Objective. In this study, we have assessed sympathovagal imbalance (SVI) by spectral analysis of heart rate variability (HRV) that contributes to the genesis of early-onset PIH. Methods. Body mass index (BMI), basal heart rate (BHR), blood pressure (BP) and HRV indices such as LFnu, HFnu, LF-HF ratio, mean RR, SDNN and RMSSD were assessed in normal pregnant women (Control group) and pregnant women having risk factors for PIH (Study group) at all the trimesters pregnancy. Retrospectively, those who did not develop PIH (Study group I) were separated from those who developed PIH (Study group II). Study group II was subdivided into early-onset and late-onset PIH. Sympathovagal balance (LF-HF ratio) was correlated with BMI, BHR and BP. Results. LF-HF ratio was significantly high in study group II compared to study group I and control group, and in early-onset PIH group compared to the late-onset category at all the trimesters of pregnancy, which was significantly correlated with BHR and BP. Alteration in HFnu in early-onset category was more prominent than the alteration in LFnu. Conclusion. Though the SVI in PIH is contributed by both sympathetic overactivity and vagal withdrawal, especially in early-onset type, SVI is mainly due to vagal inhibition. 1. Introduction Hypertensive disorders of pregnancy contribute significantly to still births and neonatal and maternal morbidity and mortality, especially in developing countries of south-east Asia [1]. In India, pregnancy-induced hypertension (PIH) accounts for about 50,000 deaths a year [2]. The major cause of maternal and fetal deaths in PIH is due to its late diagnosis and inadequate treatment. The clinical and laboratory characteristics of hypertension associated with or induced by pregnancy are difficult to differentiate from those of hypertension independent of pregnancy [3]. Pregnancy may induce hypertension in women who are normotensive before pregnancy and may aggravate hypertension in those who are hypertensive before pregnancy [4]. As a result, usually precarious delay occurs in the initiation of appropriate treatment for PIH. Though the etiology of PIH is not exactly known, it has been well established that the disease is characterized by low circulating volume and high vascular resistance [5, 6]. Usually, two physiological factors that largely contribute to the genesis of hypertension are decreased size of the vascular compartment (vasoconstriction) and increase volume of the compartment (increased blood volume) [7]. However, in this dysfunction, hypertension develops inspite of low blood volume,
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