Increased Pacing Threshold After an Automatic Defibrillator Shock in Dogs: Effects of Class I and Class II Antiarrhythmic Drugs

A high energy shock delivered by an automatic defibrillator may interfere with pacemaker function. To provide insight into the changes that occur in the threshold for ventricular pacing after the shock from an automatic defibrillator, we measured the time to capture during asynchronous ventricular pacing in dogs from endocardial or epicardial sites, after a 30 joule shock was delivered via conventional automatic defibrillator (AICD) patch electrodes. After a 30 joule shock, there was a transient loss of ventricular capture. The duration of capture loss was related to current strength. During endocardial pacing at threshold current, the time to capture was 4.9 +/- 1.2 s, whereas at current values twice threshold the time to capture from endocardial pacing was 2.2 +/- 0.9 s. No difference was found between endocardial and epicardial pacing sites in the time to capture. To ascertain the mechanism of capture loss we: (1) examined the effects of converting the pacing catheter to a current sink (transiently shunting to ground); (2) altered excitability by an infusion of flecainide; (3) blocked sympathetic input (propranolol). No change in time to capture was noted by shunting the pacer to ground. After an infusion of flecainide the time to capture from endocardial pacing was significantly prolonged to 14.9 +/- 2.2 s at the threshold value (P less than .01) and 5.6 +/- 2.1 s at twice threshold (P less than .05). Conversely, intravenous propranolol had no effect on the time to capture after shock from endocardial pacing. These data indicate that there is a transient increase in pacing threshold after the shock from an automatic defibrillator.(ABSTRACT TRUNCATED AT 250 WORDS)     

Is Antiarrhythmia Device Implantation Safe Under Dual Antiplatelet Therapy?

Background: Device implantations in patients on dual antiplatelet‐therapy (DA‐therapy) continue to rise. The aim of our study was to compile and analyze data on complications of antiarrhythmia device implantation under DA‐therapy. Methods: We prospectively collected data on all device implantations in our department from January 2008 until February 2009. The control group was comprised of patients on acetylsalicylic acid alone or no antiplatelet medication at all (318 subjects). The DA‐therapy group consisted of 109 patients of whom 71 were analyzed retrospectively (implantations from 2002 to 2007). Results: Procedure times were significantly longer in DA‐therapy patients receiving a pacemaker for the first time. In contrast, procedure times did not differ significantly between the two study groups for implantable cardioverter defibrillator (ICD) implantations and for pacemaker replacements. Fluid losses via drainage systems and drainage times were significantly increased in the DA‐therapy group as compared with the control group after pacemaker but not after ICD implantations. Importantly, there were no significant differences in complication rates, particularly the hematoma rate, between the DA‐therapy and the control group. Conclusions: When drainage systems are used, antiarrhythmia device implantation is safe and can be performed without significantly increased risk of clinically relevant hematoma in patients on continued DA‐therapy. (PACE 2010; 394–399)     

Electrogram Signals Recorded from Acute and Chronic Pacemaker Implantation Sites in Pacemaker Patients

Electrogram signals recorded from typical pacemaker implantation sites may be useful for a variety of pacemaker system functions including pacemaker follow-up, atrial and ventricular sensing (event detection), and triggered electrogram storage. We quantified the electrical characteristics of pacemaker pocket electrograms using a subcutaneous electrode array (SEA) in a population of 48 patients undergoing initial or replacement pacemaker implantation. SEA recorded intrinsic R wave amplitudes measured peak to peak averaged 118 μV and 65 μV for the two recorded SEA electrograms and were significantly different (P < 0.001); paced R wave amplitudes averaged 180 μV and 110 μV. P wave amplitudes averaged 39 μV and 26 μV. No statistically significant difference in amplitudes were observed between acute versus chronic pacemaker pocket or indication for pacing (A V block, sick sinus syndrome). Signal to noise ratios, using R wave amplitude as signal, were lower in the SEA electrogram on average (11 dB) compared to the intracardiac electrogram (27 dB), but sufficient for diagnostic assessment. R wave/P wave ratios for SEA signals were lower than surface and intracardiac values 3.1 and 2.7 compared to a range of 6.2–9.8, indicating a relative enhancement of P waves to R waves in SEA signals. In summary, SEA electrograms are of sufficient amplitude and signal quality (signal to noise ratio) to hold promise for future implantable device features such as electrogram telemetry, enhanced sensing, and diagnostic data storage.