Abstract
BackgroundHeart rate acceleration and deceleration capacities are novel parameters that can quantify sympathetic and vagal modulation. However, how acceleration and deceleration capacities associated with circadian blood pressure (BP) variation remains unknown.MethodsA total of 141 patients with essential hypertension were included in our study. Based on the nocturnal decline rate of systolic BP (SBP), patients were divided into two groups, as dippers and nondippers. Baseline demographic characteristics, ambulatory blood pressure monitoring (ABPM) parameters, Holter recordings, and echocardiographic parameters were collected.ResultsThe absolute values of acceleration capacity (AC) (−7.75 [−8.45 ~ −6.3] ms vs. −6.6 [−8.25 ~ −5.2] ms, p = .047) and deceleration capacity (DC) (7.35 [6.1 ~ 8.1] ms vs. 6.3 [5.1 ~ 7.6] ms, p = .042) were significantly higher in dippers than in nondippers. By multivariate logistic regression analysis, left atrial diameter (LAd) was found to be an independent risk factor for nondipper status in acceleration capacity model (odds ratio 1.174, 95% confidence interval 1.019–1.354, p = .027) and deceleration model (odds ratio 1.146, 95% confidence interval 1.003–1.309, p = .045). Sleep SBP was positively correlated to acceleration capacity (r = .256, p = .002) and negatively correlated to deceleration capacity (r = −.194, p = .021).ConclusionsThe absolute values of acceleration capacity and deceleration capacity were higher in patients with dipper hypertension than in patients with nondipper hypertension. However, acceleration and deceleration capacities were not independent risk factors for blunted BP variation. Sleep SBP seemed to be better correlated to the impairment of autonomic nervous system (ANS) function than other ABPM parameters.
Highlights
Hypertension, which is one of the commonest chronic disease, plays an important role in target organ damage and serves as an independent risk factor for stroke, coronary artery disease, and renal insufficiency (Messerli, Williams, & Ritz, 2007)
We found that heart rate acceleration capacity was negatively correlated with nocturnal decline rate of systolic blood pressure (BP) (SBP) (r = −.176, p = .037)
When it comes to the relationship between ambulatory blood pressure monitoring (ABPM) parameters and acceleration capacity, and deceleration capacity, acceleration capacity was positively correlated to 24 hr SBP and sleep SBP, and negatively correlated to dip rate
Summary
Hypertension, which is one of the commonest chronic disease, plays an important role in target organ damage and serves as an independent risk factor for stroke, coronary artery disease, and renal insufficiency (Messerli, Williams, & Ritz, 2007). Dipper is considered to be a normal physiologic status, while nondipper is related to increase risk of target organ damage and cardiovascular mortality (Hermida, Ayala, & Portaluppi, 2007; Ohkubo et al, 2002). Previous studies have shown that ANS was involved in the control of circadian BP variation (Dauphinot et al, 2010; Kohara, Nishida, Maguchi, & Hiwada, 1995). In their studies, indices of heart rate variability were used to reflect the function of ANS. To the best of our knowledge, there was no study investigating the association of acceleration and deceleration capacities with circadian variation of BP. Our study was designed to investigate the effect of ANS function quantified by the use of acceleration and deceleration capacities on circadian BP rhythm
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