Influence of heart rate variability and psychosocial factors on carotid stiffness, elasticity and impedance at menopause.

BACKGROUND AND AIMS:The risk for cardiovascular diseases (CVD) increases after menopause. Heart rate variability (HRV), a measure of autonomic control, is a strong predictor of CVD. We undertook this study to test the association of ultrasound indices of early carotid atherosclerosis with HRV, symptoms, hormonal conditions, metabolic state, indicators of stress, and psychosocial factors in women at peri- and postmenopause, registering ambulatory R-R interval monitoring. METHODS:In a cross-sectional design we studied 100 women at peri- and early postmenopause collecting anthropometry, symptoms, stress-related measurements, metabolic variables, cortisol, FSH and estradiol. We evaluated carotid ultrasonographic indices, and HRV was recorded for 4 h calculating time (SDNN, pNN50, rMSSD) and frequency domains (LF, HF, LF/HF) in women according to menopausal stage, estradiol levels, body mass index and waist circumference. RESULTS:Carotid indices were similar in peri- and postmenopausal women. For HRV measurements, SDNN was increased at postmenopause. Women with estradiol levels <109.2 pmol/L had increased intima-media thickness (IMT), resistive index, and systolic diameter. Using multivariate analysis, we found the associations of IMT positively with non-HDL-cholesterol, resistive index positively with LF-HRV, but negatively with effort/reward imbalance, carotid β stiffness index inversely with estradiol, and arterial distensibility positively with HF-HRV and creatinine concentrations, but negatively with non-HDL-cholesterol. CONCLUSIONS:Carotid thickness was related mainly with lipid alterations. Indices of early carotid damage were related with various components of HRV as a manifestation of autonomic imbalance, indicating CVD risk. Other factors involved were time since last menses and psychological stress. Low creatinine was associated with diminished carotid distensibility. This suggests that estrogen, lifestyle, behavior and autonomic regulation participate in vascular damage.