Factors involved in correct analysis of intracardiac electrograms captured by Medtronic Inc. pacemakers during tachycardias

Background: To thoroughly investigate the diagnostic information obtained by pacemakers, it is important that the stored intracardiac electrograms (EGMs) are analyzed. However, in Medtronic pacemakers, only a single intracardiac recording channel is available and thus EGM channel selection is critical. Methods: The study population comprised 150 patients who underwent implantation of Medtronic's dual chamber pacemakers with a single intracardiac EGM memory channel. We first set the electrogram channel to “summed,” and the automatic EGM diagnosis during the tachycardia was compared with the manual analysis findings. When the results were not identical for the 2 methods, the atrial EGM (AEGM) and ventricular EGM channels were sequentially selected and the results of each EGM selection were compared to conclude which channel was more valuable for diagnosis of high-rate episodes. The post-ventricular atrial blanking (PVAB) period was adjusted to the shortest interval with a relevant margin to avoid any far-field R wave over-sensing. Results: A total of 130 patients were eventually enrolled. High-rate episodes were observed in 115/130 patients (88%). The results of the automated tachycardia diagnosis obtained using the “summed” EGM differed from those obtained manually in 43/115 patients (37%). Changing the intracardiac EGM channel from “summed” to “AEGM” enabled a much better manual diagnosis with intracardiac EGMs because of improved atrial potential sensing, clearer manifestation of atrial electrograms within the PVAB, and more prominent atrial electrograms fused with the ventricular potentials. The ventricular EGM channel was not as useful as the AEGM channel for tachycardia diagnosis. Conclusions: In Medtronic pacemakers with single intracardiac EGM channel recording capability, AEGM is the most useful of the 3 EGM channel settings; PVAB should also be set to a much shorter value to achieve a more accurate automatic diagnosis

Early Tumor Shrinkage as a Predictor of Favorable Treatment Outcomes in Patients With Extensive-Stage SCLC Who Received Programmed Cell Death-Ligand 1 Inhibitor Plus Platinum-Etoposide Chemotherapy: A Prospective Observational Study

Introduction: In recent years, programmed cell death-ligand 1 (PD-L1) inhibitor plus platinum-etoposide chemotherapy was found to have favorable clinical outcomes in patients with extensive-stage SCLC (ES-SCLC). The usefulness of early tumor shrinkage (ETS) has been reported in various types of cancers. Nevertheless, there have been few reports evaluating ETS in ES-SCLC. Therefore, this study aimed to evaluate the role of ETS in the clinical outcomes of patients with ES-SCLC receiving chemoimmunotherapy. Methods: We prospectively identified 46 patients with ES-SCLC who received PD-L1 inhibitor plus platinum-etoposide chemotherapy at 10 institutions in Japan between September 2019 and October 2021. Of them, 35 patients were selected for analyses. Results: The responders (progression-free survival [PFS] ≥ 6.0 mo) had significantly greater tumor shrinkage at the first evaluation than the nonresponders (PFS < 6.0 mo) (65.0% versus 53.7%, p = 0.03). We defined the cutoff value for ETS as a 57% change from the baseline on the basis of the receiver operating characteristic results to determine the optimal tumor shrinkage rate at the first evaluation for identifying responders. The patients with ES-SCLC who achieved ETS had longer PFS and overall survival than those who did not achieve ETS (5.6 versus 4.0 mo, log-rank test p = 0.001 and 15.0 versus 8.3 mo, log-rank test p = 0.02). In the multivariate analyses, ETS was significantly associated with PFS and overall survival (hazard ratio = 0.27, 95% confidence interval: 0.12–0.63, p = 0.002 and hazard ratio = 0.34, 95% confidence interval: 0.13–0.85, p = 0.02). Conclusions: Our prospective observational study indicated that ETS was related to favorable clinical outcomes for patients with ES-SCLC receiving PD-L1 inhibitor plus platinum-etoposide chemotherapy