Poster 026: From Shock to Sinus: Recovery After VA-ECMO and Catheter Ablation in Tachycardia-Induced Cardiomyopathy Presenting as Refractory Cardiogenic Shock

Background: Tachycardia-induced cardiomyopathy (TIC) is an uncommon but reversible cause of severe left ventricular dysfunction. In unusual situations, sustained supraventricular tachycardia (SVT) may precipitate refractory cardiogenic shock. Prompt recognition of TIC and timely initiation of mechanical circulatory support are critical for survival and full myocardial recovery.

Methods: A 47-year-old man with no prior medical history presented with two months of progressive dyspnea, worsening at rest while travelling. Upon admission to a regional hospital, he suffered cardiac arrest and achieved return of spontaneous circulation after 10 minutes of advanced CPR. He remained in severe cardiogenic shock (SCAI stage E) despite maximal vasoactive support, prompting activation of the mobile ECMO team. Venoarterial ECMO (VA-ECMO) cannulation was performed on-site, followed by air transfer to our institution. Coronary and pulmonary angiography ruled out coronary artery disease and pulmonary embolism. Right heart catheterisation (RHC) revealed a mean pulmonary artery pressure of 36 mmHg and right atrial pressure of 18 mmHg. During angiography, the patient developed a narrow-complex regular tachycardia at 180 bpm, unresponsive to three electrical cardioversions. Laboratory studies revealed severe metabolic acidosis and acute kidney injury (KDIGO stage 3), prompting continuous renal replacement therapy. After correction of acidosis, 6 mg of adenosine restored sinus rhythm. Transthoracic echocardiography showed a left ventricular end-diastolic diameter of 60 mm, severe global hypokinesis with an ejection fraction of 23%, preserved right ventricular function (TAPSE 23 mm), mild mitral regurgitation, trivial pericardial effusion, and an apical thrombus.

Outcome: After five days of VA-ECMO support and confirmation of neurological recovery, a clamp trial guided by RHC demonstrated stable haemodynamics (RA 2 mmHg, PCWP 5 mmHg, mPAP 14 mmHg), allowing successful decannulation. We identified the aetiology of shock as TIC secondary to permanent junctional reciprocating tachycardia (PJRT). Electroanatomical mapping revealed the earliest retrograde activation at the floor of the coronary sinus ostium. Radiofrequency ablation terminated the tachycardia, and post-ablation testing failed to reinduce the arrhythmia. Follow-up echocardiography showed improvement in EF to 44%. The patient achieved neurological and renal recovery, with no need for mechanical and vasopressor support.
This case highlights the diagnostic complexity of cardiogenic shock secondary to TIC, where profound shock can obscure the arrhythmogenic substrate. Early VA-ECMO preserved end-organ perfusion and created the diagnostic window necessary to exclude structural and ischaemic causes. Electrophysiological study confirmed PJRT as the trigger, and ablation facilitated rapid ventricular recovery, demonstrating the reversibility of TIC with timely rhythm control. Notably, this case occurred in a resource-limited setting, where a mobile ECMO team, capable of travelling to peripheral hospitals for emergency cannulation and safe retrieval, was essential. Such programmes are especially valuable in Latin America, where access to tertiary care is often delayed.

Conclusion: Early recognition of TIC as a reversible cause of cardiogenic shock is crucial. VA-ECMO can serve as a bridge to diagnosis and definitive rhythm control. This case also underscores the transformative role of mobile ECMO teams in expanding access to life-saving mechanical support in low-resource regions.