(Circulation. 2001;103:2321.)
© 2001 American Heart Association, Inc.
Editorials |
From the Stroke Program, University of Texas-Houston Medical School.
Correspondence to James C. Grotta, MD, Professor of Neurology and Director, Stroke Program, The University of Texas-Houston Medical School, MSB 7.044, 6431 Fannin St, Houston, TX 77030.
Key Words: Editorials stroke ultrasonics
Prevention of stroke shares much in common with prevention of other vascular events because the underlying pathological process, namely, atherosclerosis, is the same. Attesting to this is the recent demonstration that statins,1 ACE inhibitors,2 and more well-known measures, such as control of hypertension and smoking, are as effective in preventing stroke3 as they are in preventing other cardiovascular events.
However, there is a pathological process, namely,
embolization, that leads to arterial occlusion in the
cerebral circulation much more frequently than in the coronary
bed. Consequently, the detection and prevention of embolic events is
critical to reducing the burden of stroke. Emboli may cause either
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 or from atherosclerotic plaques in the
arteries of the neck are variable in their size and
consistency. When the cardiac chambers are dyskinetic or
fibrillating, leading to stasis and the formation of thrombus, distal
emboli are usually large, they lodge in the initial branches of the
circle of Willis, and the resultant strokes are devastating. The
posterior wall of the most proximal portion of the internal carotid
artery just distal to the bifurcation is a common site of
atherosclerosis because of the unique
hemodynamic effects caused by the flow divider. Emboli
from such large-artery atheroma may consist of a thrombus
or pieces of calcified plaque, but they may also be microscopic if
composed only of fibrin-platelet material. If such
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