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Background: Left posterior fascicular ventricular tachycardia (LPF-VT) is frequently misdiagnosed as supraventricular tachycardia with aberrant right bundle branch block (RBBB) and left anterior hemiblock (LAHB). The purpose of the present study was to define the morphological ECG characteristics of LPF-VT and attempt to differentiate it from RBBB and LAHB aberrancy.Methods and Results: A systematic Medline search was used to identify or locate ECG tracings from patients with LPF-VTs. ECGs with LPF-VT were also collected from patients who underwent ablation of this arrhythmia at the Tel Aviv and Sheba Medical Centers. These ECGs were compared with ECGs of consecutive patients with RBBB and LAHB and no obvious cardiac pathology by echocardiography. Overall, 183 ECGs of LPF-VT were compared with 61 ECGs showing RBBB and LAHB. Univariate analysis demonstrated differences in QRS axis, limb (I, aVr), and precordial (V1, V2, V6) ECG leads. On multivariate logistic regression analysis, LPF-VT was more often associated with atypical RBBB-like V1 morphology (odds ratio, 5.1; P=0.004), positive QRS in aVr (odds ratio, 19.2; P<0.001), V6 R/S ratio ≤1 (odds ratio, 6.7; P=0.01), and QRS ≤140 ms (odds ratio, 7.7; P<0.001). Using these 4 variables, a prediction model was developed that predicted LPF-VT with sensitivity and specificity of 82.1% and 78.3%, respectively. Patients with 3 of 4 positive variables had high probability of having LPF-VT, whereas patients with ≤1 positive variable always had RBBB plus LAHB.Conclusions: The morphological ECG characteristics of LPF-VT were defined, and a high accurate tool for correctly differentiating LPF-VT from RBBB and LAHB aberrancy was developed. [ABSTRACT FROM AUTHOR]

Background: Atrioventricular nodal reentrant tachycardia (AVNRT) is considered a sporadic disease occurring in ≈22.5 cases per 10 000 in the general population. We define the prevalence and characteristics of familial AVNRT among patients who underwent radiofrequency ablation.Methods and Results: Ablation reports of all patients with familial AVNRT (at least 2 first-degree family members) who underwent radiofrequency ablation in our institution and in another hospital were reviewed. There were 1587 patients from our institution, of whom 20 had ≥1 first-degree relatives with AVNRT. This indicates a familial AVNRT prevalence of 127 cases per 10 000 (95% confidence interval, 82-196/10 000). First-degree relatives of patients with AVNRT presented a hazard ratio of at least 3.6 for exhibiting AVNRT compared with the general population. After inclusion of 4 families with familial AVNRT who underwent ablation at another hospital our population study comprised a total of 24 families (50 patients) with AVNRT. Patients at ablation were younger in the familial AVNRT group when compared with the sporadic AVNRT group (44.2±19 versus 54.8±18 years old, P=0.0001). The male/female ratio was similar, with female predominance. The supraventricular tachycardia mechanism was typical slow/fast reentry in most cases in both groups. The most common familial relationship in our 24 families included a parent and a child in 67% of cases and less often 2 siblings (29%).Conclusions: Familial AVNRT prevalence is higher than previously believed suggesting that this arrhythmia may have a genetic component. Autosomal dominance with incomplete penetrance is the most likely mode of inheritance. [ABSTRACT FROM AUTHOR]

Background: Information on long-term clinical outcome of patients with Brugada syndrome treated with electrophysiologically guided class 1A antiarrhythmic drugs (AAD) is limited.Methods and Results: An aggressive protocol of programmed ventricular stimulation was performed in 96 patients with Brugada syndrome (88% males; mean age, 39.8±15.9 years). Ten patients were cardiac arrest survivors, 27 had presented with syncope, and 59 were asymptomatic. Ventricular fibrillation was induced in 66 patients, including 100%, 74%, and 61% of patients with cardiac arrest, syncope, and no symptoms, respectively. All but 6 of the 66 patients with inducible ventricular fibrillation underwent electrophysiological testing on quinidine (n=54), disopyramide (n=2), or both (n=4). Fifty-four (90%) patients were electrophysiological responders to >1 AAD with similar efficacy rates (≈90%) in all patients groups. Patients with no inducible ventricular fibrillation at baseline were left on no therapy. After a mean follow-up of 113.3±71.5 months, 92 patients were alive, whereas 4 died from noncardiac causes. No arrhythmic event occurred during class 1A AAD therapy in any of electrophysiological drug responders and in patients with no baseline inducible ventricular fibrillation. Arrhythmic events occurred in only 2 cardiac arrest survivors treated with implantable cardioverter-defibrillator alone but did not recur on quinidine. All cases of recurrent syncope (n=12) were attributed to a vasovagal (n=10) or nonarrhythmic mechanism (n=2). Class 1A AAD therapy resulted in 38% incidence of side effects that resolved after drug discontinuation.Conclusions: Our data suggest that electrophysiologically guided class 1A AAD treatment has a place in our therapeutic armamentarium for all types of patients with Brugada syndrome. [ABSTRACT FROM AUTHOR]

The article presents a study that hypothesized the role of recurrent ventricular tachycardia in improving scar substrates with multiple exit sites (MES) identified during pace-mapping. The study conducted high-density mapping in all subjects to delineate scar. Pace-mapping reveals the specificity of electrograms that exhibit MES and pace-mapped induction for sites critical to reentry.

Background: Data on the age at first arrhythmic event (AE) in Brugada syndrome are from limited patient cohorts. The aim of this study is 2-fold: (1) to define the age at first AE in a large cohort of patients with Brugada syndrome, and (2) to assess the influence of the mode of AE documentation, sex, and ethnicity on the age at first AE., Methods and Results: A survey of 23 centers from 10 Western and 4 Asian countries gathered data from 678 patients with Brugada syndrome (91.3% men) with first AE documented at time of aborted cardiac arrest (group A, n=426) or after prophylactic implantable cardioverter-defibrillator implantation (group B, n=252). The vast majority (94.2%) of the patients were 16 to 70 years old at the time of AE, whereas pediatric (<16 years) and elderly patients (>70 years) comprised 4.3% and 1.5%, respectively. Peak AE rate occurred between 38 and 48 years (mean, 41.9±14.8; range, 0.27-84 years). Group A patients were younger than in Group B by a mean of 6.7 years (46.1±13.2 versus 39.4±15.0 years; P <0.001). In adult patients (≥16 years), women experienced AE 6.5 years later than men ( P =0.003). Whites and Asians exhibited their AE at the same median age (43 years)., Conclusions: SABRUS (Survey on Arrhythmic Events in Brugada Syndrome) presents the first analysis on the age distribution of AE in Brugada syndrome, suggesting 2 age cutoffs (16 and 70 years) that might be important for decision-making. It also allows gaining insights on the influence of mode of arrhythmia documentation, patient sex, and ethnic origin on the age at AE., (© 2017 American Heart Association, Inc.)

Objective: Intact endothelialization machinery is essential to facilitate vessel healing after stent placement and to prevent restenosis. Circulating endothelial progenitor cells (EPC) have been demonstrated in the peripheral blood and shown to display endothelial functional properties, along with the ability to traffic to damaged vasculature. We reasoned that robust in-stent intimal growth could be partially related to impaired endothelialization resulting from reduced circulating EPC number or function., Methods and Results: Sixteen patients with angiographically-demonstrated in-stent restenosis were compared with patients with a similar clinical presentation that exhibited patent stents (n=11). Groups were similar with respect to the use of drugs that could potentially influence EPC numbers. Circulating EPC numbers were determined by the colony-forming unit assay, and their phenotype was characterized by endothelial-cell markers. Adhesiveness of EPC from both groups to extracellular matrix and to endothelial cells was also assayed. Patients with in-stent restenosis and with patent stents displayed a similar number of circulating EPC. Fibronectin-binding was compromised in patients with in-stent restenosis as compared with their controls exhibiting patent stents. Patients with diffuse in-stent restenosis exhibited reduced numbers of EPC in comparison with subjects with focal in-stent lesions., Conclusions: Reduced numbers of circulating EPC in patients with diffuse in-stent restenosis and impaired adhesion of EPC from patients with restenosis provides a potential mechanism mediating the exuberant proliferative process. These markers, if further validated, could provide means of risk stratifying patients for likelihood of developing in-stent restenosis.