationship depends on the relative elastance of the interventricular septum and left ventricular free wall, and not simply on the ratio of the interventricular septal surface area to the left ventricular surface area. (Circ Res 54: 719730, 1984)