Congestive heart failure in dogs significantly reduced coronary blood flow responses to vasodilators (P<0.01), but responses were normal after correcting for elevated left ventricular diastolic pressure.
Does increased left ventricular diastolic pressure limit coronary vasodilation in congestive heart failure?
Reduced coronary blood flow response to vasodilators in heart failure is primarily due to increased extravascular compressive forces from elevated LVEDP rather than intrinsic endothelial dysfunction.
p-value: p=<0.01
OBJECTIVE: The increase in coronary blood flow (CBF) in response to endothelium-dependent vasodilators is reduced in congestive heart failure (CHF) suggesting endothelial dysfunction. However, increases in extravascular compressive forces secondary to elevated left ventricular diastolic pressure (LVEDP) in CHF might contribute to this abnormality. METHODS: We measured CBF responses to intracoronary doses of the endothelium-dependent vasodilators acetylcholine (ACH) and bradykinin (BK) and the endothelium-independent vasodilator sodium nitroprusside (SNP) in the same eight dogs before (control) and after CHF was produced by 23+/-3 days of rapid ventricular pacing. In five of the dogs with CHF the zero-flow pressure (P(zf)), which reflects extravascular compressive forces in the maximally vasodilated coronary circulation (adenosine) was measured and found to strongly correlate with LVEDP (r=0.91). Coronary vascular resistance (CVR) at each concentration of vasodilator before and after the development of CHF was corrected for estimated coronary back pressure: CVR=(P(Ao)-LVEDP)/CBF, where P(Ao) is mean aortic pressure. RESULTS: CHF resulted in a significant decrease in CBF and increase in heart rate and LVEDP compared to control (P<0.05). The CBF responses to ACH, BK and SNP were all significantly reduced in the failing hearts (P<0.01). However, after correction for the elevated LVEDP in CHF, the response of CVR to the endothelium-dependent vasodilators was not different from normal. CONCLUSION: These findings suggest that endothelium mediated vasodilation is preserved in CHF, but that increased extravascular compressive forces act to limit the increase in CBF.
Jay H. Traverse (Sat,) conducted a other in Congestive heart failure (n=8). Intracoronary acetylcholine, bradykinin, and sodium nitroprusside vs. Baseline (before congestive heart failure induction) was evaluated on Coronary blood flow (CBF) responses to vasodilators (p=<0.01). Congestive heart failure in dogs significantly reduced coronary blood flow responses to vasodilators (P<0.01), but responses were normal after correcting for elevated left ventricular diastolic pressure.