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Abstract Disclosure: R. Subramani: None. R. Subramani: None. V. Zeykan: None. Introduction: Tachycardia-induced cardiomyopathy related to thyrotoxicosis is an uncommon yet serious complication affecting fewer than 1% of individuals with hyperthyroidism. Restoring a euthyroid state can potentially reverse the abnormal cardiac structure and function. Here we report a case of tachycardia-induced cardiomyopathy secondary to thyrotoxicosis Case Summary: A 52-year-old woman with a history of hypertension presented with recent-onset exertional dyspnea, a nonproductive cough, and paroxysmal nocturnal dyspnea. On examination, she exhibited tachycardia (heart rate: 150/min), tachypnea, hypertension, and was afebrile. Physical findings included a mildly enlarged, firm, non-tender thyroid gland bilaterally, without exophthalmos or tremors. Auscultation revealed bilateral crackles in the left lower lung fields. Laboratory analysis revealed undetectable TSH (0.02 uIU/mL), elevated free T4 (5.3 ng/dL), free T3 (16.30 pg/mL), thyroid stimulating immunoglobulin (TSI) at 216%, and NT proBNP at 8528 pg/mL. Neck ultrasound and CT confirmed diffuse enlargement of the thyroid gland. Transthoracic echocardiography (TTE) displayed severely depressed left ventricular systolic function, estimating an ejection fraction (EF) of 25-30%. Initial management involved intravenous beta-blockers for heart rate control, IV Lasix, and IV hydrocortisone. Subsequently, the patient received propylthiouracil, propranolol, and prednisone, resulting in symptomatic improvement. A follow-up TTE after 6 months revealed an improved EF of 50%. Discussion: The pathophysiologic mechanisms underlying thyrotoxic cardiomyopathy encompass several factors, including tachycardia-induced cardiomyopathy, direct myopathic effects induced by the T3 hormone, and concurrent autoimmune myocarditis associated with Graves' disease. Thyroid hormone exerts a comprehensive impact on nearly all tissue and organ systems, heightening basal metabolic rate and subsequently increasing preload, myocardial contractility, and cardiac output. While thyrotoxicosis-related congestive heart failure (CHF) is relatively uncommon among patients hospitalized for acute CHF, addressing hyperthyroidism and CHF through definitive treatment yields a more favorable prognosis compared to cases of acute CHF stemming from other etiologies. The intricate interplay of these mechanisms highlights the importance of a comprehensive approach in managing thyrotoxic cardiomyopathy, emphasizing the need for targeted interventions to address both the underlying thyroid dysfunction and associated cardiac manifestations. Presentation: 6/3/2024
Subramani et al. (2024) studied this question.