Drugs acting on cardiovascular (CV) prevention are, by definition, interconnected with age-induced arterial changes. However, this question has been poorly investigated along long-term treatment. This goal requires a major prerequisite: to determine statistical links associating age-induced changes in arterial stiffness and wave reflections with drug classes acting on CV prevention. We studied 347 subjects where CV prevention involved hypertension, diabetes mellitus and hypercholesterolaemia; and included six drug classes: diuretics, β-blocking agents, angiotensin II (ANGII) and calcium-channel (CCB) blockers, insulin therapy and statins. For each class, the total population was divided into two subgroups according to the presence or absence of the corresponding class. Statistical comparisons between subgroups involved brachial and central blood pressure measurements, aortic pulse wave velocity (PWV), augmentation index (AIx), used as a marker of wave reflections. Non-invasive measurements included tonometry and pulse wave analysis. Appropriate adjustments indicated among results the respective role of age, sex, mean blood pressure (MBP), standard risk factors and other confounding variables. CCB and statins did not exhibit statistical association with PWV or AIx. β-Blocking agents were significantly linked with heart rate reduction and resulting increase in AIx and central pulse pressure (PP). Increased PWV independent of age, MBP, CV risk factors were noticed under diuretics, ANGII blockers and insulin, pointing to intrinsic modifications of the arterial wall. Treatment of CV prevention involves alterations of the arterial wall depending on drug class. β-Blocking agents and insulin are associated with the higher increases of central PP. © 2011 Macmillan Publishers Limited All rights reserved.
CITATION STYLE
Lieber, A., Millasseau, S., Mahmud, A., Bourhis, L., Mairesse, S., Protogerou, A., … Safar, M. E. (2011). Cardiovascular prevention: Relationships between arterial aging and chronic drug treatment. Journal of Human Hypertension, 25(9), 524–531. https://doi.org/10.1038/jhh.2011.28
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