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.

BackgroundProlongation of the QT interval is considered a risk factor for cardiac adverse events and mortality. Left bundle branch block (LBBB) lengthens the QT interval. The corrected QT interval (QTc) is most likely overestimated because its prolongation is caused by increases in depolarization duration and not in repolarization.ObjectivesIn this study, we aimed to apply corrected JT interval (JTc) as an appropriate measure of ventricular repolarization for predicting QTc in a formula.Patients and MethodsThe study population consisted of 101 patients with sinus rhythm (SR) and narrow QRS complexes (< 120 milliseconds). All patients underwent electrophysiology studies or ablation. A diagnostic catheter was positioned in the right ventricular apex (RVA) to induce LBBB at two different cycle lengths (CLs; 600 and 700 mv). The intrinsic QRS complex, QT time, and JT time were measured during SR and subsequent RVA pacing. The JTc was derived simply by subtracting the QRS duration from the QTc.ResultsStimulation from the RVA increased the QTc from 456.20 ± 38.63 ms to 530.67 ± 47.73 ms at a CL of 600 (P < 0.0001) and to 502.32 ± 47.26 ms at 700 CL (P < 0.0001). JTc showed no significant changes with stimulation from the RVA (102.97 ± 11.35 ms vs. 103.59 ± 10.67 ms, P = 0.24). There was no significant correlation between JTc and QRS complex duration. A significant correlation was seen between QRS and QTc at both CLs. The ROC curve indicated that sensitivity of 80% and specificity of 67% were obtained with JTc duration of 92.6 ms.ConclusionsRight ventricular pacing increases the QT interval without increasing the JT interval. Our results confirm that JTc, as an index of repolarization, is independent of ventricular depolarization. Therefore, it can be applied for predicting QTc in patients with LBBB.

Background:General anesthesia and deep sedation can be used during cardiac EPS to relief pain and provide comfort and immobility, but many electrophysiologists avoid sedation for better arrhythmia induction.Objective:To determine anesthesia effects in ablation procedures in adults, we used intravenous anesthetic agents in patients who underwent slow pathway ablation.Patients and Methods:One hundred patients who were to undergo radiofrequency catheter ablation were randomly assigned to with and without intravenous anesthesia groups. All patients had palpitation with a documented electrocardiography (ECG) compatible with atrio-ventricular nodal reentrant tachycardia (AVNRT). We used propofol, fentanyl and midazolam for intravenous sedation. Electrophysiological parameters were checked for the two groups and compared before and after the ablation.Results:Electrophysiological parameters were not significantly different in the two groups. In the anesthetic group, patients were more satisfied with the procedure (P value < 0. 001).Conclusions:Intravenous anesthesia could be done safely in patients who underwent electrophysiological procedures. It had no effect on arrhythmia induction or slow pathway ablation in patients with documented AVNRT.

BackgroundWith increasing use of cardiac resynchronization therapy (CRT), treating physicians should be familiar with different electrocardiographic (ECG) patterns of left ventricular (LV) lead and biventricular (BiV) pacing. However, there are a few publications on ECG patterns during BiV pacing.PurposeThis study was sought to determine different ECG patterns in patients with BiV pacing.MethodsTwelve-lead ECGs during BiV pacing (right ventricular leads at apex and LV leads in one of the lateral coronary veins) were analyzed in 181 consecutive patients (121 male; mean age, 62.0 ± 13.5 years) with advanced heart failure and baseline left bundle branch block pattern after at least 6-month of uncomplicated CRT.ResultsDuring BiV pacing, 65% of the patients showed a dominant R wave in V1. There was a right axis deviation in 57% in frontal plane. However, a left superior axis emerged in 34% and normal frontal plane axis in 9%. Sequential BiV pacing (73% vs. 58%, P = 0.04) and pacing from posterolateral coronary vein (80% vs. 60%, p = 0.045) were more likely to present with a dominant R wave in V1. In sequential pacing, AV interval was significantly longer in patients with negative complex in V1 than in those with positive complex (124 ± 21 vs. 116 ± 8.0, p = 0.005). A Q/q wave was detected in 85% of patients in lead I and 78% in lead aVL.ConclusionsBiV pacing from lateral coronary venous branches and right ventricular apex characteristically presented with dominant R wave in V1, Q/q wave in leads I and aVL, and right or left superior axis. However, a negative complex in V1, QRS axis in other quadrants, and lack of Q/q wave in leads I and aVL did not necessarily indicate a problem.

Long-term loss of AV synchrony induced by VVI pacing is associated with the impairment of LAA contraction. Thrombus formation in the LAA is not increased by VVI pacing in patients with relatively good left ventricular (LV) function and sinus rhythm.

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