Abstract
Objective Whether the inferior ability of atenolol to reduce central (aortic) compared to peripheral (brachial) blood pressure (BP) is related to its heart rate (HR)-dependent or -independent effects, or their combination, remains unclear. To provide further mechanistic insight into this topic, we studied the acute effects of atenolol versus nebivolol and ivabradine on systolic blood pressure amplification (SBPA; peripheral systolic BP minus central systolic BP) in a model of sick sinus syndrome patients with a permanent dual-chamber cardiac pacemaker in a nonrandomized single-blind single-group clinical trial. Methods We determined hemodynamic indices noninvasively (Sphygmocor XCEL) before and at least 3 h after administration of oral atenolol 50 or 100 mg, nebivolol 5 mg, or ivabradine 5 or 7.5 mg during atrial pacing at a low (40 bpm), middle (60 bpm), and high (90 bpm) HR level in 25 participants (mean age 65.5 years, 12 men). Results At the low HR level, i.e., when the drugs could exert their HR-dependent and HR-independent effects on central BP, only atenolol produced a significant decrease in SBPA (mean change 0.74 ± 1.58 mmHg (95% CI, 0.09–1.40; P = 0.028)), indicating inferior central vs peripheral systolic BP change. However, we observed no significant change in SBPA with atenolol at the middle and high HR levels, i.e., when HR-dependent mechanisms had been eliminated by pacing. Conclusion The findings of our trial with a mechanistic approach to the topic imply that the inferior ability of atenolol to reduce central vs peripheral BP can be explained by the combination of its heart rate-dependent and -independent effects. This trial is registered with NCT03245996.
Highlights
One reason why ß-blockers (BB) are not recommended as first-line antihypertensives in uncomplicated arterial hypertension in guidelines with a global impact is their inferior ability to reduce cardiovascular events, especially stroke, compared to other antihypertensive drug classes [1,2,3]. eir weaker cardiovascular protection can partly be associated with less central blood pressure (BP) reduction compared to peripheral BP reduction [4,5,6]
To provide mechanistic insight into the question whether atenolol’s inferior effect on central BP is associated with its heart rate (HR)-dependent or HR-independent properties, or their combination, we studied the acute effects of atenolol versus nebivolol and ivabradine on systolic BP amplification (SBPA; peripheral systolic BP minus central systolic BP) at different HR levels in a model of sick sinus syndrome patients with a permanent dual-chamber cardiac pacemaker
We showed a decrease in SBPA with atenolol at the low HR level, indicating an inferior central systolic BP change compared to peripheral systolic BP change
Summary
Whether the inferior ability of atenolol to reduce central (aortic) compared to peripheral (brachial) blood pressure (BP) is related to its heart rate (HR)-dependent or -independent effects, or their combination, remains unclear. At the low HR level, i.e., when the drugs could exert their HRdependent and HR-independent effects on central BP, only atenolol produced a significant decrease in SBPA (mean change 0.74 ± 1.58 mmHg (95% CI, 0.09–1.40; P 0.028)), indicating inferior central vs peripheral systolic BP change. E findings of our trial with a mechanistic approach to the topic imply that the inferior ability of atenolol to reduce central vs peripheral BP can be explained by the combination of its heart rate-dependent and -independent effects. Conclusion. e findings of our trial with a mechanistic approach to the topic imply that the inferior ability of atenolol to reduce central vs peripheral BP can be explained by the combination of its heart rate-dependent and -independent effects. is trial is registered with NCT03245996
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