Reduction of homocysteine in elderly with heart failure improved vascular function and blood pressure control but did not affect inflammatory activity.
We have previously shown that hyperhomocysteinaemia is common in elderly heart failure patients, and is associated with endothelial dysfunction, impaired vasodilatory capacity and a low-grade inflammation. In the present study we examined if supplementation with B6, B12 and folate could normalize the hyperhomocysteinaemia and if so, in turn, would improve the associated parameters. This was an open study without placebo control on heart failure patients with plasma homocysteine > 15 microM. Measurements of cutaneous vascular reactivity, blood pressure, inflammatory activity and endothelial function were performed before and after intervention with intra-individual comparisons. The treatment reduced homocysteine to near normal values and enhanced the hyperaemic response to acetylcholine related to the response to heat. The mean arterial blood pressure and pulse rate was reduced. There was no effect on inflammatory activity, plasma levels of von Willebrand factor, subjective health quality or the hyperaemic responses to sodium nitroprusside or local warming. Hyperhomocysteinaemia in heart failure patients is multifactorial in origin. Folate deficiency, inflammatory activity and reduced renal function could be contributing. It is suggested that supplementation with B-vitamins can improve the vasodilatory capacity and reduce the blood pressure but additional studies are required to confirm this.
Andersson
Sven E
SE
Department of Internal Medicine, Lund University Hospital, S-226 85 Lund, Sweden. sven.ea@telia.com
Edvinsson
Marie-Louise
ML
Edvinsson
Lars
L
D000109:Acetylcholine; D000368:Aged; D001794:Blood Pressure / Q000187:drug effects*; D001808:Blood Vessels / Q000503:physiopathology*; D016207:Cytokines / Q000097:blood; D019587:Dietary Supplements; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D005260:Female; D006304:Health Status; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006710:Homocysteine / Q000037:antagonists & inhibitors* / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D008297:Male; D009599:Nitroprusside; D012039:Regional Blood Flow / Q000187:drug effects; D012867:Skin / Q000098:blood supply; D014664:Vasodilation / Q000502:physiology; D014815:Vitamins / Q000097:blood / Q000627:therapeutic use
D016207:Cytokines; D014815:Vitamins; D006710:Homocysteine; D009599:Nitroprusside; D000109:Acetylcholine