Can drugs help patients with lower limb ischaemia?

Abstract

The prevalence of symptomatic arterial disease of the lower limbs is 2 per cent of the population aged 45-60, but it has a relatively benign course, with 70 per cent of patients requiring no therapy. Of the numerous drugs used in the treatment of the disease, there is no evidence to suggest that antilipaemic drugs, anticoagulants, vasodilators or rheological agents confer any benefit to the patient. The initial use of antiplatelet drugs and prostaglandins has been disappointing despite the undoubted importance of the platelet/endothelial interaction in the aetiology of atherosclerosis. As it is unlikely that we can reverse advanced disease, this is hardly surprising. Long term use of these drugs may prevent deterioration in those patients with progressive disease, and controlled trials on this aspect of treatment are now required. Symptomatic relief in the claudicant may perhaps be obtained with naftidrofuryl and suloctodil and with the former in more severe ischaemia, but their use should not replace the beneficial effects of exercise and cessation of smoking.

Pharmacological Approaches to the Treatment of Intermittent Claudication???

“…However, expert opinions generally hold these drugs to be of very limited or no value (Boobis & Bell 1982;Cameron et al 1988;Coffman 1988;Drug and Therapeutics Bulletin 1990;Verstraete 1982). However, expert opinions generally hold these drugs to be of very limited or no value (Boobis & Bell 1982;Cameron et al 1988;Coffman 1988;Drug and Therapeutics Bulletin 1990;Verstraete 1982).…”

“…They have hypolipidaemic and fibrinolytic actions in addition to a vasodilatory effect, but they are of no proven benefit in intermittent claudication (Boobis & Bell 1982). They have hypolipidaemic and fibrinolytic actions in addition to a vasodilatory effect, but they are of no proven benefit in intermittent claudication (Boobis & Bell 1982).…”

“…Endothelial damage causes platelet aggregation and adhesion, and atherosclerosis or mural thrombus development is thus promoted (Boobis & Bell 1982). Endothelial damage causes platelet aggregation and adhesion, and atherosclerosis or mural thrombus development is thus promoted (Boobis & Bell 1982).…”

Effect of Intensive Walking Exercise on Skeletal Muscle Blood Flow in Intermittent Claudication

“…' Despite new approaches in interventional angiology, physical training is a wellestablished therapy for peripheral arterial occlusive disease (PAOD) according to Fontaine stage II. 2 From clinical studies, increased functional capillary density, altered muscle metabolism, and improved blood flow have been postulated as possible factors.3-5 The measurement of skeletal muscle blood flow-the target for therapeutic interventions-is difficult in patients. 2 From clinical studies, increased functional capillary density, altered muscle metabolism, and improved blood flow have been postulated as possible factors.3-5 The measurement of skeletal muscle blood flow-the target for therapeutic interventions-is difficult in patients.…”

“…However, on which mechanism the improvement in painfree walking distance is predominantly based is still a matter of controversy . '3 The purpose of our experimental study was: (1) to quantify the effects of daily treadmill exercise for a period to one year on skeletal muscle blood flow in PAOD Fontaine stage II, (2) to evaluate the effect of supplementary oral administration of BF (600 mg/day), and (3) to investigate whether the effect of treadmill exercise can be enhanced by BF (3 mg/kg body weight [BW]) injected into the abdominal aorta. For this reason, various animal models have been established.~'° Most of them, however, do not allow quantification of skeletal muscle blood flow during exercise .…”