Hypertension. 2007;50:167-171
Published online before print April 9, 2007,
doi: 10.1161/HYPERTENSIONAHA.107.088799
(Hypertension. 2007;50:167.)
© 2007 American Heart Association, Inc.
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Sixth International Workshop on Structure and Function of the Vascular System |
Mechanism(s) of Systolic Blood Pressure Reduction and Drug Therapy in Hypertension
Michel E. Safar
From the Paris Descartes University, Faculty of Medicine, APHP, Diagnosis Center, Hôtel-Dieu Hospital, Paris, France.
Correspondence to Michel Safar, Diagnosis Center, Hôpital Hôtel-Dieu, 1 place du Parvis Notre-Dame, 75181 Paris Cedex 04, France. E-mail michel.safar@htd.aphp.fr
An extract of the first 250 words of the full text is provided, because this article has no abstract.
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Introduction
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Antihypertensive drug therapy is a major modality of cardiovascular
(CV) disease prevention, especially for stroke, congestive heart
failure, and renal insufficiency. Coronary risk is also consistently
prevented by antihypertensive treatment, but to a lesser extent.
14 The Prime Study
2 has shown that drug-induced blood pressure
(BP) reduction in hypertensive subjects is associated with a
significant decrease of coronary risk. However, when treated
and untreated subjects are compared, at any given value of systolic
BP (SBP), this risk remains higher in treated than in untreated
subjects, suggesting the persistence of residual coronary complications.
Results of therapeutic trials also indicate that coronary risk
is associated with a particular hemodynamic pattern in treated
hypertensive subjects.
3 Although diastolic BP (DBP) is significantly
lowered by drug treatment to <90 mm Hg (80% of the patients),
SBP remains above 140 mm Hg in 60%, indicating an increase of
pulse pressure (PP), which is the difference between SBP and
DBP.
4 It is widely accepted that SBP and PP rise sharply with
age and that this increase is a major manifestation of vascular
aging and stiffening, which are now considered major predictors
of CV risk, independent of the mean BP (MBP) level.
4 The purpose
of this review is to analyze the mechanism(s) of SBP in untreated
and chronically treated hypertensive subjects and to determine
which pathophysiological factors are susceptible to attenuating
consistently coronary and CV complications in hypertensive populations.
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Pathophysiological Modifications of SBP Along the Arterial Tree
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Ventricular ejection in humans is associated with 2 principal
events. First, the coronary circulation is transiently interrupted,
as the principal
. . . [Full Text of this Article]
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