Abstract

Background: Autonomic regulation of heart rate is impaired in hypertensive patients. The aim of this study is to elucidate the relation between HRV measures as assessed in time‐frequency and frequency domains and clinical and echocardiographic features of hypertension with and without left ventricular hypertrophy.Methods: Forty patients with hypertension were divided into two groups according to gender adjusted echocardiographic signs of left ventricular hypertrophy: group 1–20 patients with hypertension and normal LVMI; group 11–20 patients with hypertension and echocardiographic signs of left ventricular hypertrophy. The control group consists of 20 age‐matched healthy subjects. HRV analysis was accomplished using frequency‐domain analysis (fast Fourier transform) and time‐frequency analysis (smoothed pseudo‐Wigner distribution).Results: HRV components, very low frequency power (VLFP), low frequency power (LFP), high frequency power (HFP), and total power (TP) were attenuated (P > 0.05) in hypertensive patients with and without left ventricular hypertrophy. LFP/HFP and low frequency related power (LFRP) were markedly higher in group I patients than of group II and controls (P > 0.01, P > 0.0001, and P > 0.001, P > 0.05, respectively). While patients of group II had significantly lower values of VLFP, LFP, LFP/HFP ratio and LFRP as compared with group I patients (P > 0.04, P > 0.0001, P > 0.01, and P > 0.0001, respectively). The burst activity at 0.1 Hz was increased in group I patients while in group II patients it was attenuated. HRV indices associated significantly with cardiac output and systolic blood pressure in patients without signs of left ventricular hypertrophy. In patients with signs of left ventricular hypertrophy, HRV indices correlated with LVMI, related wall thickness, age, and body surface area.Conclusion: HRV responds differently in different stages of hypertension, with increase response of sinus node to sympathetic influences in hypertension without left ventricular hypertrophy and withdrawal of sympathetic and parasympathetic influences in presence of left ventricular hypertrophy.

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