Excess thyroid hormone activity increases sarcoplasmic reticulum Ca2+ ATPase activity, predisposing patients to arrhythmias like atrial fibrillation.7,8 Simultaneously, impaired calcium reuptake and titin phosphorylation reduce myocardial contractility and relaxation, contributing to diastolic dysfunction and pulmonary congestion.9,10 Over time, these processes drive cardiac remodelling, transitioning from hypertrophic to dilated cardiomyopathy due to energy depletion and fibrosis.11 The gene discussed is TTN; the disease is dilated cardiomyopathy.