EFFECTS OF CORONARY VENOUS-PRESSURE ON LEFT-VENTRICULAR DIASTOLIC DISTENSIBILITY

Coronary arterial pressure and flow are known to influence left ventricular (LV) diastolic distensibibility, but the influence of coronary venous pressure is unknown. To test the hypothesis that increased coronary venous pressure leads to an increase in LV wall volume and a decrease in LV diastolic distensibility, we studied excised, blood-perfused LV isovolumic dog hearts without the pericardium. In protocol I (n = 8), to raise coronary venous pressure the pressure of right atrium (RA) and right ventricle (RV) was increased by the height of a blood reservoir connected with a cannula that opened in both the RA and RV. In protocol II (n = 7), to isolate the effect of RV enlargement on LV diastolic distensibility (direct ventricular interaction) an isovolumic RV balloon was used with coronary venous pressure held constant at 0 mm Hg. Changes in LV diastolic distensibility were assessed by shifts of the LV end-diastolic pressure-volume relation. Changes in LV wall volume were detected by subepicardial segment length at end-diastole. The mean pressures of RA and RV (protocol I) and RV balloon only (protocol II) were increased from 0 to 15 and 30 mm Hg over a range of LV volume. In protocol I, when RA·RV pressure was increased from 0 to 30 mm Hg at three levels of LV volume (22 ± 2, 31 ± 3, and 40 ± 3 ml), LV end-diastolic pressures increased significantly from 5.2 ± 0.3 to 11.2 ± 1.5, from 10.4 ± 0.3 to 18.2 ± 1.2, and from 20.2 ± 1.0 to 28.8 ± 1.2 mm Hg, respectively. In protocol II, when RV balloon pressure was increased from 0 to 30 mm Hg at the three LV volumes (21 ± 3, 31 ± 3, and 41 ± 4 ml), LV end-diastolic pressures showed smaller increases from 5.2 ± 0.2 to 6.6 ± 0.2, from 9.8 ± 0.3 to 11.6 ± 0.6, and from 19.0 ± 0.5 to 21.4 ± 0.8 mm Hg, respectively. In both protocols, the LV end-diastolic pressure-volume relation shifted upward in a nearly parallel fashion but the shift was much greater in protocol I than in protocol II. Despite constant LV volume, an increase in LV wall dimension in protocol I was significant and much greater than that in protocol II. From these results, we conclude that increased coronary venous pressure decrease LV diastolic distensibility with increasing LV wall volume, and this mechanism appears to act independently of diastolic ventricular interaction caused by RV enlargement.