Cardiac manifestations in hyperthyroidism

Abstract

Thyroid hormones have a fundamental impact on cardiac function that is mediated by genomic and nongenomic effects, alterations that condition physiological repercussions that lead to changes in frequency, contractility, rhythm and cardiac output as well as an increase in the incidence and prevalence of different cardiovascular diseases. This document presents an updated review of the implications that hyperthyroidism has in different cardiac conditions, including its importance in the evaluation of perioperative cardiovascular risk.

Keywords: cardiovascular disease; heart failure; hyperthyroidism.

Fig. 1.

The function of thyroid hormones. T4 and T3 can enter cells (such as cardiomyocytes) by passive diffusion or through the action of transporters (MCT8 and MCT10). T4 is converted to T3 by deiodinase 2 (DIO2), and T3 enters the nucleus to modify the expression of specific genes. In the heart, thyroid hormones regulate the protein-encoding genes sarcoplasmic reticulum ${\mathrm{Ca}}^{2+}$ ATPase (SERCa2) and $\alpha$-myosin heavy chain, among others. T3 can exert its function on the mitochondria by increasing the activity of proteins that increase energy in cells. Some metabolites, such as 3,5T2, can increase thermogenesis. T3 exerts nongenomic functions through interactions with membrane proteins such as integrins, modifies the function of mitogen-activated protein kinases (MAPKs) and regulates ion channels in the plasma membrane. Author FL and JCM.

Fig. 2.

Pathophysiological changes leading to a hyperdynamic circulatory state in hyperthyroidism. Adapted from Vargas Uricoechea et al. [1].