Faculty Bibliography

Performance of a New Cardiac Cryoablation System in the Treatment of Cavotricuspid Valve Isthmus-Dependent Atrial Flutter. We sought to evaluate prospectively the safety and efficacy of cryothermal energy to ablate typical atrial flutter (AFL). Ablation of cardiac tissue using cryothermal energy has recently been developed as an alternative to radiofrequency energy, which may offer certain advantages in the treatment of AFL. This prospective, multicenter nonrandomized study of a new catheter-based system for the treatment of cavotricuspid isthmus (CTI)-dependent AFL enrolled patients between 18 and 75 years of age. The CTI dependence of AFL was confirmed at electrophysiologic study with activation mapping and/or entrainment. Patients with atrial septal defect, recent myocardial infarction, left ventricular ejection fraction <0.30, or prior AFL ablation were excluded. Cryoablation of AFL was performed in 48 patients from 11 centers. The procedure was immediately successful in 45 patients (94%), and effective in 30 of 40 patients with complete data available at 6 months. Cryoablation is a promising new treatment of CTI-dependent AFL refractory to medical therapy. Further improvements in catheter design and intravascular sheaths will be tested in a larger multicenter trial

BACKGROUND: Typical atrial flutter (AFL) is a macroreentrant arrhythmia characterized by a counterclockwise circuit that passes through the cavotricuspid isthmus with passive depolarization of the left atrium. These electrical events are thought to be responsible for the classic 'sawtooth' wave of atrial flutter seen on the surface electrocardiogram characterized by a gradual downward deflection followed by a sharp negative deflection. It has been suggested that the negative flutter wave is a result of passive depolarization of the left atrium. We hypothesized that interruption of the circuit within the isthmus would prevent the reentrant wave from depolarizing the left atrium thus eliminating the component of the electrocardiogram reflecting left atrial depolarization. METHODS: We examined 100 cases of atrial flutter with the typical 'sawtooth' pattern referred for radiofrequency ablation. Ninety-seven of the 100 were successfully ablated. All cases were reviewed for termination of atrial flutter with the last intracardiac electrogram just lateral to the site of linear ablation and surface flutter wave at the moment of termination not obscured by the QRS segment or the T-wave. Seventeen of the 97 met these criteria. RESULTS: Seventeen of the 17 cases demonstrated a gradual negative deflection as the last discernible wave of atrial activity followed by an isoelectric period and resumption of normal sinus rhythm. The last generated wave lacked the sharp negative downstroke. CONCLUSION: These results suggest that the sharp negative deflection of flutter waves likely correlates with the wavefront's penetration of the interatrial septum and passive depolarization of the left atrium

The purpose of this study was to evaluate the safety and efficacy of radiofrequency (RF) ablation of typical atrial flutter by using an 8-mm electrode catheter and a 100-W RF power generator. A limitation of previous trials of catheter ablation of atrial flutter is that the data were not collected as part of a prospective multicenter clinical trial. The study results associated catheter ablation of typical atrial flutter in a cohort of 150 patients with an 88% acute efficacy rate. At 6-month follow-up, recurrent typical atrial flutter was observed in 13% of patients. Of the 12 patients with typical atrial flutter recurrence, 4 were symptomatic and 8 were asymptomatic. Procedure duration was a significant predictor of typical atrial flutter recurrence. The 12-month rate for development of atrial fibrillation was 30%. Catheter ablation of atrial flutter was associated with significant improvements in 5 of 8 domains of the Short Form 36 Survey (quality of life) and significant decreases in 13 of the 16 symptoms of the Symptom Checklist. The device- or procedure-related complication rate was 2.7%. Skin burns occurred at the dispersive pad site due to stronger RF power in 3 patients. Use of a dual dispersive pad system mitigated this problem. Thus, the results of this study associated catheter ablation of atrial flutter with high acute efficacy, a small risk of recurrent atrial flutter, and an important risk of atrial fibrillation during follow-up.

Biventricular pacing for the treatment of congestive heart failure has consistently demonstrated improvement in quality-of-life and reduction in heart failure symptoms. Though the over-the-wire systems will be helpful in overcoming many existing obstacles to optimal lead placement, anatomic variability will still limit overall success. Cardiac vein angioplasty may be required for deployment of leads into tortuous or obstructed cardiac veins. This case report describes the angioplasty of a focal cardiac vein stenosis allowing for successful implantation of a left ventricular pacing lead. The safety of this procedure is unknown, though the risks may be acceptable in certain patients

INTRODUCTION: ATP-sensitive K+ channels (K(ATP)) are expressed abundantly in cardiovascular tissues. Blocking this channel in experimental models of ischemia can reduce arrhythmias. We investigated the acute effects of amiodarone on the activity of cardiac sarcolemmal K(ATP) channels and their sensitivity to ATP. METHODS AND RESULTS: Single K(ATP) channel activity was recorded using inside-out patches from rat ventricular myocytes (symmetric 140 mM K+ solutions and a pipette potential of +40 mV). Amiodarone inhibited K(ATP) channel activity in a concentration-dependent manner. After 60 seconds of exposure to amiodarone, the fraction of mean patch current relative to baseline current was 1.0 +/- 0.05 (n = 4), 0.8 +/- 0.07 (n = 4), 0.6 +/- 0.07 (n = 5), and 0.2 +/- 0.05 (n = 7) with 0, 0.1, 1.0, or 10 microM amiodarone, respectively (IC50 = 2.3 microM). ATP sensitivity was greater in the presence of amiodarone (EC50 = 13 +/- 0.2 microM in the presence of 10 microM amiodarone vs 43 +/- 0.1 microM in controls, n = 5; P < 0.05). Kinetic analysis showed that open and short closed intervals (bursting activity) were unchanged by 1 microM amiodarone, whereas interburst closed intervals were prolonged. Amiodarone also inhibited whole cell K(ATP) channel current (activated by 100 microM bimakalim). After a 10-minute application of amiodarone (10 microM), relative current was 0.71 +/- 0.03 vs 0.92 +/- 0.09 in control (P < 0.03). CONCLUSION: Amiodarone rapidly inhibited K(ATP) channel activity by both promoting channel closure and increasing ATP sensitivity. These actions may contribute to the antiarrhythmic properties of amiodarone