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.

Reversible acute heart failure induced by thyrotoxic cardiomyopathy: A case report

“…[15] The current instance represents the occurrence of thyrotoxic cardiomyopathy, an uncommon sequela of thyrotoxicosis, in approximately 1% of patients with thyrotoxicosis and thyrotoxic cardiomyopathy (TCM), which may precipitate profound left ventricular dysfunction and culminate in cardiogenic shock, carrying a substantial mortality risk. [16] Cardiac myopathy typically manifests as a "high-output" form of cardiac insufficiency, wherein cardiac output may surge by 50% to 300% due to a multifaceted interplay of basal heart rate, contractility, ejection fraction, augmented systolic volume, and reduced systemic vascular resistance, whereas instances of low-output cardiac failure remain scarce. [17] Owing to the patient's precarious status, an expeditious diagnosis was imperative and necessitated prompt supportive measures and resuscitation.…”

Thyrotoxic Cardiomyopathy Unveiled: Insights From a Compelling Case Report

“…Thyroid hormones, particularly T3, affect cardiomyocytes through multiple mechanisms, including genomic regulation of cardiac gene expression, as well as non-genomic modulation of the plasma membrane or nuclear receptors in the cardiomyocytes [6]. Excessive thyroid hormones will lead to a hyperdynamic state by increasing the cardiac output and decreasing systemic vascular resistance.…”

“…This can result in sinus tachycardia and AF due to the shortening of the refractory period of cardiomyocytes. Therefore, neglecting or underestimating these effects can take a heavy toll on the cardiovascular system over time, resulting in devastating cardiogenic shock and death [4,5,6].…”

“…Although TCM is a rare disease with an incidence of only 1% in patients with thyrotoxicosis, it is still a fatal type of dilated cardiomyopathy, and its prompt recognition is essential because it is a reversible cause of HF [6]. Recognizing TCM can be challenging due to the unexplained signs and symptoms of HF, making it a diagnosis of exclusion [5,6]. In cases of poorly controlled thyroid function, dilated cardiomyopathy typically starts with left ventricular hypertrophy and high cardiac output.…”

“…Thus, it is imperative to maintain a high level of suspicion for thyroid disorders in patients with new-onset atrial fibrillation, heart failure, and tachycardia-induced cardiomyopathy. The most effective management strategy to control these patients' blood pressure and heart rate involves using anti-thyroid medications and treating any possible cardiovascular complications [5,6].…”