Search

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.