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Papers on CASP

Central Pressure More Strongly Relates to Vascular Disease and Outcome Than Does Brachial Pressure
The Strong Heart Study
Mary J. Roman, Richard B. Devereux, Jorge R. Kizer, Elisa T. Lee, James M. Galloway, Tauqeer Ali, Jason G. Umans, Barbara V. Howard
Hypertension 2007;50;197-203; originally published online May 7, 2007;
DOI: 10.1161/HYPERTENSIONAHA.107.089078
Hypertension is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX
72514
Copyright © 2007 American Heart Association. All rights reserved. Print ISSN: 0194-911X. Online
ISSN: 1524-4563

 

 

Regression of Left Ventricular Mass in Hypertensive Patients Treated With Perindopril/ Indapamide as a First-Line Combination
The REASON Echocardiography Study
Nicola de Luca, Jean-Michel Mallion, Michael F. O’Rourke, Eoin O’Brien, Karl-Heinz Rahn, Bruno Trimarco, Ramon Romero, Peter Wilhelmus De Leeuw, Gerhart Hitzenberger, Edouard Battegay, Daniel Duprez, Peter Sever, and Michel E. Safar, on behalf of the REASON Project*
doi:10.1016/j.amjhyper.2004.03.681

Background: Increase in left ventricular mass (LVM) may be linked to morbidity and mortality in hypertensive patients. Arterial stiffness, systolic blood pressure (BP), and pulse pressure (PP) seem to be the main determinants of LVM. The perindopril/indapamide combination normalizes systolic BP, PP, and arterial function to a greater extent than atenolol. The aim of this study was to compare the effects of perindopril (2 mg)/indapamide (0.625 mg) first-line combination with atenolol (50 mg) on LVM reduction in hypertensive patients.

 

Central blood pressures: do we need them in the management of cardiovascular disease? Is it a feasible therapeutic target?
Athanase D. Protogeroua,b, Theodore G. Papaioannoub, Jacques Blachera, Christos M. Papamichaelb, John P. Lekakisc and Michel E. Safara
Journal of Hypertension 2007, 25:265–272

It is well established that in young and healthy individuals central (aortic or carotid) systolic and pulse pressures are different from peripheral (brachial) corresponding pressures as a consequence of progressive changes in arterial stiffness and pressure wave reflections along the arterial tree. There is evidence indicating that in interventions with pharmaceutical and non-pharmaceutical agents, central pressures are subjected to greater changes than peripheral pressures, and they are more closely related to the pathophysiology of end-organ damage or cardiovascular risk. Therefore central blood pressures may be of higher clinical importance than peripheral pressures. The present review aims to provide an insight into the (patho)physiology of central blood pressures, to present the most accurate techniques for their estimation, and to discuss the available experimental and epidemiological data that support the emerging need for the evaluation of central blood pressures in clinical practice. J Hypertens 25:265–272 Q 2007 Lippincott Williams & Wilkins.

 

Differential Impact of Blood Pressure–Lowering Drugs on Central Aortic Pressure and Clinical Outcomes
Principal Results of the Conduit Artery Function Evaluation (CAFE) Study

ImageThe CAFE Investigators, for the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) Investigators
CAFE Steering Committee and Writing Committee: Bryan Williams, MD, FRCP; Peter S. Lacy, PhD; Simon M. Thom, MD, FRCP; Kennedy Cruickshank, MD; Alice Stanton, MB, PhD, FRCPI; David Collier, MBBS, PhD; Alun D. Hughes, MBBS, PhD; H. Thurston, MD, FRCP
Study Advisor: Michael O’Rourke, MD, FRACP

Circulation 2006;113;1213-1225; originally published online Feb 13, 2006;
DOI: 10.1161/CIRCULATIONAHA.105.595496

When blood pressure is measured conventionally over the brachial artery, it is assumed that these measurements accurately reflect pressures in the central circulation. This assumption is supported by irrefutable observations that brachial blood pressure parameters are powerful predictors of cardiovascular structural damage, morbidity, and mortality.1 However, central aortic pressure parameters and left ventricular load are determined not only by cardiac output and peripheral vascular resistance but also by the stiffness of conduit arteries and the timing and magnitude of pressure wave reflections.2–6 Short-term studies have shown that various classes of blood pressure–lowering drugs may have profoundly different effects on pulse wave morphology and thus central hemodynamic parameters despite similar effects on brachial artery pressures.7–11 This observation is relevant to the debate about how much of the benefit of blood pressure–lowering drugs in clinical trials can be attributed to blood pressure lowering per se or to alternative mechanisms “beyond blood pressure.”12 This debate is fundamental because it defines the principles of clinical practice for the treatment of hypertension.  

 

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