Abstract 13181: Characteristics of Diurnal Change of Pulse Rate in Resistant Hypertension
Introduction: Sympathetic hyperactivity is one of the most important causes of resistant hypertension. Ambulatory blood pressure monitoring (ABPM) allows measurement of blood pressure (BP) and pulse rate (PR) throughout the day, as well as measurement of diurnal variations in BP and PR, which are controlled by the autonomic nervous system.
Hypothesis: We hypothesized that abnormal diurnal change of BP and PR are associated with resistant hypertension.
Methods: We evaluated 1003 patients with hypertension who were enrolled in the Japan Morning Surge Home Blood Pressure Study and were using ABPM. Resistant hypertension was defined as clinic BP≧140/90 mmHg despite the use of optimal doses of 3 classes of antihypertensive drugs, including a diuretic. BP or PR dipper status was defined as (awake systolic BP (SBP) or PR-sleep SBP or PR)/awake SBP or PR ≧0.1. BP or PR nondipper status was defined as (awake SBP or PR-sleep SBP or PR)/awake SBP or PR <0.1 and ≧0. BP and PR riser status were defined as awake SBP or PR < sleep SBP or PR.
Results: The numbers of PR nondippers and PR risers in the resistant hypertensive groups were significantly greater than those in the non-resistant hypertensive groups (x2=9.35, p=0.009), but there were no significant differences in the diurnal variation of BP between the resistant hypertensive and non-resistant hypertensive groups (x2=3.10, p=0.21). In the resistant hypertensive groups, the proportion of PR risers was approximately three-fold greater than that in the non-resistant hypertensive groups after adjustment for age, gender, 24-h BP, PR, and BP variation (Hazard ratio 2.94, 95%Cl 1.25-6.91, p=0.013), but there were no significant differences in the proportion of PR nondippers (Hazard ratio 1.36, 95%Cl 0.82-2.26, p=0.23).
Conclusions: A riser pattern of PR was associated with resistant hypertension. ABPM may be useful to identify resistant hypertensive patients who have autonomic nervous system dysfunction.
Author Disclosures: H. Watanabe: None. T. Kabutoya: None. S. Hoshide: None. K. Eguchi: None. K. Kario: None.
- © 2014 by American Heart Association, Inc.