Preventing stroke: is preventing microemboli enough?

Abstract

However, there is a pathological process, namely, emboli-zation, that leads to arterial occlusion in the cerebral circula-tion much more frequently than in the coronary bed. Conse-quently, the detection and prevention of embolic events iscritical to reducing the burden of stroke. Emboli may causeeither large disabling strokes or small subclinical events,depending on the size and eventual location of the embolus.Emboli generated from the chambers or valves of the heart orfrom atherosclerotic plaques in the arteries of the neck arevariable in their size and consistency. When the cardiacchambers are dyskinetic or fibrillating, leading to stasis andthe formation of thrombus, distal emboli are usually large,they lodge in the initial branches of the circle of Willis, andthe resultant strokes are devastating. The posterior wall of themost proximal portion of the internal carotid artery just distalto the bifurcation is a common site of atherosclerosis becauseof the unique hemodynamic effects caused by the flowdivider. Emboli from such large-artery atheroma may consistof a thrombus or pieces of calcified plaque, but they may alsobe microscopic if composed only of fibrin-platelet material. Ifsuch “microemboli” are ,0.1 mm in diameter, they mightpass into the small arteriolar branches. There they may belysed by endogenous protective hemostatic defenses, or theymay cause areas of microinfarction.Much has been learned about the clinical consequences andprevention of large emboli. Because such strokes are theleading cause of disability among US adults, multicenter,randomized, clinical stroke prevention trials have been orga-nized to reduce clinically apparent strokes as the primary endpoint. These have conclusively demonstrated that antiplatelettherapy reduces the incidence of recurrent stroke by ’20% to25%