Background: The mechanisms of increased left ventricular mass (LVM) in hyperthyroidism are complex. The aim was to determine the effects of hyperthyroidism and thyreostatic therapy on LVM regarding its interrelationship with factors responsible for the heart's hemodynamic workload.
Material/methods: The study included 51 hyperthyroid subjects and 30 healthy controls. Left heart ventricle parameters evaluated using standard ultrasonocardiography were: left ventricular volume (end-systolic and end-diastolic), left ventricle posterior wall thickness at systole (LVPWs) and diastole (LVPWd) with the respective interventricular septal thicknesses (IVSs, IVSd), LVM, stroke volume (SV), cardiac output (CO), output-pressure index (OPI), and total peripheral resistance (TPR). Systolic (SBP) and diastolic (DBP) blood pressure, heart rate (HR), and body mass index (BMI) were investigated. Measurements were repeated after two weeks of thiamazole treatment and after attaining euthyreosis.
Results: Compared with controls, the hyperthyroid subjects had significant thickening of LVPWd, LVPWs, and IVSs, increased LVM, augmented SV, CO, OPI, SBP, and HR, but reduced TPR and DBP. Hyperthyroid treatment did not normalize LVM. LVM showed positive correlations with SV, CO, OPI, SBP, BMI, and serum triiodothyronine concentration and negative correlation with TPR. In multivariate regression analysis, LVM correlated with SBP, SV, and BMI (R=0.64, p<0.001).
Conclusions: 1) In hyperthyroid patients, LVM is increased, mainly due to its eccentric remodeling, probably caused by volume overload; the increased LVM does not seem to be reversible despite attainment of euthyreosis. 2) The increased LVM is probably related to the heart's hemodynamic workload and reflects adaptive changes.