After overdrive pacing excitation that is one
After overdrive pacing, excitation that is one lap behind (the second beat after the stimulus) is caused by several mechanisms. One is the prolonged conduction time that is longer than the TCL due to a long conduction pathway and/or slow conduction. The other is the dual-loop reentry . The excitation wavefront induced by the overdrive stimulation entered one circuit after going around the other, so the penetration to the other reentry circuit became the second beat after the stimulus. Entrainment mapping using the activation sequence of the last captured beat is very useful for clarifying the complex relation of these reentrant circuits.
The fourth criterion of reentry requires entrainment with shorter pacing ppar agonist lengths in order to detect antidromic penetration into the reentrant circuit . In Cases 1 and 2, entrainment with a shorter pacing cycle length demonstrated antidromic penetration to the circuit and changed the activation sequence of the last captured beats depending on the functional relation of reentrant circuits. However, it is sometimes difficult to determine changes induced by antidromic penetration, because the entrainment at shorter cycle lengths risks termination of the tachycardia and a catheter must be positioned precisely where antidromic penetration changes.
Conflicts of interest
Introduction Patients with ischemic cardiomyopathy are at an increased risk for serious ventricular arrhythmias and sudden cardiac death (SCD). Epidemiological studies indicate that more than 50% of cardiac deaths are sudden [1,2]. Antiarrhythmic drugs (AAD) do not reduce mortality in these patients [3–7]. Although earlier trials used programmed electrical stimulation (PES) for risk stratification [6–8], more recent data demonstrate the benefit of implantable cardiac defibrillators (ICDs) to treat patients with severely reduced left ventricular ejection fractions (LVEF) without performing PES [7,9]. However, as many patients will never have any ICD treatment, further risk stratification is required. The MADIT I and II studies included PES before randomization to ICD or medical therapy (PES was not mandatory but encouraged in MADIT II and was performed in 80% of the patients). In the MUSTT study, a registry of all patients recruited was maintained, and included those patients who did not experience abnormal rhythms induced during PES (non-inducible patients). Buxton et al. showed that with no antiarrhythmic therapy, the non-inducible patients had better prognosis than inducible patients . However, the mortality rate of both groups was still high, and the non-inducible patients might still benefit from ICD. The purpose of this study was to evaluate the efficacy of PES for risk stratification based on mortality for inducible patients treated with ICD vs. non-inducible patients in a “real-world” registry.
Materials and methods
Results A total of 198 patients were included in the study. Of these, 138 exhibited (+)PES and underwent ICD implantation and 60 exhibited (−)PES and were followed clinically. The mean follow-up period was 44.2±17.6 months. The baseline characteristics upon inclusion into the study are presented in Table 1. The mean age of the (−)PES patients was similar to that of the (+)PES group (68.5±8.6 and 66.3±9 years, respectively; p=0.14). The mean LVEF of all patients was 27.8±5.3% and did not differ between the two groups. More patients in the (−)PES group had a history of atrial fibrillation (28.8% vs. 15.2%, p=0.027). β-Blockers were used less often in the (−)PES group (86.7% vs. 98.6%, p<0.001). Baseline electrocardiographic characteristics were similar in the two groups. Some characteristics of ECG and PES are presented in Table 3. The primary outcome, five-year survival rate, showed a trend towards increased survival in the (+)PES group in which ICD implantation was performed compared to the (−)PES group (20% vs.. 35%, p=0.058) (Fig. 1A, Table 2). Survival rates significantly reduced in younger patients (≤68 years old) who did not undergo ICD implantation (HR, hazard ratio=0.3; Fig. 1B), especially in young patients with severely reduced LVEF (≤25%) (HR=0.1; Table 2). Of note, the cut-off of 68 years old was chosen for subgroup analysis because it was the median age in the study.