Thyrotoxic Cardiomyopathy: State of the Art

Abstract

Thyroid hormones, mainly triiodothyronine, have genomic and non-genomic effects on cardiomyocytes related to the contractile function of the heart. Thyrotoxicosis, which is the set of signs and symptoms derived from the excess of circulating thyroid hormones, leads to increased cardiac output and decreased systemic vascular resistance, increasing the volume of circulating blood and causing systolic hypertension. In addition, the shortening of the refractory period of cardiomyocytes produces sinus tachycardia and atrial fibrillation. This leads to heart failure. Approximately 1% of patients with thyrotoxicosis develop thyrotoxic cardiomyopathy, a rare but potentially fatal form of dilated cardiomyopathy. Thyrotoxic cardiomyopathy represents a diagnosis of exclusion, and prompt identification is crucial as it is a reversible cause of heart failure, and heart function can be recovered after achieving a euthyroid state using antithyroid drugs. Radioactive iodine therapy and surgery are not the best initial therapeutic approach. Moreover, it is important to manage cardiovascular symptoms, for which beta blockers are the first-line therapeutic option.

Keywords: Cardiomyopathies; heart failure; hyperthyroidism; thyroid; thyrotoxicosis.

Figure 1:. Thyrotoxic cardiomyopathy research timeline

Figure 2:. Thyroid hormone production and regulation of cardiac gene expression

Figure 3:. Genomic and non-genomic effects of excess thyroid hormones on the cardiovascular system

Figure 4:. Thyrotoxic cardiomyopathy diagnostic algorithm

Figure 5:. Thyrotoxic cardiomyopathy therapeutic algorithm