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Heart, Lung and Circulation

Pseudo-Conduction in the Mitral Isthmus After Ablation

  • Wei-Tso Chen
    Affiliations
    Heart Rhythm Center, Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan

    Division of Cardiology, Department of Medicine, Hualien Tzu Chi Hospital, Hualien, Taiwan
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  • Ibrahim Ahliah
    Affiliations
    Heart Rhythm Center, Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
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  • Fa-Po Chung
    Correspondence
    Corresponding author at: Heart Rhythm Center and Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, No. 201, Sec. 2, Shih-Pai Road, Taipei, Taiwan, National Yang Ming Chiao Tung University, Taipei, Taiwan.
    Affiliations
    Heart Rhythm Center, Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan

    Institute of Clinical Medicine and Cardiovascular Research Institute, National Yang Ming Chiao Tung University, Taipei, Taiwan
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      A 56-year-old patient with a history of hypertension, dyslipidaemia, and long-standing atrial fibrillation underwent pulmonary vein isolation, endocardial mitral line ablation, and alcohol ablation of the vein of Marshall in 2018. He complained of palpitation due to recurrent atrial flutter, which was poorly controlled by amiodarone. Therefore, catheter ablation was arranged. Pre-ablation echocardiography showed normal left ventricular ejection fraction and computed tomography demonstrated an enlarged coronary sinus (CS). The initial rhythm in the electrophysiology laboratory was incessant atrial flutter (Figure 1A). The CS catheter was placed from the right jugular vein and the electrograms showed an activation sequence from distal to proximal electrodes (Figure 1B). The activation map showed clockwise peri-mitral flutter with epicardial bridging connections at the lateral mitral isthmus (Figure 1C). Radiofrequency (RF) energy was delivered via ThermoCool SmartTouch SF ablation catheter (Biosense Webster, Irvine, CA, USA) at the lateral mitral isthmus from endocardium (50 W, Ablation index 500) and epicardium (via CS, 20∼25 W, 20 S for each lesion). The tachycardia was terminated during ablation. After ablation, the CS electrogram activated from distal to proximal portion during left atrial appendage (LAA) pacing, whilst differential pacing confirmed bidirectional block according to the endocardial activation map. Dissociation between endocardial and epicardial activation due to partial mitral block was suspected. However, high-density mapping created by PENTARAY Catheter (Biosense Webster) inside CS during LAA pacing revealed a slanted line of block (Figure 2A, Supplementary Video A) with the earliest activation site at the roof of CS ostium. The middle CS activation was through the myocardial connection between the LA posterior wall and CS. Hence, the inconsistent activation pattern between the CS roof and CS floor could be observed during LAA pacing (Figure 2B). No tachycardia could be induced by atrial burst pacing with isoproterenol infusion after ablation and the patient was uneventful during the 6-month follow-up period.
      Figure thumbnail gr1
      Figure 1(A) Twelve-lead electrocardiogram (ECG) morphology of incessant atypical atrial flutter. (B) Distal to proximal coronary sinus activation during atypical atrial flutter. (C) An activation map of atrial flutter showed clockwise peri-mitral flutter with epicardial bridging connections at the lateral mitral isthmus. Wavefronts of activation are coloured from red to purple.
      Figure thumbnail gr2
      Figure 2(A) Post-ablation activation map during left atrial appendage (LAA) pacing showed a slanted block inside the coronary sinus (CS). (B) As a result of the slanted line of block, the CS catheter on the floor of the CS recorded an activation wavefront from distal to proximal electrodes.

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