(Circulation. 2000;101:1641.)
© 2000 American Heart Association, Inc.
Editorials |
From the Departments of Radiology and Medicine, Brigham and Womens Hospital and Harvard Medical School, Boston, Massachusetts.
Correspondence to Norman K. Hollenberg, MD, PhD, Brigham and Womens Hospital, 75 Francis St, Boston, MA 02115.
Key Words: Editorials angiotensin hypertension
In his seminal review, Folkow1 pointed out that recognition of structural cardiovascular changes in association with hypertension is longstanding: In 1836, Richard Bright described both left ventricular and aortic wall thickening in Brights disease. Moreover, George Johnson some 50 years later first reported wall thickening in arterioles, but the functional and hemodynamic consequences appear to have been overlooked until Folkow began to develop the theme some 30 years ago, a field of interest that has grown over the past 3 decades.
Until about 10 to 15 years ago, the underlying pathogenetic sequence seemed straightforward. Muscle hypertrophies in the face of an increased workload. An increase in arterial blood pressure represents an increase in workload for the heart and the arterial tree. Hypertrophy of the heart and vascular tree, then, not only come as no surprise but might have been anticipated.
If elevated blood pressure represents the central element in
pathogenesis, why does control of blood pressure with the ß-blocking
agent atenolol not reverse the hypertrophic process in the study by
Schiffrin et al in this issue of Circulation and earlier
studies?2 3 The ratio of small-artery wall thickness
to lumen was as increased after a year of treatment with atenolol as it
was at baseline. It has been common experience that it is much easier
to normalize blood pressure than to normalize vascular structure in
patients with essential hypertension4 5 6 and in animal
models.7 8 9 The duration of treatment seems to be the
crucial factor. In a long-term follow-up study, up to 6
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C. Vecchione, D. Carnevale, A. Di Pardo, M. T. Gentile, A. Damato, G. Cocozza, G. Antenucci, G. Mascio, U. Bettarini, A. Landolfi, et al. Pressure-Induced Vascular Oxidative Stress Is Mediated Through Activation of Integrin-Linked Kinase 1/{beta}PIX/Rac-1 Pathway Hypertension, November 1, 2009; 54(5): 1028 - 1034. [Abstract] [Full Text] [PDF] |
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