Venous endothelial function in heart failure: comparison with healthy controls and effect of clinical compensation.
BACKGROUND
Endothelial function has been extensively evaluated at the arterial bed in several cardiovascular scenarios. Venous endothelial dysfunction, however, has not been thoroughly explored particularly in heart failure (HF).


OBJECTIVE
To characterize venous endothelial function in severe HF.


RESULTS
Venous endothelial function was evaluated by the dorsal hand vein technique using a tripod holding a linear variable differential transformer. Dorsal hand veins were pre-constricted with phenylephrine and dose-response curves were constructed after acetylcholine and sodium nitroprusside administration. Maximum vasodilator response to acetylcholine, a marker of endothelium-dependent venodilation, was significantly lower (47+/-53% versus 102+/-54%, respectively, p=0.0004) in HF (n=27) patients compared to healthy controls (n=20). No difference in the endothelium-independent venodilator response was observed (p=0.87). Maximum vasodilator response to acetylcholine was also significantly lower on admission compared to the response immediately before hospital discharge in patients with acute decompensated HF (p<0.01). Improvement in venous endothelial function paralleled weight loss (mean difference of -3.8 kg, p<0.01) and improvement in the 6-minute walk test (mean difference of 107 m, p<0.01). There was no significant change in angiotensin-converting enzyme inhibitor or beta-blocker use during hospital stay.


CONCLUSIONS
HF patients experience marked endothelium-dependent venous dysfunction with partial recovery during in-hospital management.
Rabelo
Eneida R
ER
Cardiovascular Division of Hospital de Clínicas de Porto Alegre, The Post-Graduation Program in Biology, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Ruschel
Karen
K
Moreno
Heitor
H
Rubira
Marcelo
M
Consolim-Colombo
Fernanda M
FM
Irigoyen
Maria Cláudia
MC
Rohde
Luis E
LE
D000109:Acetylcholine / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006225:Hand / Q000098:blood supply; D006333:Heart Failure / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D009599:Nitroprusside / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology; D014680:Veins / Q000503:physiopathology; D015431:Weight Loss
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D014665:Vasodilator Agents; D009599:Nitroprusside; D000109:Acetylcholine