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.
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 hypertensiveparticipants of the CARTaGENE study using propensity score analyses and multivariate linear regressions. RESULTS: Of the 20 004 participants, 2575 were treated hypertensivepatients 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.
Authors: Tuuli Teeäär; Martin Serg; Kaido Paapstel; Mare Vähi; Jaak Kals; John R Cockcroft; Mihkel Zilmer; Jaan Eha; Priit Kampus Journal: Int J Hypertens Date: 2020-04-26 Impact factor: 2.420