Atherogenic lipoproteins affect large artery and left ventricular structure in premenopausal subclinical hypothyroid women

Subclinical hypothyroidism (sHT) has been claimed to be a risk factor for aortic atherosclerosis and myocardial infarction. An atherogenic lipoprotein profile may underlie the cardiovascular involvement in sHT as in the case of overt hypothyroidism. Aim of the study was to explore myocardial and large artery structures in sHT, and their possible relation to the serum lipoprotein profile and oxidative stress. Eighteen women (aged 39±10 years) with sHT, and 20 age matched healthy euthyroid women were studied. Smoker, obese and post-menopausal subjects were excluded. Left ventricular (LV) structure and function were assessed by M-mode ultrasound (LV mass, endocardial fractional shortening, FS%), and by acoustic densitometry (AD, Agilent Technologies). The average value of integrated backscatter signal (IBS, dB) reflected from a region of interest at mid-septum and the amplitude of its cyclic variation through the cardiac cycle (CV-IBS, dB) were then obtained. Carotid artery intima-media thickness (IMT) was obtained by standard US approach. Total cholesterol (TC), LDL cholesterol (LDLc), plasma oxidised lipoproteins (Ox-Lip) and total antioxidant power (FRAP) were also determined. sHT patients showed significantly higher serum TC (p=0.02), and LDLc (p=0.03) levels than controls. Moreover, CV-IBS was significantly reduced (p=0.01) and IMT significantly increased (p=0.0002) in sHT patients than controls. IMT correlated directly with age, mean blood pressure, TC, LDLc, FRAP and Ox-Lip (with r-values between 0.62 for age and 0.43 for Ox-Lip). In a multivariate model, TC remained independently associated with IMT (r=0.44, p<0.05). CV-IBS was reciprocally related to TC (r=-0.55, p<0.02) and LDLc (r=-0.45, p<0.02). A significant correlation between TC and TSH was also observed (p=0.01). In conclusion, in fertile women with sHT an atherogenic lipoprotein profile is associated with increased carotid IMT and subclinical LV dysfunction. These associations seem to be mediated, at least in part, by an increased oxidative stress.