A new experimentally validated formula to calculate the QT interval in the presence of left bundle branch block holds true in the clinical setting.

BACKGROUND: The evaluation of the QT interval in the presence of left bundle branch block (LBBB) is associated with the challenge to discriminate native QT interval from the prolongation due to the increase in QRS duration. The newest formula to evaluate QT interval in the presence of LBBB suggests: modified QT during LBBB = measured QT interval minus 50% of LBBB duration. The purpose of this study is therefore to validate the abovementioned formula in the clinical setting. METHODS: Validation in two separate groups of patients: Patients who alternated between narrow QRS and intermittent LBBB and patients with narrow QRS who developed LBBB after transcatheter aortic valve implantation (TAVI). RESULTS: The acquired mean native QTc intervals and those calculated by the presented formula displayed no significant differences (p > .99 and p > .75). CONCLUSIONS: In this study we proved for the first time the validity and applicability of the experimentally acquired formula for the evaluation of the QT interval in the presence of LBBB in a clinical setting.

Is there a prognostic relevance of electrophysiological studies in bundle branch block patients?

BACKGROUND: The present European guidelines suggest a diagnostic electrophysiological (EP) study to determine indication for cardiac pacing in patients with bundle branch block and unexplained syncope. We evaluated the prognostic relevance of an EP study for mortality and the development of permanent complete atrioventricular (AV) block in patients with symptomatic bifascicular block and first-degree AV block. HYPOTHESIS: The HV interval is a poor prognostic marker to predict the development of permanent AV block in patients with symptomatic bifascicular block (BFB) and AV block I°. METHODS: Thirty consecutive patients (mean age, 74.8 ± 8.6 years; 25 males) with symptomatic BFB and first-degree AV block underwent an EP study before device implantation, according to current guidelines. For 53 ± 31 months, patients underwent yearly follow-up screening for syncope or higher-degree AV block. RESULTS: Thirty patients presented with prolonged HV interval during the EP study (mean, 82.2 ± 20.1 ms; range, 57-142 ms), classified into 3 groups: group 1, <70 ms (mean, 62 ± 4 ms; range, 57-67 ms; n = 7), group 2, >70 to ≤100 ms (mean, 80 ± 8 ms; range, 70-97 ms; n = 18), and group 3, >100 ms (mean, 119 ± 14 ms; range, 107-142 ms; n = 5). According to the guidelines, patients in groups 2 and 3 received a pacemaker. The length of the HV interval was not associated with the later development of third-degree AV block or with increased mortality. CONCLUSIONS: Our present study suggests that an indication for pacemaker implantation based solely on a diagnostic EP study with prolongation of the HV interval is not justified.

Spot diagnosis of inferior axis and concordant R-pattern predicts left ventricular inflow tract tachycardia: Ablation from the great cardiac vein of an underdiagnosed entity.

BACKGROUND: The present literature holds an enormous variation concerning origin and ablation site of idiopathic ventricular arrhythmias (VA), ranging from 2.5 to 15% for the origin within the coronary venous system (CVS). The aim of the study was to detect positive predictive ECG morphology patterns to discriminate VA stemming from the CVS. METHODS: 110 consecutive patients (P) with 111 premature ventricular capture beat (PVC) morphologies undergoing successful ablation for VA were retrospectively analyzed concerning their ECG patterns. RESULTS: 20/110 P (18%) displayed their VA origin in the CVS with anterior/anterolateral left ventricular inflow tract (LVIT) (epicardial/GCV) in 16 P (14%), anterior/anterolateral LVIT (endo- and epicardial/GCV) in 3 P (3%), and anterior interventricular vein (AIV) 1 P (<1%). ECG morphology of all GCV cases demonstrated an inferior axis and concordant R-pattern in all precordial leads resulting in 100% sensitivity. One VA demonstrating this pattern was ablated outside at the LVOT resulting in 95% specificity for origin in the anterior/anterolateral LVIT. 3/20 P that were ablated in the CVS required additional endocardial ablation from the anterior/anterolateral LVIT resulting in 80% specificity for sole successful ablation in the CVS. CONCLUSION: An inferior axis and concordant R-pattern in all precordial leads serve as diagnostic markers for an LVIT origin in the surface ECG and suggest a high primary ablation success via the GCV.

New formula for evaluation of the QT interval in patients with left bundle branch block.

BACKGROUND: Left bundle branch block (LBBB) and QT prolongation both are associated with a worse prognosis. LBBB lengthens the QT interval. To date it is not known whether QT prolongation during LBBB differs in repolarization from QT prolongation during narrow QRS. OBJECTIVE: The purpose of the present proof-of-concept-study was to develop a formula that allows comparison of the adjusted QT interval during LBBB with reference values and thereby allows interpretation of the QT interval irrespective of QRS widening. METHODS: Sixty consecutive patients with sinus rhythm (SR) and narrow QRS underwent electrophysiologic study for ablation. In all patients, the intrinsic QRS ,QT, and JT times were measured during SR, and ventricular pacing from both the right ventricular apex (RVA) and the right ventricular outflow tract (RVOT) caused LBBB. We determined prolongation of the QT during as compared to SR (ΔQT). ΔQT was then divided by the QRS length during pacing QRS (QRSb). This describes the percentage of the QRS duration at LBBB, which must be subtracted from the measured QT (QTb) to determine the modified QT interval (QTm). RESULTS: The ratio of ΔQT to paced QRS was calculated as 48.3% (RVA) and 48.8% (RVOT) (mean 48.5%). The ratio intrinsic of JTi to paced JT was 1.0055 (RVA) and 1.0087 (RVOT). There was no significant difference in intrinsic JT vs paced JT (P = .2). CONCLUSION: Right ventricular pacing causes prolongation of the QT due to a paced LBBB without prolongation of the JT time. In our study, we showed that QT prolongation caused by LBBB constitutes 48.5% of the QRS width. This is the value that must be subtracted from the measured QT in LBBB in order to estimate the modified QT. Thus, the resulting formula for "modified QT" estimation in LBBB is QTm = QTb - 48.5% * (QRSb).