Cutaneous vascular reactivity is reduced in aging and in heart failure: association with inflammation.
In the present study, we have investigated whether changes in vascular reactivity in congestive heart failure (CHF) patients can be detected in the cutaneous microvessels and whether these changes are due to endothelial dysfunction, are affected by increasing age and related to an ongoing inflammation. The responses to local warming and iontophoretically administered endothelium-dependent and -independent vasodilators were investigated in healthy young adults, healthy elderly adults and elderly adults with CHF. The results were correlated with plasma concentrations of vascular risk factors and markers for endothelial dysfunction and inflammation. The vasorelaxant responses were reduced in the elderly groups and were attenuated further in the CHF group. This group also had increases in levels of several markers associated with inflammation, higher blood glucose and homocysteine levels, a lower low-density lipoprotein-cholesterol and a rise in the concentration of von Willebrand factor, indicating a prothrombotic endothelial function. The severity of the heart failure, measured as the plasma level of brain natriuretic peptide, correlated with the intensity of inflammation and to the changes in vascular risk factors and endothelial function. It is concluded that the reactivity of the cutaneous microvessels is reduced with age, and the presence of CHF causes a further impairment. There is endothelial dysfunction in CHF, but it is uncertain to what extent this contributes to the reduced vasodilatory capacity. The inflammatory response appears central for many of the manifestations of the CHF syndrome.
Andersson
S E
SE
Department of Internal Medicine, Lund University Hospital, S-226 85 Lund, Sweden. Sven.Andersson@skane.se
Edvinsson
M-L
ML
Edvinsson
L
L
D000328:Adult; D000368:Aged; D000375:Aging / Q000502:physiology*; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000503:physiopathology*; D006358:Hot Temperature; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000097:blood; D007478:Iontophoresis; D008297:Male; D008833:Microcirculation / Q000502:physiology; D020097:Natriuretic Peptide, Brain / Q000097:blood; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012867:Skin / Q000098:blood supply*; D014664:Vasodilation / Q000502:physiology; D014665:Vasodilator Agents
D018836:Inflammation Mediators; D014665:Vasodilator Agents; D020097:Natriuretic Peptide, Brain