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Left atrial appendage (LAA) may be the source for initiation and maintenance of atrial fibrillation (AF). This report shows restoration of sinus rhythm in the atria during radiofrequency wide-area LAA electrical isolation, whereas AF persists in the LAA., (© 2018 Wiley Periodicals, Inc.)

A 70-year-old woman with persistent atrial fibrillation underwent pulmonary vein isolation and linear ablation with a contact sensor catheter. During cavotricuspid isthmus ablation, a steam pop resulted in cardiac tamponade, and the patient developed severe hypotension despite successful pericardial puncture and minimal residual pericardial effusion. Right coronary artery angiography revealed extravasal contrast medium accumulation posterior of the Crux Cordis. Emergent cardiac surgery confirmed isolated disruption of the artery in the absence of additional heart perforation. Although contact sensor catheters may reduce complications, steam pops can still occur and result in dramatic complications., (© 2016 Wiley Periodicals, Inc.)

Although novel cryoablation systems have recently been introduced into clinical practice for catheter ablation of supraventricular tachycardia, the feasibility of catheter cryoablation of VT is unknown. Thus, the present study evaluates catheter cryoablation of the ventricular myocardium (1) in healthy sheep and (2) of VT in chronic myocardial infarction (MI). In three healthy sheep, 21 ventricular lesions (12 left and 9 right ventricle) were created with a catheter cryoablation system. Different freeze/thaw characteristics were used for lesion creation. The mean nadir temperature was -84.1 degrees C +/- 0.9 degrees C, mean lesion volume was 175.8 +/- 170.3 mm3, and 5 of 21 lesions were transmural. Lesion dimensions were 7.5 +/- 3.1 mm (width) and 4.2 +/- 2.5 mm (depth). Left ventricular lesions were significantly larger than right ventricular lesions (262 +/- 166 vs 60.5 +/- 91.6 mm3, P=0.0025). There was no difference in lesion volume with respect to different freeze/thaw characteristics. Anatomically (n=3) or electrophysiologically (n=3) guided catheter cryoablation was attempted in six sheep 105 +/- 56 days after MI, three of six animals had reproducibly inducible VT with a mean cycle length of 215 +/- 34 ms prior to ablation. In these animals, five VTs were targeted for ablation. A mean of 6 +/- 3 applications for nine left ventricular lesions were applied, six of nine lesions were transmural. The mean lesion volume was 501 +/- 424 mm3. No VT was inducible in two of three animals after cryoablation using an identical stimulation protocol. Therefore, catheter cryoablation of VT in healed MI is feasible, and no acute complications were observed.

The determinants of slow pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT) are still unknown, and great differences in the AH interval during slow pathway conduction are observed between patients. In 35 patients with typical AVNRT who underwent successful slow pathway ablation (defined as complete elimination of dual pathway physiology), the A2H2 interval at the "jump" during programmed atrial stimulation and the AH interval during AVNRT (as a reflection of slow pathway conduction time) and the fluoroscopic distance between the successful ablation site and the His-bundle recording site and between the coronary sinus ostium (CSO) and the His-bundle recording site were determined. The mean (+/- SEM) AH interval during slow pathway conduction was 323 +/- 12 ms with programmed stimulation and 310 +/- 10 ms during AVNRT. The mean number of energy applications was 8 +/- 1 (range 1-21). The mean distances between (1) the successful ablation site and the His bundle recording site and (2) between the CSO and the His-bundle recording site were 24 +/- 1 and 28 +/- 1 mm in the RAO and 23 +/- 1 and 28 +/- 1 mm in the LAO projections, respectively. The AH interval during slow pathway conduction correlated significantly with the distance between the successful ablation site and the His-bundle (P < 0.001) but not with the distance between CSO and His-bundle recording site. There is a significant correlation between the AH interval during slow pathway conduction and the distance of the successful ablation site from the His bundle. This relationship (1) suggests that, in addition to functional factors, anatomic factors influence slow pathway conduction and (2) may be helpful in determining the initial energy application site during slow pathway ablation.

Treatment of ventricular tachyarrhythmias in the setting of chronic myocardial infarction requires accurate characterization of the arrhythmia substrate. New mapping technologies have been developed that facilitate identification and ablation of critical areas even in rapid, hemodynamically unstable ventricular tachycardia. A noncontact mapping system was used to analyze induced ventricular tachycardia in a closed-chest sheep model of chronic myocardial infarction. Twelve sheep were studied 96 +/- 10 days after experimental myocardial infarction. During programmed stimulation, 15 different ventricular tachycardias were induced in nine animals. Induced ventricular tachycardia had a mean cycle length of 190 +/- 30 ms. In 12 ventricular tachycardias, earliest endocardial activity was recorded from virtual electrodes, preceding the surface QRS onset by 30 +/- 7 ms. Noncontact mapping identified diastolic activity in ten ventricular tachycardias. Diastolic potentials were recorded over a variable zone, spanning more than 30 mm. Timing of diastolic potentials varied from early to late diastole and could be traced back to the endocardial exit site. Entrainment with overdrive pacing was attempted in nine ventricular tachycardias, with concealed entrainment observed in seven. Abnormal endocardium in the area of chronic myocardial infarction identified by unipolar peak voltage mapping was confirmed by magnetic resonance imaging. These data suggest that induced ventricular tachycardia in the late phase of myocardial infarction in the sheep model is due to macroreentry involving the infarct borderzone. The combination of this animal model with noncontact mapping technology will allow testing of new strategies to cure and prevent ventricular tachycardia in the setting of chronic myocardial infarction.

The Wearable Cardioverter Defibrillator (WCD) automatically detects and treats ventricular tachyarrhythmias without the need for assistance from a bystander, while at the same time allowing the patient to ambulate freely. It represents an alternative to emergency medical services for outpatient populations with a temporary risk of sudden cardiac death. While the original devices used a monophasic truncated exponential waveform for cardioversion/defibrillation shocks, a new, biphasic shock was developed for the next device generation. In 12 patients undergoing electrophysiological testing for ventricular tachyarrhythmias, termination of electrically induced ventricular fibrillation (VF) was attempted via the WCD. In 22 episodes, induced VF was promptly terminated by the first 70 J (n=12) or 100 J (n=10) biphasic shocks. Time between arrhythmia initiation and shock delivery was 22 +/- 6 seconds (70 J) and 21 +/- 6 seconds (100 J) (P=NS). The measured transthoracic impedance was 71 +/- 5 Ohms (64-79 Ohms) for the 70 J shock and 64 +/- 8 Ohms (47-72 Ohms) for the 100 J shock. The present study demonstrates that a single low energy biphasic shock delivered by the WCD, reliably terminates electrically induced VF (100% of episodes). The results of this study suggest that there is an acceptable safety margin to the maximum output of the device (150 J). Despite our promising data, we recommend that programming all shocks for maximum energy output should be done when using the WCD in ambulatory patients.

Dual AV node physiology often persists after successful slow pathway (SP) ablation, and the mechanism of tachycardia elimination is unresolved. Therefore, AV node conduction curves were analyzed following successful ablation (4 +/- 1 energy applications) in 85 consecutive patients (58 women, age 50 +/- 2 years) with typical AVNRT. Twenty-seven patients (32%) had complete elimination (group 1) whereas 58 (68%) patients had persistence (group 2) of dual AV node physiology. A significant increase in the AV node Wenckebach cycle length (WB-CL) was observed in both groups (310 +/- 9 to 351 +/- 15 ms in group 1, and 325 +/- 8 to 369 +/- 9 ms in group 2, P < 0.05). A decrease in the fast pathway (FP) ERP (339 +/- 15 to 279 +/- 12 ms) and an increase in the maximum FP AH interval (141 +/- 5 to 171 +/- 7) were observed only in group 1 (P < 0.05). In group 2, no change in the SP ERP (267 +/- 7 to 280 +/- 10 ms) was observed, and the change in the maximum SP-AH following ablation showed a significant inverse relation to the maximum SP-AH at baseline in group 2. In conclusion, (1) an increase in the WB-CL is observed independent of the persistence or elimination of dual physiology after successful ablation; (2) when dual physiology is eliminated, significant changes in the FP ERP and the maximum FP-AH occur; (3) when dual physiology persists, FP physiology and the SP ERP remain unchanged, and a significant inverse relation between the change in the maximum SP-AH following ablation and the maximum baseline SP-AH is observed.

Previous studies have shown that platelets are activated during atrial fibrillation (AF). However, prophylactic therapy with aspirin is not associated with a reduction of thromboembolic complications in patients with AF. Stimulation of platelet thrombin and ADP receptors causes a release of P-selectin, which is not affected by aspirin. The purpose of this study was to assess the influence of AF on platelet P-selectin expression. Blood samples from 30 patients were studied ex vivo. Nineteen patients had chronic AF (> 3 months), 11 patients were in sinus rhythm (SR). P-selectin expression was determined by flow cytometry (antibody binding capacity [BC]) at baseline and after platelet stimulation with adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP). To determine the effect of heart rate and atrial pressure (RAP), measurements were repeated after 10 minutes of ventricular pacing (120 beats/min) in patients with SR. P-selectin expression was increased in patients with AF at baseline (AF: 1329 +/- 81 BC vs SR: 968 +/- 108 BC; P < 0.05) and after stimulation with ADP (AF: 1445 +/- 101 BC vs SR: 1061 +/- 109 BC; P < 0.05) and TRAP (AF: 13,783 +/- 2442 BC vs SR: 5977 +/- 800 BC; P < 0.05). RAP (2.0 +/- 0.5 vs 6.0 +/- 0.8 mmHg; P < 0.01) and atrial rate (75 +/- 5 vs 114 +/- 5 beats/min; P < 0.001) increased during ventricular pacing. However, P-selectin levels remained stable. AF was accompanied by increased P-selectin expression. In contrast, increased ventricular rate and elevated atrial pressure alone had no effect on platelet activity. Further studies are needed to determine if platelet ADP receptor inhibitors offer a therapeutic benefit in patients with AF.