In CRT-D candidates with a history of AF, 25% experience recurrent AF within 6 months of implant. Atrial detection and ventricular detection, shock, and resynchronization therapies are not compromised by the addition of atrial therapies to a CRT-D device.

Programmed ventricular stimulation was performed on 36 patients after recent cardiac surgery using implanted right ventricular epicardial temporary wires and with catheters positioned percutaneously at two right ventricular endocardial sites. Patients were followed for a mean of 18.5 months (range 3 to 36 months). Epicardial wires were nonfunctional in 10 patients (28%) due to excessively high pacing thresholds. Overall, 22 patients (61%) had inducible sustained ventricular tachycardia; epicardial wires were functional in 15 (68%) of these patients. Six patients without inducible ventricular tachycardia with epicardial stimulation were inducible using endocardial stimulation. Of the 24 patients in whom epicardial and endocardial ventricular stimulation could be performed, concordant results were obtained in only 17 (71%), despite similar epicardial and endocardial ventricular effective and functional refractory periods. A total of 14 arrhythmic events occurred during the follow-up period. Of the 22 patients with an inducible sustained ventricular tachycardia, 12 (64%) had subsequent arrhythmic events. Only 2 of the 14 noninducible patients had follow-up arrhythmic events, one of which was caused by medication proarrhythmia. Endocardial ventricular stimulation had a superior sensitivity (83% versus 30%, P < 0.0001) and an improved negative predictive value (86% versus 61%, P < 0.05) compared with epicardial ventricular stimulation. These results indicate that noninducibility using epicardial programmed ventricular stimulation does not reliably portend a low risk for recurrent ventricular tachyarrhythmias. Epicardial programmed stimulation, used alone, may be inadequate for postoperative electrophysiological evaluation of patients at risk for ventricular arrhythmias.

The incidence and timing of rate response parameter reprogramming in activity responsive pacing systems during the year after implantation was evaluated in two groups of patients: 24 patients in whom a VVI,R system was implanted (Activitrax, Medtronic, Inc.), and 21 patients in whom a DDD,R system was implanted (Synchrony, Siemens Pacesetter, Inc.). Activity parameter changes in Activitrax patients were made based on the presence of symptoms, while in Synchrony patients, changes were based on objective data obtained using a sensor indicated rate histogram with a slow and fast walk protocol. No significant difference in the incidence of activity parameter reprogramming was noted at various time intervals during the first year in Activitrax patients; in Synchrony patients a greater incidence of reprogramming changes was noted at the 1-month follow-up visit compared to later follow-up visits (P less than 0.02). Further, the incidence of changes at 1 month was greater for Synchrony compared to Activitrax patients (P less than 0.001), while no difference was detected between groups at subsequent follow-up intervals. Use of the slow and fast walk protocol, by permitting serial evaluation of sensor response, demonstrated alterations in sensor drive rates with similar levels of activity over the initial 4 to 6 postimplant weeks. This may result from postoperative changes at the pacemaker insertion site. Based on this experience, predischarge programming may not predict long-term rate response requirements. We recommend evaluation of sensor function using an exercise protocol performed at 4 to 6 postimplant weeks in all rate responsive pacing systems that utilize a piezoelectric crystal.

Data from numerous experimental infarction studies indicate that rapid myocardial cell depolarization following ischemia causes the flow of injury currents. These currents were measured in the canine myocardium by monitoring voltage gradients across infarct boundaries using silver chloride plunge electrodes, followed by placement of a 100 omega resistor between the electrodes and again measuring the voltage gradients. Current flow was calculated from these measurements with the following results: 1) TQ currents developed within 15 seconds after occlusion and persisted for 120 to 150 minutes, often attaining a magnitude of 1 microA. 2) ST currents also developed within 15 seconds and attained 2 to 3 microA within 15 to 30 minutes, then usually subsided to some degree. 3) T currents were biphasic and attained 2 to 5 microA. Initially, current flowed from normal to ischemic myocardium but usually reversed within 30 minutes after occlusion. 4) The current flow was often disproportionate to the voltage gradient between 120 and 180 minutes after occlusion, possibly indicating electrical uncoupling of the infarcting cells from normal cells. These data indicate that intramyocardial current flow develops early after acute coronary occlusion. These currents may be sufficient to induce reexcitation.

No abstract