Riddhi Shah

Spinal cord stimulation protects against atrial fibrillation induced by tachypacing

BACKGROUND Spinal cord stimulation (SCS) has been shown to modulate atrial electrophysiology and confer protection against ischemia and ventricular arrhythmias in animal models. OBJECTIVE To determine whether SCS reduces the susceptibility to atrial fibrillation (AF) induced by tachypacing (TP). METHODS In 21 canines, upper thoracic SCS systems and custom cardiac pacing systems were implanted. Right atrial and left atrial effective refractory periods were measured at baseline and after 15 minutes of SCS. Following recovery in a subset of canines, pacemakers were turned on to induce AF by alternately delivering TP and searching for AF. Canines were randomized to no SCS therapy (CTL) or intermittent SCS therapy on the initiation of TP (EARLY) or after 8 weeks of TP (LATE). AF burden (percent AF relative to total sense time) and AF inducibility (percentage of TP periods resulting in AF) were monitored weekly. After 15 weeks, echocardiography and histology were performed. RESULTS Effective refractory periods increased by 21 ± 14 ms (P = .001) in the left atrium and 29 ± 12 ms (P = .002) in the right atrium after acute SCS. AF burden was reduced for 11 weeks in EARLY compared with CTL (P <.05) animals. AF inducibility remained lower by week 15 in EARLY compared with CTL animals (32% ± 10% vs 91% ± 6%; P <.05). AF burden and inducibility were not significantly different between LATE and CTL animals. There were no structural differences among any groups. CONCLUSIONS SCS prolonged atrial effective refractory periods and reduced AF burden and inducibility in a canine AF model induced by TP. These data suggest that SCS may represent a treatment option for AF.

Usefulness of monitoring congestive heart failure by multiple impedance vectors

Introduction: We investigated trends in intrathoracic impedance measured between multiple implanted electrodes for monitoring pulmonary edema secondary to congestive heart failure (CHF) in an experimental model. Methods: Biventricular ICDs were implanted in 16 dogs and 5 sheep. Continuous RV pacing (230–250 bpm) was applied over several weeks. Meanwhile, impedance was measured every hour along 4 intrathoracic and 2 intracardiac vectors. Four cardiogenic impedance vectors were also monitored. Cardiac function was assessed biweekly by catheterization and echocardiography. Left atrial (LA) pressure was measured daily by an implanted LA pressure sensor. Results: All animals developed CHF after 2–4 weeks of pacing as evidenced by changes in function (EF, 52 vs. 34%; LV end-diastolic volume, 65 vs. 97 ml; LV end-diastolic pressure, 7 vs. 16 mmHg; LA volume, 17 vs. 33 ml; LA pressure, 7 vs. 26 mmHg), clinical symptoms, or autopsy. Steady state impedance decreased during CHF: LV-Can, 17±9%; LV-RV, 15±8%; LV-RA, 13±6%; RV-Can, 13±8%; RVcoil-Can, 8±6%; RA-Can, 6±6%. Change in LV-Can impedance was greater than that of RA-Can, RV-Can, and RVcoil-Can (P<0.05). LV-Can impedance correlated well with LA pressure (r2=0.73), while RV-Can and RVcoil-Can were weakly correlated (r2=0.43 and r2=0.52, respectively). Changes in LV-RV and LV-RA impedances were also larger than those of RVcoil-Can and RA-Can (P<0.05). Meanwhile, all impedances were associated with circadian variability at baseline (5±2%) which diminished during CHF (2±1%); P=0.02. Furthermore, significant variations were observed in cardiogenic impedances during progression into CHF as evidenced by reduced peak-to-peak amplitude and increased fractionation of the signals. Conclusions: All impedance vectors decreased during CHF. Impedance measurement employing left heart sensors correlated well with LA pressure, and may improve detection of CHF onset compared to sensing by RA or RV leads alone. This approach has important clinical implications for managing heart failure patients in the ambulatory setting.

Impact of Tachyarrhythmia Detection Rate and Time from Detection to Shock on Outcomes in Nationwide US Practice

Although higher detection rates and delayed detection improve survival in implantable cardioverter defibrillator clinical trials, their effectiveness in clinical practice has limited validation. To evaluate the effectiveness of programming strategies for reducing shocks and mortality, we conducted a nationwide assessment of patients with implantable cardioverter defibrillators or cardiac resynchronization therapy defibrillators with linked remote monitoring data. We categorized patients based on the presence or absence of high rate detection and delayed detection: higher rate delayed detection (HRDD), higher rate early detection (HRED), lower rate delayed detection (LRDD), and lower rate early detection (LRED). Cox regression was used to compare mortality and shock-free survival. There were 64,769 patients (age 68 ± 12 years; 27% female; 46% cardiac resynchronization therapy defibrillator; follow-up 1.7 ± 1.1 years). In the first year, 13% of HRDD, 14% of HRED, 18% of LRDD, and 20% in the LRED group experienced a shock. After adjustment, HRDD was associated with lower risk of shock than HRED (hazard ratio [HR] 0.93, 95% confidence interval [CI] 0.89 to 0.98, p = 0.002), LRDD (HR 0.63, 95% CI 0.60 to 0.66, p <0.001), and LRED (HR 0.58, 95% CI 0.55 to 0.61, p <0.001). HRDD was also associated with lower risk of mortality than HRED (adjusted HR 0.80, 95% CI 0.75 to 0.86, p <0.001), LRDD (HR 0.76, 95% CI 0.70 to 0.83, p <0.001), and LRED (HR 0.68, 95% CI 0.62 to 0.73, p <0.001). Similar results were observed in patients with or without a shock in the first 6 months after implant. In conclusion, high rate programming is associated with lower risk of shocks or death compared with delayed detection. Optimal outcomes are observed in patients programmed with both high rate and delayed detection.