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BP control reduces lacunar stroke risk but not all events; leaves open targeted prevention of atherothrombotic and cardioembolic mechanisms.
Despite widespread treatment of hypertension, stroke continues to be the third leading cause of death in the United States. Antihypertensive therapy is more effective in preventing hemorrhagic strokes than ischemic strokes. In order to understand the reasons why antihypertensive therapy is only partially successful in the eradication of ischemic strokes, differences in the pathogenesis and treatment of subtypes of stroke must be considered. There are three main stroke subtypes of ischemic strokes: small-vessel arteriopathic (lacunar), large-artery atherothrombotic, and cardioembolic. Hypertension is the major cause of lacunar strokes but plays a lesser role in the pathogenesis of atherothrombotic strokes. Antihypertensive therapy prevents the majority of lacunar strokes but may not have a major impact on the occurrence of atherothrombotic strokes. Due to impaired cerebral autoregulation, overtreatment of hypertension, especially in the elderly and in patients with previous strokes, may paradoxically lead to stroke (J-curve). Assuming that the majority of lacunar strokes are prevented by judicious antihypertensive therapy, future therapeutic efforts should concentrate on the prevention of atherothrombotic and cardioembolic strokes. In this regard, refinement of surgical techniques, pharmacologic approaches aimed at plaque stabilization, and the application of transesophageal echocardiography for the diagnosis of embolic strokes (and anticoagulation for a probable source) are promising. Besides the obvious reasons of noncompliance and inadequate therapy, overly aggressive treatment of hypertension in the elderly and stroke mechanisms unrelated to blood pressure may explain the occurrence of strokes despite our efforts to treat hypertension.
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Géza Simon (2002) studied this question.
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