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Heart rate dependent and independent effects of beta-blockers on central hemodynamic parameters: a propensity score
Rémi Goupil1, Dominique Dupuis, Stéphan Troyanov
1aHôpital du Sacré-Cœur de Montréal, Université de Montréal, Montreal bCHU de Québec, Hôtel-Dieu de Québec, Université Laval, Quebec City, Québec, Canada.
Insights
Beta-blockers may worsen central hemodynamics through heart rate-dependent and independent mechanisms. This study reveals that beta-blocker use is associated with an unfavorable central hemodynamic profile in treated hypertensive patients.
Area of Science:
- Cardiovascular medicine
- Pharmacology
Background:
- Central hemodynamic parameters are superior predictors of cardiovascular risk compared to peripheral blood pressure.
- Beta-blockers are hypothesized to reduce central blood pressure less effectively than peripheral blood pressure, potentially due to heart rate reduction.
Purpose of the Study:
- To investigate the association between beta-blocker use, heart rate, and central hemodynamic indices in treated hypertensive individuals.
- To elucidate the mechanisms underlying the effects of beta-blockers on central hemodynamics.
Main Methods:
- Utilized propensity score matching and multivariate linear regressions on data from the CARTaGENE study.
- Analyzed 2575 treated hypertensive patients with valid pulse wave analysis, matching 457 beta-blocker users with non-users.
Main Results:
- Beta-blocker users exhibited less favorable central pulse pressure, pulse pressure amplification, augmentation index, and augmented pressure compared to non-users.
- Adjusting for heart rate significantly altered the observed differences in central pulse pressure, indicating both heart rate-dependent and independent effects.
Conclusions:
- The unfavorable central hemodynamic profile associated with beta-blocker use has both heart rate-dependent and independent components.
- These findings were consistent across frequently used beta1-selective beta-blockers like atenolol, metoprolol, and bisoprolol.
Objectives:
Central hemodynamic parameters are better predictors of the cardiovascular burden than peripheral blood pressure (BP). Beta-blockers are known to reduce central BP to a lesser extent than peripheral BP, a hypothesized mechanistic consequence of heart rate (HR) reduction.
Methods:
The association between beta-blocker use, HR and central hemodynamics indices was studied in treated hypertensive participants of the CARTaGENE study using propensity score analyses and multivariate linear regressions.
Results:
Of the 20 004 participants, 2575 were treated hypertensive patients with valid pulse wave analysis. Using propensity score analyses, beta-blocker users (n = 605) were matched to nonusers having similar clinical characteristics with (Model 1) and without (Model 2) adjustment for HR. This resulted in 457 and 510 pairs with adequate balance, except for a HR difference in Model 2 (62.5 ± 10.5 vs. 70.4 ± 11.5 bpm, p < 0.001). In Model 1, the central pulse pressure (PP) was 46.5 ± 12.9 mmHg with beta-blocker compared with 45.4 ± 11.0 mmHg without (p = 0.045). PP amplification, augmentation index and augmented pressure were also less favorable with the use of beta-blocker. The HR difference in Model 2 further increased the difference in central PP observed with beta-blocker to 46.5 ± 13.0 vs. 43.3 ± 11.3 without (p < 0.001). These findings were similar when atenolol, metoprolol and bisoprolol were assessed separately using multivariate linear regression models.
Conclusion:
This study shows that the unfavorable central hemodynamic profile of beta-blocker has both HR-dependent and HR-independent components that are similar for all frequently used β1-selective beta-blocker.
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