White-coat hypertension and autonomic nervous system dysregulation - PubMed (original) (raw)
White-coat hypertension and autonomic nervous system dysregulation
Serina A Neumann et al. Am J Hypertens. 2005 May.
Abstract
Background: White-coat hypertension, defined as high blood pressure (BP) on clinical assessment but normal BP elsewhere or on ambulatory measurement, is a common but poorly understood phenomenon. The current study asks whether individuals with white-coat hypertension have abnormal autonomic-cardiac regulation, similar to that observed in sustained or persistent hypertension.
Methods: Participants were men (ages 40 to 70 years; 63% white, 37% African American) not receiving any cardiovascular medications who were classified as persistent hypertensive (n = 40), white-coat hypertensive (n = 40), or normotensive (n = 40) on the basis of clinic and daytime ambulatory BP, using a threshold criterion for hypertension of 140/90 mmHg. Persistent and white-coat hypertensive subjects were matched on ethnicity and clinic BP, and white-coat hypertensive subjects and normotensive subjects were matched on race and daytime ambulatory BP. Frequency domain analysis of resting beat-to-beat heart rate variability (HRV) was used to estimate parasympathetic and sympathetic control of the heart.
Results: Relative to normotensive subjects, both persistent and white-coat hypertensive subjects had lower high-frequency (HF) (P < .03) and low-frequency (LF) power (P < .051) and thus less parasympathetic activity. In addition, white-coat and persistent hypertensive subjects had significantly greater LF/HF ratios, indicating greater sympathetic-to-parasympathetic activity, as compared with normotensive subjects (P < .03).
Conclusions: These findings suggest similarities between persistent and white-coat hypertensive subjects reflecting attenuated parasympathetic control of the heart. In addition, the association between white-coat hypertension and autonomic dysregulation, particularly diminished parasympathetic tone, may serve as a mechanism for increased risk for cardiovascular events in affected individuals.
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