P2324A novel high risk ECG feature in Brugada Syndrome Probands: Localized QRS prolongation on right precordial leads

Abstract

Best Posters in new targets in cardiovascular drug assessment / Best Posters in Brugada syndrometed to our center with acute coronary syndrome during the period from January 2015 till December 2016 was done. Patients with AF at the time of presentation or those with history of AF were excluded from the study. Patients were divided into two groups, a group received ivabradine as indicated by their clinical status and the other group did not receive it, and the incidence of new onset AF in both groups was calculated. Results: Of the 488 patients included in our study, 73 patients received ivabradine (14.95%) and 415 patients did not receive it (85.05%). Regarding the occurrence of AF, 35 patients in the ivabradine group developed AF (47.95%) while 123 patients in the no-ivabradine group developed AF (29.64%) with a statistically significant difference between both groups. (P=0.003)

Higher Dispersion Measures of Conduction and Repolarization in Type 1 Compared to Non-type 1 Brugada Syndrome Patients: An Electrocardiographic Study From a Single Center

“…By contrast, QRS dispersion reflects spatial dispersion of CVs, increases in which can lead to unidirectional conduction block and reentry ( 44 ). Higher QRS dispersion ( 5 ) and increased fragmentation of the QRS complex ( 45 , 46 ), have been associated with pro-arrhythmic outcomes in BrS patients.…”

“…For instance, slow and discontinuous conduction of action potentials through working myocardium, due to reduced sodium channel activity, may lead to higher degrees of spatial and temporal dispersion in conduction ( 3 ). These could potentially be detected as prolonged QRS intervals ( 4 ) and higher QRS dispersion ( 5 ). Moreover, heterogeneous time-course in full repolarization between the different myocardial layers, due to regional difference in transient outward potassium channel activity, leads to increased transmural repolarization gradients that can be measured electrographically using QT dispersion (QT d ) ( 6 , 7 ), interval from the peak to the end of the T-wave ( 8 ) [T peak – T end , reflecting transmural dispersion of repolarization, TDR ( 9 )], (T peak – T end )/QT ratio ( 10 , 11 ) and T peak – T end dispersion.…”

Risk stratification in early stage arrhythmogenic cardiomyopathy and provocable brugada ECG

“…During a last ESC meeting in Barcelona 2017 another risk factor gained further importance: Localized right precordial QRS prolongation [10]. This risk factor was tested in more than 200 patients with a sensitivity of 78% and a specificity of 87%.…”

“…In about 10 -15% of cases there seems to be an association between arrhythmogenic cardiomyopathy and Brugada syndrome by the so-called connexome -a linkage of desmosomal proteins, sodium channel complexes and gap junctions including desmosomal genes like plakophilin-2 [2], desmoglein-2 [3], desmoplakin [4], and plakoglobin (in animal models). Risk assessment in these cases is of utmost importance by spontaneous coved-type ST elevation in right precordial leads as the only independent risk marker [5], QRS fragmentation [6], positive R wave in lead a VR [7], 1° AV block [8], inducibility dur-ing electrophysiological examination [9], and as a new finding localized right precordial QRS prolongation demonstrated in the last ESC meeting in Barcelona 2017 [10] with a sensitivity of 78% and a specificity of 87%.…”