Infection is an important complication of cardiac implantable electronic device procedures. To further study the factors associated with infection, we retrospectively reviewed the records of 3,205 consecutive patients who had undergone de novo or revision cardiac electronic device implantation at our institution from March 2011 through March 2015. We recorded all infections and specified whether they were related to the characteristics of the patient, device, or procedure. To identify predictors of infection, we performed multivariate analysis. Device infections were identified in 85 patients (2.7%), at a mean follow-up time of 27 ± 11 months. The main predictors of device infection were use of an implantable cardioverter-defibrillator or a cardiac resynchronization therapy defibrillator device (odds ratio [OR]=16; 95% CI, 4.14-61.85; =0.0001), stage 3 chronic kidney disease (OR=9.41; 95% CI, 1.77-50.04;=0.009), a revision procedure (OR=8.8; 95% CI, 3.37-23.2; =0.0001), or postoperative hematoma (OR=6.9; 95% CI, 1.58-30.2;=0.01). We also identified 2 novel predictors of infection: a low body mass index of <20 kg/m (OR=1.03; 95% CI, 1.01-1.06; =0.005), and use of povidone-iodine rather than chlorhexidine-alcohol for topical antisepsis (OR=4.4; 95% CI, 2.01-9.4;=0.03). We conclude that comorbidities, device characteristics, procedure types, and postoperative noninfective complications all increase the risk of device infection after a cardiac implantable electronic device procedure.

Background The aim of the present study was to determine whether postprocedural antibiotic reduces the risk of infection related to the cardiac implantable electronic device (CIED) implantations. Methods The present investigation is a randomized, prospective, single‐blinded controlled trial. All consecutive patients who presented for new CIED implantation, generator replacement, or upgrade were randomized into the following three groups: (A) no antibiotic, (B) intravenous (IV) antibiotic for 1 day, (C) 1 day IV plus 7 days oral antibiotic. Follow‐up was performed on 10‐12 days; 1, 3, 6 months; and then every 6 months for 2 years. The primary endpoint was any evidence of infection at the generator pocket or systemic infection related to the procedure at short‐term (6‐month) and long‐term (2‐year) follow‐ups. Results Of the 450 patients (72 patients with cardiac resynchronization device) included in the study, the primary endpoint of short‐term infection was reached in one patient (0.2%) in group A and no patients in groups B and C. The endpoint of long‐term infection was reached in nine patients (2%) with equal frequency between three randomized groups (three patients in each group). On multivariable analysis, the only independent predictor of infection was defibrillator implantation (odds ratio, 8.5; 95% confidence interval, 1.6‐45). Conclusions The results of this prospective study showed no benefit for the postoperative antibiotic for the prevention of CIED infection.

The Brugada syndrome (BrS) is an inherited arrhythmia characterized by ST‐segment elevation in V1–V3 leads and negative T wave on standard ECG. BrS patients are at risk of sudden cardiac death (SCD) due to ventricular tachyarrhythmia. At least 17 genes have been proposed to be linked to BrS, although recent findings suggested a polygenic background. Mutations in SCN5A, the gene coding for the cardiac sodium channel Nav1.5, have been found in 15–30% of index cases. Here, we present the results of clinical, genetic, and expression studies of a large Iranian family with BrS carrying a novel genetic variant (p.P1506S) in SCN5A. By performing whole‐cell patch‐clamp experiments using HEK293 cells expressing wild‐type (WT) or p.P1506S Nav1.5 channels, hyperpolarizing shift of the availability curve, depolarizing shift of the activation curve, and hastening of the fast inactivation process were observed. These mutant‐induced alterations lead to a loss of function of Nav1.5 and thus suggest that the p.P1506S variant is pathogenic. In addition, cascade familial screening found a family member with BrS who did not carry the p.P1506S mutation. Additional next generation sequencing analyses revealed the p.R25W mutation in KCNH2 gene in SCN5A‐negative BrS patients. These findings illustrate the complex genetic background of BrS found in this family and the possible pathogenic role of a new SCN5A genetic variant.