Abstract 12607: Renin Angiotensin Aldosterone System Inhibition Prevents the Arterial Stiffness Elevation Resulting in the Amelioration of Inappropriate Cardiovascular Response During Exercise in Patients With Hypertension
Introduction: Patients with hypertension (HT) are known to show an increased activity of renin-angiotensin-aldosterone system (RAAS) secondary to sympathetic hyperactivity. The RAAS hyperactivity was reported to induce vascular endothelial dysfunction and elevated functional arterial stiffness resulting in an inappropriate cardiovascular response during exercise such as an excessive blood pressure (BP) elevation. This study investigated whether a long-term RAAS inhibition ameliorated the inappropriate cardiovascular response during exercise in HT patients.
Methods: Eighty HT patients (64±14 years, 48 males) were divided into two groups based on antihypertensives: angiotensin II receptor blocker (ARB) group and L-type calcium channel blocker (CCB) group. Patients were followed up for one year, after their BP was controlled below 140/90 mmHg. Patients received a cycle ergometer test, and blood examination before and after the follow-up period. We determined systolic blood pressure (SBP) elevation during the exercise test as the change from baseline SBP to peak SBP (ΔSBP). We assessed the changes in plasma renin, aldosterone, noradrenaline (NORA) and adrenaline (ADRN), and brachial-ankle pulse wave velocity (PWV) before and after the exercise test (ΔNORA and ΔADRN as sympathetic activity parameters and ΔPWV as a functional arterial stiffness).
Results: ΔSBP after the follow-up period was significantly lower in the ARB group than in the CCB group (P<0.001). ΔADRN and ΔPWV increased significantly after the follow-up period in the CCB group as compared with baseline assessment (P<0.05, respectively) despite no significant changes in the ARB group. Those after the follow-up period were significantly lower in the ARB group than in CCB group (P<0.05, P<0.001).
Conclusions: RAAS inhibition prevented the arterial stiffness elevation resulting in the amelioration of inappropriate cardiovascular response during exercise in HT patients.
Author Disclosures: K. Yabu: None. T. Masuda: None. M. Ogura: None. R. Shimizu: None. D. Kamekawa: None. A. Akiyama: None. Y. Kamada: None. S. Tanaka: None. N. Hamazaki: None. A. Aoyama: None. T. Nakamura: None. E. Maekawa: None. M. Tojo: None. J. Ako: None.
- © 2015 by American Heart Association, Inc.