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Effects of coronary venous pressure on left ventricular diastolic distensibility
J Watanabe1, M J Levine, F Bellotto
1Department of Medicine, (Cardiovascular Division), Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Mass. 02215.
Insights
Increased coronary venous pressure reduces left ventricular (LV) diastolic distensibility by increasing LV wall volume. This effect is independent of right ventricular (RV) enlargement, highlighting a novel mechanism impacting cardiac function.
Area of Science:
- Cardiovascular Physiology
- Cardiac Mechanics
- Hemodynamics
Background:
- Coronary arterial pressure and flow are established determinants of left ventricular (LV) diastolic distensibility.
- The specific impact of elevated coronary venous pressure on LV diastolic properties remains largely unexplored.
- Understanding these relationships is crucial for comprehending diastolic dysfunction.
Purpose of the Study:
- To investigate the hypothesis that increased coronary venous pressure leads to augmented LV wall volume and diminished LV diastolic distensibility.
- To differentiate the effects of elevated coronary venous pressure from direct ventricular interaction caused by right ventricular (RV) enlargement.
Main Methods:
- Utilized excised, blood-perfused, isovolumic canine left ventricular (LV) preparations without the pericardium.
- Protocol I: Increased coronary venous pressure by elevating right atrial (RA) and right ventricular (RV) pressures.
- Protocol II: Isolated RV enlargement using an RV balloon catheter while maintaining constant coronary venous pressure (0 mm Hg).
- Assessed LV diastolic distensibility via shifts in the LV end-diastolic pressure-volume relationship and LV wall volume changes using subepicardial segment length.
Main Results:
- Elevating RA/RV pressure (Protocol I) significantly increased LV end-diastolic pressure and LV wall dimensions across various LV volumes compared to baseline.
- RV balloon inflation (Protocol II) resulted in smaller increases in LV end-diastolic pressure and wall dimensions.
- The LV end-diastolic pressure-volume relation shifted upward more substantially in Protocol I than in Protocol II, indicating greater reduction in diastolic distensibility.
- LV wall dimension increased significantly in Protocol I, even at constant LV volume, to a greater extent than in Protocol II.
Conclusions:
- Increased coronary venous pressure significantly decreases LV diastolic distensibility.
- This reduction in distensibility is associated with an increase in LV wall volume.
- The observed effects of elevated coronary venous pressure are independent of diastolic ventricular interactions mediated by RV enlargement.
Abstract:
Coronary arterial pressure and flow are known to influence left ventricular (LV) diastolic distensibility, 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 decreases LV diastolic distensibility with increasing LV wall volume, and this mechanism appears to act independently of diastolic ventricular interaction caused by RV enlargement.