Heart rate acceleration and deceleration capacities associated with circadian blood pressure variation

Heart 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.

A 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.

The 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).

The 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.