Introduction We describe the progressive increase in the QRS durations (QRSd) and the subsequent decrease in the left ventricular ejection fractions (LVEF) of two patients post pacemaker implantation. We aim to highlight the need for contemporary cardiac implantable electronic devices (CIEDs) to include QRSd monitoring in the standard device data capture. This would ultimately allow for early interventions to be made to prevent chronic heart failure (CHF) hospitalizations. Methods The echocardiographic studies of two patients (pre and post pacemaker implantation) were analyzed, in order to determine changes in QRSd and LVEF data leading up to CHF hospitalization events. Results Patient 1 had a QRSd of 66 msec in June of 2018, one month before pacemaker implantation. Six months after implantation, Patient 1 had an increased QRSd of 156 msec. This was accompanied with a stark decrease in LVEF, from 55% at the time of implantation to below 35% in October of 2020. Patient 2 had a QRSd of 160 msec and a LVEF of 43% prior to the implantation of a pacemaker in 2016. Patient 2 similarly showed a progressive increase in their QRSd and was found to have a significantly decreased LVEF of 17% when hospitalized for decompensated heart failure around 5 years after pacemaker insertion. Conclusion Chronic RV apical pacing can be associated with adverse effects, leading to compromised cardiac function and resulting in pacing-induced cardiomyopathy (PICM). Progressive paced QRS widening can be indicative of CHF development and correlates with a decline in ejection fraction. The addition of device based QRS width monitoring to the current trend toolkit in implantable devices could alert electrophysiologists and patients of the potential for PICM, in the absence of serial 12 lead comparisons. This pre-emptive alert is essential in an era where remedy in the form of cardiac resynchronization and physiological pacing therapy is readily available.

The prevalence of atrial fibrillation (AF) is forecasted to increase manifold, emphasizing the need for efficacious treatments. Pulmonary vein isolation (PVI) to eliminate ectopic triggers is now established as a fundamental component of the invasive treatment of AF, however its efficacy in persistent AF remains suboptimal. The atrial myocardium undergoes adverse fibrotic remodeling as AF progresses, favoring arrhythmia initiation and maintenance. Reductions in left atrial bipolar voltage have been suggested to identify regions of such pathological remodeling, and represent novel targets for ablation to target the arrhythmogenic substrate. Early observational studies targeting these low voltage areas (LVA) have been encouraging, however results from more recent randomized trials are more mixed. Importantly, there is significant heterogeneity in the techniques for identifying LVAs and the strategies for ablation. In reality, the atrial arrhythmogenic substrate is multi-faceted rather than being limited to fibrosis and there remains uncertainty as to how accurately LVAs represent regions of fibrosis. Additionally, bipolar voltage is influenced by numerous physiological and biophysical factors. The present review summarizes the current evidence for LVA ablation in AF. We then analyze the components of the atrial arrhythmic substrate, its relationship to LVAs and the limitations in LVA assessment. Finally we discuss novel techniques for delineating the atrial substrate.

Background: Spontaneous ventricular premature contractions (PVCs) in the post infarct milieu is assumed to be due to automaticity. However, the mechanism has not been studied with appropriate mapping tools. Objective: To study the mechanism of spontaneous PVCs with high density intramural mapping in a canine model, to test the hypothesis that post-infarct PVCs are due to re-entry rather than automaticity. Methods: In 15 anesthetized dogs, using 768 intramural unipolar electrograms, simultaneous recordings were made. After 30 mins of stabilization, recordings were made during the first 10 minutes of ischemia, and activation maps were constructed of individual beats. Acute ischemia was produced by clamping the left anterior descending coronary artery proximal to the first diagonal branch. The analysis was limited to the activation pattern of spontaneous ventricular beats. Results: In all experiments ST-T alternans occurred. In 8 of 15 dogs spontaneous ventricular beats occurred. In all 8 of these experiment earliest, ectopic activity occurred in the endocardium, well within the ischemic zone. From there, activity spread rapidly along the subendocardium, with endo-to epicardial spread along the non ischemic myocardium. Epicardial breakthrough always occurred at the border of the ischemic myocardium. In 3 dogs, delayed potentials were observed, which were earliest at the ischemic epicardium and extended transmurally with increasing delay towards the endocardium, where they culminated in a premature beat. Conclusion: Graded responses that occur with each sinus beat intramurally, when able to propagate from epicardium to endocardium is the mechanism by which PVCs are generated in post-infarct myocardium.