Key result
Heart rate reduction with ivabradine increased flow-mediated vasodilation and reduced carotid-femoral pulse wave velocity in stable CAD.
Why the study?
Heart rate is associated with cardiovascular mortality and experimental studies showed vascular effects of ivabradine, but its effects on endothelial function and arterial stiffness in stable coronary artery disease needed clinical evaluation.
Does heart rate reduction with ivabradine improve endothelial function and reduce arterial stiffness in patients with stable coronary artery disease?
RCT (n=23)
Does heart rate reduction with ivabradine improve endothelial function and reduce arterial stiffness in patients with stable coronary artery disease?
Heart rate reduction with ivabradine improves endothelium-dependent vasodilation and reduces arterial stiffness in patients with stable coronary artery disease.
Answers are grounded in this paper and cite their sources.
May improve vascular surrogates in stable CAD; extends limited RCT data on heart rate reduction.
INTRODUCTION: Epidemiological and clinical studies have shown a relevant association between heart rate and cardiovascular mortality. Experimental studies identified vascular effects of heart rate reduction with the If channel inhibitor ivabradine. Therefore, the effects of heart rate reduction on endothelial function and indices of arterial stiffness were examined in patients with stable coronary artery disease in a prospective, placebo-controlled clinical crossover study. METHODS AND RESULTS: Twenty-three patients (18 men and 5 women) with a resting heart rate (HR) of at least 70 beats per minute (bpm) and stable coronary artery disease were enrolled in this study. In a cross-over design, all patients were treated with ivabradine (Iva, 7.5 mg b.i.d.) and placebo for 6 months each. Iva reduced heart rate by 11.4 bpm (Iva 58.8 ± 8.2 bpm vs. placebo 70.2 ± 8.3 bpm, P < 0.0001). Augmentation index (AIx75), carotid-femoral pulse wave velocity (cfPWV) and central aortic blood pressure were measured using applanation tonometry (SphygmoCor). HRR by Iva increased AIx75 by 12.4% (Iva 24.3 ± 10.5% vs. placebo 21.3 ± 10.1%, P < 0.05) and reduced cfPWV by 14.1% (Iva 6.3 ± 1.7 m/s vs. placebo 7.3 ± 1.4 m/s, P < 0.01). Iva increased mean central blood pressure by 7.8% (Iva 107.5 ± 15.4 mmHg vs. placebo 99.1 ± 12.2 mmHg, P < 0.001). Endothelial function was determined measuring the flow-mediated vasodilation (FMD) of the brachial artery. HRR by Iva increased FMD by 18.5% (Iva 7.3 ± 2.2% vs. placebo 6.0 ± 2.0%, P < 0.001). Aortic distensibility was characterized by MRI. HRR by Iva increased aortic distensibility by 33.3% (Iva 0.003 ± 0.001/mmHg vs. placebo 0.002 ± 0.010/mmHg, P < 0.01) and circumferential cyclic strain by 37.1% (Iva 0.062 ± 0.027 vs. placebo 0.039 ± 0.018, P < 0.0001). CONCLUSION: Heart rate reduction with Iva increased endothelium-dependent vasodilation and reduced arterial stiffness in patients with stable CAD. These findings corroborate and expand the results collected in experimental studies and indicate the importance of heart rate as a determinant of vascular function.
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Hohneck et al. (2019) conducted an RCT in stable coronary artery disease (n=23). ivabradine vs. placebo was evaluated on flow-mediated vasodilation (FMD) of the brachial artery (p=< 0.001). Heart rate reduction with ivabradine increased flow-mediated vasodilation and reduced carotid-femoral pulse wave velocity in stable CAD.
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