Increased extravascular forces limit endothelium-dependent and -independent coronary vasodilation in congestive heart failure

Jay H. Traverse, Yingjie Chen, Melanie Crampton, Shauna Voss, Robert J Bache

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16 Scopus citations


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 (Pzf), 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=(PAo-LVEDP)/CBF, where PAo 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.

Original languageEnglish (US)
Pages (from-to)454-461
Number of pages8
JournalCardiovascular Research
Issue number3
StatePublished - 2001

Bibliographical note

Funding Information:
This study was supported by U.S. Public Health Service Grants HL20598, HL58067 and HL21872 from the National Heart, Lung and Blood Institute. Jay H. Traverse was supported by a Scientist Development Grant from the American Heart Association.


  • Coronary circulation
  • Endothelial function
  • Heart failure
  • Nitric oxide
  • Vasoconstriction/dilation


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