The increasing prevalence of congestive heart failure has focused importance on the search for potentially reversible etiologies of cardiomyopathy. The concept that incessant or chronic tachycardias can lead to ventricular dysfunction that is reversible is supported by both animal models of chronic rapid pacing as well as human studies documenting improvement in ventricular function with tachycardia rate or rhythm control. Sustained rapid pacing in experimental animal models can produce severe biventricular systolic dysfunction. Hemodynamic changes occur as soon as 24 h after rapid pacing, with continued deterioration in ventricular function for up to 3 to 5 weeks, resulting in end-stage heart failure. The recovery from pacing-induced cardiomyopathy demonstrates that the myopathic process associated with rapid heart rates is largely reversible. Within 48 h after termination of pacing, hemodynamic variables approach control levels, and left ventricular ejection fraction shows significant recovery with subsequent normalization after 1 to 2 weeks. In humans, descriptions of reversal of cardiomyopathy with rate or rhythm control of incessant or chronic tachycardias have been reported with atrial tachycardias, accessory pathway reciprocating tachycardias, atrioventricular (AV) node reentry and atrial fibrillation (AF) with rapid ventricular responses. Control of AF rapid ventricular responses has been demonstrated to improve ventricular dysfunction with cardioversion to sinus rhythm, pharmacologic ventricular rate control and AV junction ablation and permanent ventricular pacing. The investigation of potential tachycardia-induced cardiomyopathy in patients with heart failure requires further prospective confirmation in larger numbers of patients, with study of mechanisms, patient groups affected and optimal therapies.

Intravenous ibutilide given in repeated doses is effective in rapidly terminating atrial fibrillation and flutter and under monitored conditions is an alternative to current cardioversion options.

Ablation and pacing therapy improves a broad range of clinical outcomes for patients with medically refractory atrial fibrillation. The calculated 1-year mortality rates after this therapy are low and comparable with medical therapy.

These data demonstrate that ibutilide is able to rapidly terminate atrial fibrillation and atrial flutter.

Background-Despite the success of catheter ablation of cavotricuspid isthmus-dependent atrial flutter (AFL), important postablation outcomes are ill-defined. The purpose of our study was to analyze long-term outcomes after catheter ablation of cavotricuspid isthmus-dependent AFL. Methods and Results-A meta-analysis was performed of articles reporting clinical outcomes after catheter ablation of AFL published between January 1988 and July 2008. The analysis included 158 studies comprising 10 719 patients (79% men, 59.8Ϯ0.5 years old, 46% left atrial enlargement, 46% heart disease, 42% with history of atrial fibrillation, 14.3Ϯ0.4 months of follow-up). The overall acute success rate adjusted for reporting bias was 91.1% (95% CI, 89.5 to 92.4), 92.7% (95% CI, 90.0 to 94.8) for 8-to 10-mm tip/or irrigated radiofrequency catheters, and 87.9% (95% CI, 84.2 to 90.9) for 4-to 6-mm tip catheters (PϾ0.05). Atrial flutter recurrence rates were significantly reduced by use of 8-to 10-mm tip or irrigated radiofrequency catheters (6.7% versus 13.8%, PϽ0.05) and by use of bidirectional cavotricuspid isthmus block as a procedural end point (9.3% versus 23.6%, PϽ0.05). The AFL recurrence rate did not increase over time. The overall occurrence rate of atrial fibrillation after AFL ablation was 33.6% (95% CI, 29.7 to 37.3) but was 52.7% (95% CI, 47.8 to 57.6) in patients with a history of atrial fibrillation before ablation and 23.1% (95% CI, 17.5 to 29.9) in those without atrial fibrillation before ablation (PϽ0.05). The incidence of atrial fibrillation increased over time in both groups; however, 5 years after ablation, the incidence of atrial fibrillation was similar in those with and without atrial fibrillation before ablation. The acute complication rate was 2.6% (95% CI, 2 to 3). The mortality rate during follow-up was 3.3% (95% CI, 2.4 to 4.5). Antiarrhythmic drug use after ablation was 31.6% (95% CI, 25.6 to 37.8

Background-Delivery of inappropriate shocks caused by misdetection of supraventricular tachycardia (SVT) remains a substantial complication of implanted cardioverter/defibrillator (ICD) therapy. Whether use of optimally programmed dual-chamber ICDs lowers this risk compared with that in single-chamber ICDs is not clear. Methods and Results-Subjects with a clinical indication for ICD (nϭ400) at 27 participating centers received dual-chamber ICDs and were randomly assigned to strictly defined optimal single-or dual-chamber detection in a single-blind manner. Programming minimized ventricular pacing. The primary end point was the proportion of SVT episodes inappropriately detected from the time of programming until crossover or end of study. On a per-episode basis, 42% of the episodes in the single-chamber arm and 69% of the episodes in the dual-chamber arm were due to SVT. Mortality (3.5% in both groups) and early study withdrawal (14% single-chamber, 11% dual-chamber) were similar in both groups. The rate of inappropriate detection of SVT was 39.5% in the single-chamber detection arm compared with 30.9% in the dual-chamber arm.

Appropriate ventricular arrhythmia detection is excellent for all ICD systems evaluated; however, specificity of supraventricular arrhythmia discrimination by the S-ICD system is better than discrimination by 2 of 3 TV systems.

Acute complications resulting from permanent pacemaker implantation are well known and include perforation of the right atrium or right ventricle. Recently, several reports have described the occurrence of perforation and pericarditis as late complications following pacemaker implantation. These complications may occur days to weeks following uncomplicated pacemaker implantation and may lead to death if they are not recognized early. Five patients with late complications caused by active-fixation leads are reported and the clinical features of their presentation and management are reviewed. Late perforation of the right atrium or right ventricle is an uncommon complication after pacemaker implantation but should be suspected by the general cardiologist in a patient who has a device implanted within a week to several months prior to the development of chest pain.