Calf and Forearm Blood Flow in Hypercholesterolemic Patients

Abstract

Patients with hypercholesterolemia without vascular disease have an impaired endothelium-dependent (nitric oxide-mediated) vasodilation in coronary and peripheral vascular beds. This study was designed to establish whether hypercholesterolemia (and its reduction) affects also the microcirculation vasomotion during postischemic hyperemia in both calf and forearm. Thirteen male patients, aged 36.2+/-8.5 years, mean +/-SD, with heterozygous familial hypercholesterolemia and 10 male control subjects, aged 32.2+/-3.6 years free from vascular lesions were studied. Plasma lipids, hematologic parameters, and limb vasoreactivity were evaluated while the patients were treated only with diet and during therapy with simvastatin. Calf and forearm blood flows were determined by venous occlusion strain gauge plethysmography at rest, during reactive hyperemia, and after sublingual isosorbide dinitrate administration. Calf resting flow rate of the hypercholesterolemic patients during and without treatment was similar to that of the controls. Calf resting vascular resistance was greater in the untreated hypercholesterolemic subjects than in the normal controls, but during treatment this difference was abolished. Peak flow during reactive hyperemia and flow debt repayment were lower in the untreated hypercholesterolemic subjects as compared to the controls, but they were normalized following hypocholesterolemic therapy. No differences were observed in forearm blood flow measurements between hypercholesterolemic subjects (without and during therapy) and control subjects. 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. Hypercholesterolemia does not affect vasodilation in the forearm as determined by postocclusive reactive hyperemia, while in the calf hypercholesterolemia is associated with higher resting vascular resistance, lower peak flow during reactive hyperemia, and lower flow debt repayment. These abnormalities are corrected by the hypocholesterolemic treatment.

Abnormal endothelial function in female patients with hypothyroidism and borderline thyroid function

“…It is believed that its early phase (peak reactive hyperemia forearm blood flow, and max dfl%) is related to vessel wall structure abnormalities and not to endothelial function [24]. In our study, no differences were observed in the early phase of reactive hyperemia, an observation in agreement with this assumption ( Table 2).…”

Arterial Reactivity in Lower Extremities Is Progressively Reduced as Cardiovascular Risk Factors Increase

“…We did not find differences in resting lower extremity shear rate, flow, or normalized flow between groups, in contrast with one study (31), but in agreement with others (21,22,26,(32)(33)(34). Other studies found no differences in forearm hyperemia with risk factors (21,22,35), and also found that leg hyperemia may be reduced even when arm hyperemia is not (21,22). Also in agreement with our study, those studies showed that lower extremity HypQ measures compared with resting flow measures more clearly distinguished groups with different levels of risk (21,22).…”

“…Relatively greater reductions in lower compared with upper extremity HypQ have been demonstrated in subjects with hypercholesterolemia and in subjects with peripheral arterial disease (21,22). However, regional differences in hyperemic shear rate have not been studied in persons with risk factors.…”

Angiotensin II Type 1 Receptor Antagonism Improves Hypercholesterolemia-Associated Endothelial Dysfunction

“…Reactive hyperemia-induced increase in FBF is a frequently used marker of endothelium-dependent vasorelaxation, especially because of the noninvasive approach. 18,19 However, there are certain limitations compared with the reference method of FBF measurement during intra-arterial infusion of acetylcholine. Hyperemic blood flow is not exclusively dependent on the endothelium, because in addition to endothelium-derived vasoactive agents, other local metabolic factors may contribute to vasodilatation after ischemia.…”