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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.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.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.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.