Key result
Beta-blockers precipitate cardiogenic shock in a patient with AF-related tachycardiomyopathy despite sinus rhythm restoration.
Case Report (n=1)
Beta-blockers may precipitate cardiogenic shock in vulnerable patients with AF-related tachycardiomyopathy and thyroid dysfunction even after apparent recovery and restoration of sinus rhythm.
Alerts to beta-blocker shock risk after sinus rhythm recovery in tachycardiomyopathy; leaves open safe rate-control strategies in thyroid dysfunction.
Abstract A 75–year–old woman with no known cardiovascular disease was admitted for acute decompensated heart failure. She reported months of progressive exertional dyspnea. Electrocardiography revealed atrial fibrillation with rapid ventricular response (∼140 bpm). Transthoracic echocardiography showed reduced left ventricular ejection fraction (LVEF 40%) with diffuse hypokinesia, severe atrial dilation with atrial functional moderate–to–severe mitral and tricuspid regurgitation, pulmonary hypertension and left pleural effusion. Laboratory tests showed reduced TSH (0.26 μIU/mL) with normal free thyroid hormones, and no liver or kidney damage. During hospitalization, multiple attempts at rate control were performed using high–dose beta–blockers (metoprolol up to 200 mg/day, followed by propranolol up to 160 mg/day) and digoxin, with poor ventricular rate control. After exclusion of left atrial appendage thrombosis, electrical cardioversion successfully restored sinus rhythm, with rapid improvement of LVEF to 52%, consistent with tachycardiomyopathy. The patient was discharged in sinus rhythm (60 bpm) on metoprolol 100 mg/die, flecainide 100 mg/die, anticoagulation, diuretics, canreonate and antithyroid therapy (metimazole 5 mg/die); catheter ablation of AF was scheduled. Within 24 hours, she was readmitted with syncope. On admission, she was hypotensive (70/50 mmHg) with sinus bradycardia (45 bpm), severe metabolic derangement (lactate 7.4 mmol/L), and acute kidney injury (creatinine 3.4 mg/dL). Echocardiography showed severe functional mitral and tricuspid regurgitation with global hypokinesia and LVEF 40%. Iatrogenic beta–blocker–induced hemodynamic collapse was suspected. She required inotropes and withdrawal of negative chronotropic drugs. Hemodynamics progressively improved, and serial echocardiography demonstrated complete recovery of LVEF (60%) and marked reduction of valvular regurgitation. Coronary angiography was normal. At 3–month follow–up, her echocardiogram showed persistence of normal LVEF together with mild mitral and tricuspid regurgitation. She underwent successful AF ablation. Conclusion This case illustrates the vulnerability of patients with AF–related tachycardiomyopathy and thyroid dysfunction. Even after apparent recovery and restoration of sinus rhythm, beta–blockers may precipitate cardiogenic shock. Early rhythm–control strategies, cautious pharmacological therapy and prolonged in–hospital observation are crucial in this population.
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Galluzzo et al. (2026) conducted a case report in Atrial fibrillation-related tachycardiomyopathy (n=1). Beta-blockers was evaluated on Cardiogenic shock. In a patient with AF-related tachycardiomyopathy and thyroid dysfunction, beta-blocker therapy precipitated cardiogenic shock even after apparent recovery and restoration of sinus rhythm.
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