Calf and forearm blood flow in hypercholesterolemic patients

Patients with hypercholesterolemia without vascular disease have an impaire d endothelium-dependent (nitric oxide-mediated) vasodilation in coronary an d peripheral vascular beds. This study was designed to establish whether hy percholesterolemia (and its reduction) affects also the microcirculation va somotion during postischemic hyperemia in both calf and forearm. Thirteen m ale patients, aged 36.2 +/- 8.5 years, mean +/- SD, with heterozygous famil ial hypercholesterolemia and 10 male control subjects, aged 32.2 +/- 3.6 ye ars free from vascular lesions were studied. Plasma lipids, hematologic par ameters, and limb vasoreactivity were evaluated while the patients were tre ated only with diet and during therapy with simvastatin. Calf and forearm b lood flows were determined by venous occlusion strain gauge plethysmography at rest, during reactive hyperemia, and after sublingual isosorbide dinitr ate administration. Calf resting flow rate of the hypercholesterolemic pati ents during: and without treatment was similar to that of the controls. Cal f resting vascular resistance was greater in the untreated hypercholesterol emic subjects than in the normal controls, but during treatment this differ ence was abolished. Peak flow during reactive hyperemia and flow debt repay ment were lower in the untreated hypercholesterolemic subjects as compared to the controls, but they were normalized following hypocholesterolemic the rapy. No differences were observed in forearm blood flow measurements betwe en hypercholesterolemic subjects (without and during therapy) and control s ubjects. The blood flow and vascular resistance after isosorbide dinitrate were modified in a similar manner in the hypercholesterolemic (without and during therapy) and control subjects at both calf and forearm. Hypercholest erolemia does not affect vasodilation in the forearm as determined by posto cclusive reactive hyperemia, while in the calf hypercholesterolemia is asso ciated with higher resting vascular resistance, lower peak flow during reac tive hyperemia, and lower flow debt repayment. These abnormalities are corr ected by the hypocholesterolemic treatment.