GRAVE DANGER: RARE CASE OF COMPLETE HEART BLOCK SECONDARY TO GRAVES DISEASE

ABSTRACT

Background: Complete heart block (CHB) is a cardiac conduction disorder commonly due to age-related degeneration of the conduction system. Other etiologies include hypothyroidism, Lyme disease or COVID-19, infiltrative cardiomyopathy, myocarditis, and atrioventricular (AV) nodal blocking agents. Hyperthyroidism is an extremely rare cause of CHB. Case We present the case of a 40-year-old previously healthy male who presented after two syncopal episodes. He denied any home medications, recreational drug use, or prior syncopal episodes. He did endorse worsening palpitations, heat intolerance, anxiety, insomnia and diarrhea for one month. Initial EKG was normal. Labs revealed an undetectable thyroid stimulating hormone (TSH), and high T4 of 3.26 ng/dL. Potassium was 3.1 mMol/L which was replaced to normal levels. In the emergency department, he had another syncopal episode. Telemetry showed a 20 second episode of CHB. Patient was admitted and started on methimazole. Decision-making Labs showed positive TSH receptor antibodies and thyroid stimulating immunoglobulins, confirming a diagnosis of Graves’ disease. COVID-19 IgG antibodies were positive with negative COVID-19 PCR, indicative of remote COVID 19 infection. Cardiac MRI did not show any myocarditis or infiltrative disease, and otherwise revealed a structurally normal heart. Lyme disease antibodies were negative. Toxicology screen was negative. Thyroid ultrasound showed diffuse heterogeneity of the gland. 72 hour telemetry monitoring revealed no further conduction abnormalities. At this point, CHB wes attributed to hyperthyroidism. As this was reversible, and CHB resolved after initiation of methimazole, a permanent pacemaker was not placed. He was discharged with a 30-day event monitor which did not show any conduction abnormalities. Conclusion: This case highlights a rare sequela of hyperthyroidism induced CHB. Although the pathophysiology is not well understood, a proposed mechanism is the direct toxic effect of T3 leading to focal inflammation of the AV node. Further studies are needed to evaluate the pathophysiology and chronicity of this process, which will assist in the decision to implant a permanent pacemaker.