In patients with LV systolic dysfunction, use of APAs is associated with improved survival and reduced morbidity. This association is retained after adjustment for baseline characteristics. APA use is associated with retained but reduced benefit from enalapril.

Electric shock is the only effective therapy against ventricular fibrillation. However, shocks are also known to cause electroporation of cell membranes. We sought to determine the impact of electroporation on ventricular conduction and defibrillation. We optically mapped electrical activity in coronary-perfused rabbit hearts during electric shocks (50 to 500 V). Electroporation was evident from transient depolarization, reduction of action potential amplitude, and upstroke dV/dt. Electroporation was voltage dependent and significantly more pronounced at the endocardium versus the epicardium, with thresholds of 229+/-81 versus 318+/-84 V, respectively (P=0.01, n=10), both being above the defibrillation threshold of 181.3+/-45.8 V. Epicardial electroporation was localized to a small area near the electrode, whereas endocardial electroporation was observed at the bundles and trabeculas throughout the entire endocardium. Higher-resolution imaging revealed that papillary muscles (n=10) were most affected. Electroporation and conduction block thresholds in papillary muscles were 281+/-64 V and 380+/-79 V, respectively. We observed no arrhythmia in association with electroporation. Further, preconditioning with high-energy shocks prevented reinduction of fibrillation by 50-V shocks, which were otherwise proarrhythmic. Endocardial bundles are the most susceptible to electroporation and the resulting conduction impairment. Electroporation is not associated with proarrhythmic effects and is associated with a reduction of vulnerability.

The safety of pacemaker and defibrillator implantations in orally anticoagulated patients using standard techniques has not been thoroughly evaluated. This article describes a prospectively collected experience in such patients. Patients presenting for device implantation who were treated with warfarin were allowed to continue therapy provided that the INR was < 3.5. Implantations involved cannulation of the left axillary vein. Except for defibrillator leads, 7 Fr introducers were used, and all were leads actively fixated. The study included 47 patients who underwent implantation of permanent pacemakers (n = 39), defibrillators (n = 5), or biventricular pacemakers (n = 3). The mean INR was 2.3. The primary indication for anticoagulation was a mechanical cardiac prosthesis in 11 (24%) patients. Atrial fibrillation was present in 33 patients. There were no instances of major bleeding or hematomas requiring evacuation. One patient had a small soft hematoma, which resolved spontaneously. At 6 weeks, all patients had well-healed scars with satisfactory pacing and sensing thresholds. In experienced centers, patients requiring treatment with warfarin may undergo implantation of pacemakers or defibrillators with minimal risk despite continuation of anticoagulation.