Possible platelet thrombi formation in dog and human femoral arteries.

Atherosclerosis is a ubiquitous condition that commonly produces vessel stenosis and progresses ultimately to vascular occlusion. It is thought by many that platelets collect on sites of atherosclerosis and exacerbate its progression. We have previously shown that platelet thrombi can form within 10 minutes in the stenosed coronary arteries of a dog and can produce acute cyclical reduction in blood flow measured with an electromagnetic flowmeter (EMF). This is followed by sudden restoration of flow as the platelet thrombus breaks loose and is carried distally (Circulation 54:365-370, 1976). In five dogs, blood flow was measured simultaneously in a femoral artery stenosed 70%, exposed proximally with an EMF, and monitored distally over intact skin with a Doppler ultrasonic flowmeter (DUF). Cyclical reductions in blood flow were detected by both the EMF and the DUF, presumably due to platelet thrombi forming in the stenosed femoral artery and then breaking loose and moving distally. These flow reductions could be consistently abolished with aspirin (ASA). In ten patients with angiographically proven substantial stenoses of the femoral or popliteal arteries who were not taking ASA, the popliteal blood flow velocity was measured with a DUF. Six of the ten patients showed cyclical blood flow velocity reductions during 30 minutes of observation. These flow velocity reductions were similar to those observed in the stenosed dog femoral arteries. One hour after taking 600 mg ASA orally, five of the six patients no longer showed flow velocity reductions. Eight male control subjects who were not on ASA and had no known stenoses had no flow velocity reductions when studied with the DUF. Since many factors, such as cigarette smoking, diabetes, and elevated plasma lipids, are known to increase human platelet aggregation, we postulate that platelet thrombi may form in stenosed peripheral arteries, hasten the development of atherosclerosis, and reduce blood flow. This postulate would be compatible with the increased incidence and accelerated development of clinically significant atherosclerosis noted in such patients. Claudication may be more than just the response to "increased demand"; thrombus degeneration may lead to the elaboration of vasospastic substances. If these findings are confirmed by further investigations, the potential for successful therapeutic intervention may be quite significant.