[Hyperinsulinism, heart rate variability and circadian variation of arterial pressure in obese hypertensive patients].

Aims : During insulin resistance, sympathetic nerve activity is increased. However insulin resistance is a common feature of obesity and essential hypertension, it is unclear if chronic hyperinsulinemia per se contributes to sympathetic overactivation. The purpose of our study was to explor the relationships between chronic hyperinsulinemia and heart rate variability (HRV), a non-intensive tool to assess autonomic function, in obese and hypertensive subjects. Methods : 24 hours Holter ECG for HRV time and frequency domain analysis was performed in 77 patients, mean age 53 ± 10 years, 52 men and 25 women, free of diabetes, without beta-blockers, divided in four groups according to three parameters, body mass index (BMI > 27 kg/m 2 in man and > 25 kg/m 2 in woman defined obesity), arterial pressure and insulinemia (fasting insulinemia > 25 mUI/L defined hyperinsulinemia): 27 patients obese, hypertensive, with hyperinsulinemia; 28 patients obese, hypertensive, without hyperinsulinemia; 12 patients non obese, hypertensive, without hyperinsulinemia; 10 patients obese, normotensive, without hyperinsulinemia. Results: In comparison with the three other groups, patients with hyperinsulinemia showed a significant decrease (p < 0.05) of SDNN and the power of total spectrum (0.01-1Hz) band, which are indexes of global HRV, and a significant decrease (p < 0.005) of SD and the normalized power of the low frequency (0.04-0.15 Hz) band, both indexes reflecting sympathetic modulation of HRV. In contrast, no significant difference was observed between the four groups for indexes of HRV reflecting parasympathetic tone. These relations were independent of mean RR. Fasting insulinemia was significantly (p < 0.0001) related with HRV in time domain (SDNN: r = -0.43; SD: r = -0.49) and spectral domain (total spectrum: r = -0.49: low frequency: r = -0.52). Conclusion: Chronic hyperinsulinemia appears to be an important determinant of HRV, particularly for the indexes reflecting sympathetic influence, independent of obesity and hypertension.