Abstract

The American Heart Association Prevention Conference IV, “Prevention and Rehabilitation of Stroke,” was held May 1-2, 1996, in Tucson, Ariz. The report of the conference presents the state of knowledge on stroke epidemiology, etiologic basis, treatment, and rehabilitation. The conference report in its entirety is published in the July 1, 1997, issue of Stroke . This executive summary appears in the July 15, 1997, issue of Circulation . Reprints of the executive summary and full text are available from the American Heart Association. Stroke results from either ischemia, due to arterial occlusion or stenosis, or hemorrhage, due to leakage or rupture of an artery. Differentiation cannot be reliably made from the history or clinical examination alone. Most—but not all—strokes have a sudden or rapid onset. Differential diagnosis of sudden change in focal neurological status includes seizures or postepileptic paralysis, hemorrhage into a tumor (itself a form of stroke), and migraine. Neuroimaging helps to differentiate between these and the cause of short-lived symptoms (transient ischemic attack [TIA]) usually due to ischemia but possibly due to new-onset infarction or hemorrhage. More precise classification of stroke into a pathogenic subtype evades the best clinical skills. ### Ischemic Stroke Mechanism Embolism to the brain. Embolism to the brain may be arterial or cardiac in origin. Commonly recognized cardiac sources include atrial fibrillation (AF), sinoatrial disorder, recent acute myocardial infarction (AMI), marantic or subacute bacterial endocarditis, cardiac tumors, and valvular disorders, both native and artificial. Myocardial infarction. Stroke is an important complication in patients with AMI, occurring in 1% to 3% of all infarctions and in 2% to 6% of patients with anterior wall infarctions. Atrial fibrillation . Pooling of blood in the dysfunctional atrium leads to clots and emboli. AF increases risk of thromboembolism up to 18 times. Risk of stroke in patients with AF can be reduced …

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