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Cardiovascular prevention: relationships between arterial aging and chronic drug treatment
A Lieber1, S Millasseau, A Mahmud
1Université Paris Descartes, Assistance Publique-Hôpitaux de Paris, Hôtel-Dieu, Centre de Diagnostic et de Thérapeutique, Paris, France.
Abstract:
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.
Insights
Cardiovascular prevention drugs impact arterial stiffness differently. Diuretics, angiotensin II blockers, and insulin increase arterial stiffness, while beta-blockers and insulin raise central pulse pressure.
Area of Science:
- Cardiovascular Pharmacology
- Vascular Physiology
- Arterial Biomechanics
Background:
- Cardiovascular (CV) prevention drugs are linked to arterial changes, but long-term effects on arterial stiffness and wave reflections are understudied.
- Understanding these drug-specific arterial modifications is crucial for optimizing long-term CV prevention strategies.
Purpose of the Study:
- To determine statistical associations between age-induced changes in arterial stiffness and wave reflections with specific drug classes used in CV prevention.
- To investigate the impact of diuretics, beta-blocking agents, angiotensin II blockers, calcium-channel blockers, insulin therapy, and statins on arterial properties.
Main Methods:
- Studied 347 subjects with hypertension, diabetes mellitus, and hypercholesterolemia undergoing CV prevention.
- Utilized non-invasive tonometry and pulse wave analysis to measure brachial/central blood pressure, aortic pulse wave velocity (PWV), and augmentation index (AIx).
- Compared subgroups based on drug class usage, adjusting for age, sex, mean blood pressure, and other risk factors.
Main Results:
- Calcium-channel blockers and statins showed no association with PWV or AIx.
- Beta-blocking agents were linked to decreased heart rate, increased AIx, and central pulse pressure.
- Diuretics, angiotensin II blockers, and insulin therapy were associated with increased PWV, independent of other factors, suggesting intrinsic arterial wall changes.
Conclusions:
- CV prevention treatments alter arterial properties in a drug-dependent manner.
- Diuretics, angiotensin II blockers, and insulin therapy appear to intrinsically modify the arterial wall, increasing stiffness.
- Beta-blocking agents and insulin therapy are associated with increased central pulse pressure, highlighting differential vascular effects.
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