Abstract 15342: Does Ivabradine Affect Sympathetic Overdrive and Arterial Stiffening in Hypertensive Patients With Metabolic Syndrome?
Introduction: Hypertension and metabolic syndrome are related to sympathetic overdrive and arterial stiffening, while there are no data whether ivabradine modulates sympathetic activity and vascular abnormalities in this setting.
Hypothesis: To assess the effect of ivabradine on muscle sympathetic nerve activity (MSNA) and arterial stiffness in hypertensive patients with metabolic syndrome.
Methods: We studied 36 patients with essential hypertension [age: 56±10 years, 30 males, office blood pressure (BP): 148/92±14/11 mmHg] on antihypertensive therapy with a fixed combination of perindopril/amlodipine. Patients were randomized with a ratio 2:1 to ivabradine (5 mg twice daily) or no ivabradine (control group). Metabolic syndrome was defined according to the Adult Treatment Panel III criteria. In all participants at baseline and at 6 months follow-up arterial stiffness was evaluated on the basis of carotid to femoral pulse wave velocity (PWV) while sympathetic drive was assessed by MSNA estimations based on established methodology (microneurography).
Results: Patients on ivabradine (n=24) compared to controls (n=12) did not differ regarding baseline BP, creatinine, glucose and lipid profile (p=NS or all). There was no significant difference in the reduction of office BP between the two study groups (p=NS). However, hypertensive patients in the ivabradine group were characterized by a reduction in carotid to femoral PWV from 11.5±0.9 m/sec to 9.8±1.2 m/sec (p<0.001) and sympathetic nerve traffic as reflected by MSNA levels from 86.2±2.5 bursts per 100 heart beats to 74.8±2.4 bursts per 100 heart beats (p<0.001) at 6 months. No significant changes in PWV and MSNA were observed in the control group (p=NS).
Conclusions: In hypertensive patients with metabolic syndrome, treatment with ivabradine reduces sympathetic activation and arterial stiffening as reflected by lower MSNA and PWV levels at 6 months follow-up. These findings suggest that ivabradine could exhibit additional therapeutic properties in the setting of dysmetabolic hypertension.
Author Disclosures: K. Dimitriadis: None. C. Tsioufis: None. E. Koutra: None. T. Kalos: None. I. Liatakis: None. E. Andrikou: None. P. Vasileiou: None. I. Andrikou: None. D. Tousoulis: None.
- © 2015 by American Heart Association, Inc.