Ritter, Philippe

AbstractBackgroundThe Micra clinical trials have enrolled more than 2500 patients without any reported device‐related infections that required removal during follow‐up. Leadless pacemakers might be more resistant to bacterial seeding due to smaller surface area and a greater tendency for encapsulation.ObjectiveTo analyze the incidence and outcomes of serious infectious events (SIEs: bacteremia or endocarditis) that developed during follow‐up in patients with history of Micra leadless pacemaker implantation.MethodsSIE and outcomes were characterized based upon adverse event reports. Among 720 patients implanted with Micra in the investigational device exemption trial, we identified 16 patients who had documented 21 SIEs during follow‐up.ResultsAmong patients with SIEs, mean age was 71.9 ± 11.7 years. SIEs occurred at a mean 4.8 ± 4.5 months after implant and patients were followed for 13.1 ± 9.1 months after documentation of SIE. All events were adjudicated as unrelated to the Micra device or procedure. Bacteremia was documented to be related to a gram‐positive organism in 13 events (seven Staphylococcus, three Streptococcus, two Enterococcus, and one uncharacterized gram‐positive bacteria), and gram‐negative organisms in three events. In five events, the type of organism was not characterized (two patients with endocarditis). No persistent cases of bacteremia after antibiotic cessation were seen over the duration of follow‐upConclusionIn this small series of Micra patients who developed SIEs postimplant, the occurrence of bacteremia and/or endocarditis did not appear to lead to persistent bacteremia off antibiotics; most events resolved with antibiotic treatment.

Background: Sudden cardiac death because of ventricular fibrillation (VF) is commonly unexplained in younger victims. Detailed electrophysiological mapping in such patients has not been reported. Methods: We evaluated 24 patients (29±13 years) who survived idiopathic VF. First, we used multielectrode body surface recordings to identify the drivers maintaining VF. Then, we analyzed electrograms in the driver regions using endocardial and epicardial catheter mapping during sinus rhythm. Established electrogram criteria were used to identify the presence of structural alterations. Results: VF occurred spontaneously in 3 patients and was induced in 16, whereas VF was noninducible in 5. VF mapping demonstrated reentrant and focal activities (87% versus 13%, respectively) in all. The activities were dominant in one ventricle in 9 patients, whereas they had biventricular distribution in others. During sinus rhythm areas of abnormal electrograms were identified in 15/24 patients (62.5%) revealing localized structural alterations: in the right ventricle in 11, the left ventricle in 1, and both in 3. They covered a limited surface (13±6 cm 2 ) representing 5±3% of the total surface and were recorded predominantly on the epicardium. Seventy-six percent of these areas were colocated with VF drivers ( P <0.001). In the 9 patients without structural alteration, we observed a high incidence of Purkinje triggers (7/9 versus 4/15, P =0.033). Catheter ablation resulted in arrhythmia-free outcome in 15/18 patients at 17±11 months follow-up. Conclusions: This study shows that localized structural alterations underlie a significant subset of previously unexplained sudden cardiac death. In the other subset, Purkinje electrical pathology seems as a dominant mechanism.