Complete Recovery From Tachycardiomyopathy and Atrial Fibrillation Through Targeted Mitochondrial Support: A Case Report

Background: Tachycardiomyopathy is a reversible form of heart failure caused by persistent tachyarrhythmias such as atrial fibrillation. Conventional therapy includes rate or rhythm control and neurohormonal modulation. Emerging evidence suggests that mitochondrial dysfunction may contribute to disease progression. Case presentation: We report the case of a 52-year-old male patient initially diagnosed in March 2024 with severe heart failure due to tachycardiomyopathy (LVEF 20–25%, NT-proBNP 6260 pg/mL, NYHA IV) in the context of persistent atrial fibrillation. Laboratory tests at admission showed elevated serum potassium and low-normal sodium, consistent with suppressed RAAS activity despite marked volume overload. After diuretic-induced decongestion, potassium and sodium normalized (4.18 and 143 mmol/L, respectively) prior to the initiation of neurohormonal therapy. Guideline-based pharmacological therapy and electrical cardioversion failed to restore rhythm or improve function. A mitochondria-targeted therapeutic approach—including ubiquinone, thiamine, L-carnitine, and NAC—was then initiated, leading to complete clinical and echocardiographic remission by March 2025 (LVEF 60%, NT-proBNP 49 pg/mL, sinus rhythm, asymptomatic). Conclusions: This case supports the therapeutic plausibility of mitochondrial-targeted interventions in patients with refractory heart failure due to tachycardiomyopathy. Further studies are warranted to validate this approach in larger populations.