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Background: Interatrial conduction occurs via discrete pathways along the coronary sinus musculature, fossa ovalis region, and Bachman's bundle. We assessed the feasibility of altering interatrial conduction by selectively ablating two of these conduction pathways using a novel mesh electrode ablation catheter. Methods: Circular radiofrequency energy catheter ablation lesions were created in the proximal coronary sinus in four dogs and in both the fossa ovalis and the proximal coronary sinus regions in seven pigs. Interatrial conduction was assessed by analyzing intracardiac electrogram and noncontact isopotential mapping data. Inducibility of atrial fibrillation was assessed before and after ablation (in six pigs). Results: Ablation lesions in the proximal coronary sinus eliminated interatrial conduction along the coronary sinus musculature in four dogs and five of seven pigs. Ablation lesions in the fossa ovalis region eliminated interatrial conduction via midseptal pathways in six of seven pigs. Atrial fibrillation, inducible in five of seven pigs at baseline, was rendered noninducible in all five. There was no adverse effect on AV nodal conduction. Conclusions: (1) Using a novel mesh electrode ablation catheter, we were able to ablate interatrial conduction pathways along the proximal coronary sinus and fossa ovalis regions. (2) This altered interatrial conduction and altered atrial fibrillation inducibility and maintenance. (3) Catheter ablation of interatrial conduction pathways may be useful in the therapy of atrial fibrillation.

Ventricular Dilatation and DFT. Introduction: Ventricular dilatation has Important electrophysiologic effects, but its effect on ventricular defibrillation threshold (DFT) is unknown. Methods and Results: A fluid-filled, latex balloon was placed in the left ventricular cavity of 19 isolated rabbit hearts. In each experiment, an undilated volume (equivalent to a left ventricular end-diastolic pressure of approximately 0 mmHg) was compared to a dilated volume achieved by adding 1.0 mL of saline (n = 10) or 5% dextrose (n = 9) to the intracavitary balloon. Left ventricular effective refractory period (ERP) and DFT were determined at each volume. Defibrillation was attempted with a monophasic shock delivered between a patch electrode positioned over the posterior left ventricle (cathode) and a metallic aortic cannula (anode). DFT was determined using a modified “down/up” protocol with 10-V steps. Ventricular dilatation increased the left ventricular end-diastolic pressure from 0 ± 0.5 mmHg to 35 ± 3 mmHg (P < 0.001), decreased the average left ventricular ERP 15% (from 116 ± 3 msec to 99 ± 3 msec; P < 0.001), and increased the average DFT 30% (from 96 ± 4 V to 125 ± 7 V; P < 0.001). In one third of experiments, the dilated DFT was ≥ 150% of the DFT at zero volume. The mechanism of the observed increase in DFT is unknown but may be related to the decrease in refractoriness observed with ventricular dilatation. Conclusion: Acute ventricular dilatation in this model increased DFT an average of 30%, an effect not previously described. This observation may have implications for patients with implantable cardioverter defibrillators.

The Brugada syndrome (BS) is now recognized as an important condition predisposing individuals with a seemingly normal heart to sudden death due to ventricular fibrillation (VF).1 Mutations in the gene encoding the cardiac sodium channel (SCN5A) have been found in 18–30% of patients with BS.2 It is believed that abnormalities in regional repolarization and/or depolarization provide the electrophysiological milieu for VF.3,4 In a recent consensus statement,5 the electrocardiographic features have been categorized as follows: type 1 (diagnostic for BS): coved ST segment elevation of ≥2 mm followed by a negative T wave in more than one of leads V1–3; type 2 (not diagnostic for BS) saddleback shaped ST segment elevation with ST elevation of ≥2 mm and a trough ≥1 mm ST elevation; or type 3 (not diagnostic for BS) coved or Saddleback ST segment elevation of

A patient who had undergone heterotopic heart transplantation and placement of an implantable cardioverter defibrillator in his native heart underwent generator change. Defibrillation testing induced ventricular fibrillation in his donor heart. To prevent this potentially lethal complication, defibrillator shock therapy must be synchronized to the donor heart R wave.

Tachycardia-Induced Cardiomyopathy. Introduction: Two years after orthotopic cardiac transplantation, a 60-year-old man presented with unexplained congestive heart failure and an incessant atrial tachycardia. Methods and Results: Electrophysiologic evaluation identified the underlying arrhythmia as automatic atrial tachycardia with site of origin at the high anterior lateral right atrial wall. Radiofrequency catheter ablation successfully eliminated the tachycardia, which resulted in prompt improvement of this patient's congestive heart failure. Conclusion: This is the first reported case of tachycardia-induced cardiomyopathy in a cardiac transplant patient. Radiofrequency catheter ablation can he used successfully in this patient population.