Long-term outcomes of minimally invasive surgical ablation for atrial fibrillation: A single-center experience.

BACKGROUND: Minimally invasive surgical atrial fibrillation (AF) ablation (MISAA) delivers radiofrequency energy via a thoracoscopic approach to perform pulmonary vein isolation and left atrial ganglionic plexi ablation. Data on long-term outcomes of MISAA are lacking. OBJECTIVE: We report 5-year follow-up data from a prospective cohort of patients who underwent MISAA at a single center. METHODS: One hundred nine consecutive patients (60 paroxysmal, 49 persistent; mean age 62.7 ± 9.3 years) underwent MISAA with left atrial appendage exclusion by a single surgeon between 2006 and 2012. Patients were followed with transtelephonic monitoring at 1, 6, and 12 months and annually thereafter for up to 5 years. Recurrence was defined as any atrial tachyarrhythmia lasting ≥30 seconds from 90 days after surgery onward. RESULTS: Mean follow-up duration was 1738.5 ± 661.5 days. Single-procedure success rate was 38% (37 of 98 patients). Atrial arrhythmias occurred in 22%, 42%, 55%, 59%, and 62% of patients by 1, 2, 3, 4, and 5 years. Seventy-eight (79.6%) patients remained AF free with or without additional interventions including catheter ablation, antiarrhythmic drugs, or cardioversion. There was no significant difference in AF-free survival between paroxysmal and persistent AF groups (P = .725). Multivariate analyses showed hypertension to be a significant predictor of AF recurrence (odds ratio 6.6, confidence interval 1.41-30.80; P = .016). Five (5.1%) patients had a stroke or transient ischemic attack during follow-up. CONCLUSION: AF-free survival was 38% at 5 years after MISAA. A total of 79.6% of patients remained AF free with or without additional intervention. Patients may have an ongoing risk of stroke even in the absence of AF recurrences.

Impact of ventricular ectopic burden in a premature ventricular contraction-induced cardiomyopathy animal model.

BACKGROUND: Frequent premature ventricular contractions (PVCs) have been associated with PVC-induced cardiomyopathy (CM) in some patients. OBJECTIVE: The purpose of this study was to understand the cardiac consequences of different PVC burdens and the minimum burden required to induce left ventricular (LV) dysfunction. METHODS: Right ventricular apical PVCs at a coupling interval of 240 ms were introduced at different PVC burdens in 9 mongrel canines. A stepwise increase in PVC burden was implemented every 8 weeks from 0% (baseline), 7%, 14%, 25%, 33% to 50% using our premature pacing algorithm. Echocardiogram and 24-hour Holter were obtained at 4- and 8-week period for each PVC burden with a single blinded reader assessing all echocardiographic parameters including those assessed by speckle tracking imaging (EchoPAC workstation, General Electric). CM was defined as left ventricular ejection fraction (LVEF) <50% or LVEF drop >10% points. Interleukin-6 and pro-brain natriuretic peptide levels were obtained at the end of each PVC burden. RESULTS: The mean LVEF (mean heart rate) at 8 weeks for each PVC burden (0%, 7%, 14%, 33%, and 50%) were 57% ± 2.9% (85 ± 13 beats/min), 54.4% ± 3% (81 ± 10 beats/min), 53.3% ± 5% (77 ± 12 beats/min), 51.1% ± 4.2% (79 ± 14 beats/min), 47.7% ± 3.8% (80 ± 14 beats/min), and 44.7% ± 1.9% (157 ± 43 beats/min). PVC-induced CM was present in 11.1%, 44.4%, and 100% of animals with 25%, 33%, and 50% PVC burden, respectively. E/A ratio and radial strain decreased while left atrial size increased beyond 33% PVC burden. No changes in pro-brain natriuretic peptide and interleukin-6 levels were noted at any PVC burden. CONCLUSION: LV systolic function (LVEF and radial strain) declined linearly as PVC burden increased. PVC-induced CM developed in some canines with 25% and 33% PVC burden, but developed in all animals with 50% PVC burden.

Prospective Evaluation of Implantable Cardioverter-Defibrillator Lead Function During and After Left Ventricular Assist Device Implantation.

OBJECTIVES: This study investigated the mechanism of lead malfunction by monitoring lead parameters throughout left ventricular assist device (LVAD) implantation. BACKGROUND: Implantable cardioverter-defibrillator (ICD) lead malfunction can occur after LVAD implantation. METHODS: ICD lead data were prospectively evaluated during and after LVAD implantation and at 12 pre-specified intraoperative time points. RESULTS: We prospectively evaluated 32 patients with ICDs who underwent LVAD implantation, of whom 20 patients underwent serial testing at 12 intraoperative steps. Post-operative right ventricle (RV) sensing had decreased by >50% from baseline in 7 patients (22%), with RV sensing improving at 1 to 7 weeks in 2 patients (28.6%). Nine patients (28.1%) had >10-ohm (Ω) high-voltage (HV) impedance changes from baseline to final impedance. In all 5 patients with >50% decrease in RV sensing and all 7 patients with a >10-Ω HV impedance change who underwent intraoperative testing, changes were not detected until after weaning from cardiopulmonary bypass. Patients with decreased RV lead sensing >50% (n = 7) had lower glomerular filtration rates (48.7 ± 21.9 ml/min/1.73 m2 vs. 68.4 ± 22.5 ml/min/1.73 m2, respectively, p = 0.0489), were more likely to have undergone concomitant RVAD placement (42.9% vs. 0%, respectively, p = 0.0071), concomitant tricuspid valve surgery (57.1% vs. 16%, p = 0.0469), or to have had cardiac tamponade or unplanned return to the operating room (57.1% vs. 12%, p = 0.0258). CONCLUSIONS: ICD lead malfunction can occur following LVAD implantation but may improve over time. Intraoperative RV sensing and HV impedance changes were not detected until after weaning from cardiopulmonary bypass, suggesting the mechanism of RV lead malfunction may be related to LV unloading and concomitant leftward septal shift. A conservative approach is warranted in many patients with ICD parameter changes after LVAD implantation because parameter abnormalities may improve over time. (Implantable Cardioverter Defibrillator (ICD) Function During Ventricular Assist Device (VAD) Implantation; NCT01576562).

Mycobacterium fortuitum causing infection of a biventricular pacemaker/implantable cardioverter defibrillator.

Increased utilization of cardiovascular implantable electronic devices (CIED) has seen a corresponding rise in related infections. Non-tuberculosis mycobacteria (NTM) are rarely the cause. Treatment involves susceptibilities, antimicrobials, and device removal. This study presents a patient who underwent a biventricular implantable cardioverter defibrillator upgrade with a multi-drug resistant Mycobacterium fortuitum located at the pocket site and a lead infection.