Reversible Ventricular Dysfunction in Tachycardia-induced Cardiomyopathy: Implications for Timing of ICD Therapy
Bethel O. Anekwe *
University of Nigeria Teaching Hospital, Enugu, K8N 2Z9, Nigeria.
Adaku S. Ndubisi
University of Nigeria Teaching Hospital, Enugu, K8N 2Z9, Nigeria.
Chimaobi Nwevo
NYC Health + Hospital/ South Brooklyn Health 11235, Brooklyn NY MBBCh, United States.
*Author to whom correspondence should be addressed.
Abstract
Tachycardia-induced cardiomyopathy is a potentially reversible cause of left ventricular systolic dysfunction that can develop in the setting of persistent or frequently recurrent tachyarrhythmias. Recognition is clinically important because ventricular recovery after rhythm control may alter decisions regarding primary-prevention implantable cardioverter-defibrillator therapy. We report the case of a 58-year-old man with hypertension who presented with several weeks of progressive exertional dyspnoea, palpitations, reduced exercise tolerance, and mild volume overload. Electrocardiography demonstrated typical atrial flutter with 2:1 atrioventricular conduction and a ventricular rate of approximately 150 beats/min. Transthoracic echocardiography showed left ventricular dilation, global hypokinesis, a left ventricular ejection fraction of 29%, and a left ventricular end-diastolic diameter of 6.6 cm. Coronary angiography did not show obstructive coronary disease, and no alternative reversible cause of cardiomyopathy was identified. As tachycardia-induced cardiomyopathy was suspected, rhythm control was prioritised. The patient underwent cavotricuspid isthmus catheter ablation, with successful termination of atrial flutter and restoration of sinus rhythm. Guideline-directed medical therapy for heart failure was continued, and primary-prevention implantable cardioverter-defibrillator implantation was deferred pending reassessment. At 3-month follow-up, symptoms had improved substantially, and repeat echocardiography demonstrated recovery of systolic function, with left ventricular ejection fraction improving from 29% to 66% and left ventricular end-diastolic diameter decreasing from 6.6 cm to 4.7 cm. These clinical and imaging findings supported deferral of permanent device therapy at that time. This case highlights the importance of identifying potentially reversible arrhythmia-mediated ventricular dysfunction and reassessing cardiac function after durable rhythm control before committing selected patients to permanent device therapy.
Keywords: Tachycardia-induced cardiomyopathy, atrial flutter, arrhythmia-mediated cardiomyopathy, catheter ablation, reverse remodelling, left ventricular dysfunction, implantable cardioverter-defibrillator, rhythm control, sudden cardiac death, device-therapy timing