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(Stroke. 1995;26:1700-1706.)
© 1995 American Heart Association, Inc.
Articles |
From the Departments of Clinical and Internal Medicine (A.R.), University of Padua, University Hospital, Padua, Italy.
Correspondence to G.P. Rossi, MD, FACC, Clinica Medica 1, Hypertension Unit, University Hospital, via Giustiniani 2, 35126 Padova, Italy.
Background Arterial hypertension is the leading cause of cardiovascular disease and is associated with an increased risk of stroke and heart attack. These complications have been largely attributed to the remodeling of the arterial wall, including accelerated atherosclerosis occurring in hypertensive patients. Although the risk of haemorrhagic stroke seems to be directly related to the level of blood pressure elevation, no such tight relationship has been found between blood pressure levels and atherosclerosis. This observation has led to the concept that a number of genetic, humoral, and cellular factors may be involved in atherogenesis in hypertensive patients.
Summary of Review The experimental and clinical evidence concerning the role of the renin-angiotensin system in cardiovascular remodeling and atherogenesis of the cerebrovascular bed as well as the data supporting an association between angiotensin II and thrombotic stroke are examined.
Conclusions The contribution of the renin-angiotensin system to the pathogenesis of accelerated carotid artery atherosclerosis and particularly of cerebrovascular disease remains to be definitively proven. However, the bulk of experimental and clinical data are consistent with the hypothesis that the renin-angiotensin system may play a detrimental role.
Key Words: carotid artery diseases hypertension renin-angiotensin ultrasonics
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