Aims
Oesophageal fistula represents a rare but dreadful complication of atrial fibrillation catheter ablation. Data on its incidence, management and outcome are sparse.
Methods and results
This international multicenter registry investigates the characteristics of oesophageal fistulae after treatment of atrial fibrillation by catheter ablation. A total of 553,729 catheter ablation procedures (radiofrequency: 62.9%, cryoballoon: 36.2%, other modalities: 0.9%) were performed at 214 centers in 35 countries. In 78 centers 138 patients (0.025%, radiofrequency: 0.038%, cryoballoon: 0.0015% (p<0.0001)) were diagnosed with an oesophageal fistula. Periprocedural data were available for 118 patients (85.5%). Following catheter ablation, the median time to symptoms and the median time to diagnosis were 18 (7.75, 25; range: 0-60) days and 21 (15, 29.5; range: 2-63) days, respectively. The median time from symptom onset to oesophageal fistula diagnosis was 3 (1, 9; range: 0-42) days. The most common initial symptom was fever (59.3%). The diagnosis was established by chest computed tomography in 80.2% of patients. Oesophageal surgery was performed in 47.4% and direct endoscopic treatment in 19.8%, and conservative treatment in 32.8% of patients. The overall mortality was 65.8%. Mortality following surgical (51.9%) or endoscopic treatment (56.5%) was significantly lower as compared to conservative management (89.5%) (odds ratio 7.463 (2.414, 23.072) p<0.001).
Conclusions
Oesophageal fistula after catheter ablation of atrial fibrillation is rare and occurs mostly with the use of radiofrequency energy rather than cryoenergy. Mortality without surgical or endoscopic intervention is exceedingly high.
HIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques.
Background
SCN5A mutations may present with different clinical phenotypes such as Brugada syndrome, long QT3 syndrome, sick sinus syndrome, atrial fibrillation, dilated cardiomyopathy, and the least known multifocal ectopic Purkinje-related premature contractions syndrome.
Case summary
We report a case of a 29-year-old woman with palpitations due to multifocal premature ventricular complexes (PVCs) and a family history of sudden death. The previous electrophysiological study had shown that PVCs arose from Purkinje fibres but catheter ablation was unsuccessful. Cardiac magnetic resonance (CMR) imaging demonstrated non-ischaemic areas of subendocardial fibrosis at multiple left ventricular (LV) segments with concomitant dilatation and mild systolic impairment. Amiodarone suppressed the ectopy but caused hyperthyroidism. Due to recent pregnancy, she received no antiarrhythmics which resulted in PVC burden increase and further deterioration of the ejection fraction (EF). After gestation, amiodarone was reinitiated and switched to flecainide after implantation of a subcutaneous defibrillator as a safety net. At follow-up, LV function had almost normalized. Genetic analysis confirmed an SCN5A mutation.
Discussion
Multifocal ectopic Purkinje-related premature contractions syndrome is associated with SCN5A mutation which in our case (R222Q) is the most common described. Flecainide can be an appropriate treatment option when ablation is ineffective. Defibrillator—even a subcutaneous type—could be implanted in cases of LV dysfunction or scar. PVCs suppression by flecainide and restoration of EF implies an arrhythmia—induced mechanism of LV impairment.
Atrial tachycardia, AV node reentry, entrainmentA 57-year-old patient presented with narrow-complex tachycardia (NCT) without discernable P waves on the ECG. He had previously undergone an aortic root and aortic valve replacement 6 years before. At electrophysiological studies, baseline measurements of AH and HV were 92 and 46 milliseconds, respectively. A stable and sustained NCT at the cycle length (CL) of 302 milliseconds was readily inducible. There was 1:1 atrioventricular relationship with a VA interval at the proximal coronary sinus (CS) of 160 milliseconds. Ventricular overdrive pacing (VOP) at a cycle length of 280 milliseconds resulted in VA block and failed to entrain the atrium. Atrial overdrive pacing (AOP) at 280 milliseconds was then performed at the high septal right atrium and coronary sinus ostium (Fig. 1A,B). Is VA linking demonstrated by this pacing maneuver?
CommentaryVA block during VOP excludes AVRT and strongly favors AT, 1 but AVNRT with retrograde block in the lower common pathway 2 is a potential differential diagnosis. AOP to assess for VA linking by comparing the VA interval on the first return beat to the VA during tachycardia can be useful to differentiate AVNRT (presence of VA linking with difference <10 milliseconds) from atrial tachycardia (absence of VA linking).3 However, VA linking could exist coincidentally in AT, and repeating this maneuver at different AOP CLs and from different atrial sites has been proposed to increase its predictive value.
1In panel A, atrial activation at the CS during AOP precedes the pacing stimulus, which represents a very long intra-atrial conduction time from the high right atrial septum to the CS ostium, and suggests a macroreentrant atrial tachycardia mechanism. Measurement of the V-V intervals following AOP confirms that the last entrained ventricular beat should
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