Beta-blocker use in hypertensive patients was associated with higher central pulse pressure than nonusers (46.5 vs. 45.4 mmHg, p=0.045), showing both HR-dependent and independent unfavorable effects.
Observational (n=2,575)
Does beta-blocker use worsen central hemodynamic parameters in treated hypertensive patients?
Beta-blockers exhibit an unfavorable central hemodynamic profile in hypertensive patients, driven by both heart rate-dependent and heart rate-independent mechanisms.
Absolute Event Rate: 46.5% vs 45.4%
p-value: p=0.045
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.
Goupil et al. (Wed,) conducted a observational in Hypertension (n=2,575). Beta-blockers vs. Nonusers was evaluated on Central pulse pressure (PP) adjusted for heart rate (p=0.045). Beta-blocker use in hypertensive patients was associated with higher central pulse pressure than nonusers (46.5 vs. 45.4 mmHg, p=0.045), showing both HR-dependent and independent unfavorable effects.
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