Abstract
Although the clinical relevance of brachial blood pressure (BP) measurement for cardiovascular (CV) risk stratification is nowadays widely accepted, this approach can nevertheless present several limitations. Pulse pressure (PP) amplification accounts for the notable increase in PP from central to peripheral arterial sites. Target organs are more greatly exposed to central hemodynamic changes than peripheral organs. The pathophysiological significance of local BP pulsatility, which has a role in the pathogenesis of target organ damage in both the macro- and the microcirculation, may therefore not be accurately captured by brachial BP as traditionally evaluated with cuff measurements. The predictive value of central systolic BP and PP over brachial BP for major clinical outcomes has been demonstrated in the general population, in elderly adults and in patients at high CV risk, irrespective of the invasive or non-invasive methods used to assess central BP. Aortic stiffness, timing and intensity of wave reflections, and cardiac performance appear as major factors influencing central PP. Great emphasis has been placed on the role of aortic stiffness, disturbed arterial wave reflections and their intercorrelation in the pathophysiological mechanisms of CV diseases as well as on their capacity to predict target organ damage and clinical events. Comorbidities and age-related changes, together with gender-related specificities of arterial and cardiac parameters, are known to affect the predictive ability of central hemodynamics on individual CV risk.
Keywords: Cardiovascular risk prediction, central pulse pressure, aortic stiffness, wave reflections, atherosclerosis, microcirculatory damage.
Current Pharmaceutical Design
Title:Central Hemodynamics in Risk Assessment Strategies: Additive Value Over and Above Brachial Blood Pressure
Volume: 21 Issue: 6
Author(s): Alexandra Yannoutsos, Elisa R. Rinaldi, Yi Zhang, Athanassios D. Protogerou, Michel E. Safar and Jacques Blacher
Affiliation:
Keywords: Cardiovascular risk prediction, central pulse pressure, aortic stiffness, wave reflections, atherosclerosis, microcirculatory damage.
Abstract: Although the clinical relevance of brachial blood pressure (BP) measurement for cardiovascular (CV) risk stratification is nowadays widely accepted, this approach can nevertheless present several limitations. Pulse pressure (PP) amplification accounts for the notable increase in PP from central to peripheral arterial sites. Target organs are more greatly exposed to central hemodynamic changes than peripheral organs. The pathophysiological significance of local BP pulsatility, which has a role in the pathogenesis of target organ damage in both the macro- and the microcirculation, may therefore not be accurately captured by brachial BP as traditionally evaluated with cuff measurements. The predictive value of central systolic BP and PP over brachial BP for major clinical outcomes has been demonstrated in the general population, in elderly adults and in patients at high CV risk, irrespective of the invasive or non-invasive methods used to assess central BP. Aortic stiffness, timing and intensity of wave reflections, and cardiac performance appear as major factors influencing central PP. Great emphasis has been placed on the role of aortic stiffness, disturbed arterial wave reflections and their intercorrelation in the pathophysiological mechanisms of CV diseases as well as on their capacity to predict target organ damage and clinical events. Comorbidities and age-related changes, together with gender-related specificities of arterial and cardiac parameters, are known to affect the predictive ability of central hemodynamics on individual CV risk.
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Cite this article as:
Yannoutsos Alexandra, Rinaldi R. Elisa, Zhang Yi, Protogerou D. Athanassios, Safar E. Michel and Blacher Jacques, Central Hemodynamics in Risk Assessment Strategies: Additive Value Over and Above Brachial Blood Pressure, Current Pharmaceutical Design 2015; 21 (6) . https://dx.doi.org/10.2174/1381612820666141023164125
DOI https://dx.doi.org/10.2174/1381612820666141023164125 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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