Differentiating the origin of outflow tract premature ventricular complexes using the QRS-right ventricular apex interval

Background For localization of outflow tract Premature ventricular complexes (PVCs) many ECG criteria have been proposed, however in some cases it is difficult to accurately localize the origin of PVCs using the surface ECG. Objective This study aims to study the relation between QRS-right ventricular apex interval and the origin of the outflow tract PVCs. Patients and Methods The study included 30 patients (27 female, age 37.20 ± 7.87, RVOT origin 18) referred for PVCs ablation and we measured the interval from the onset of the earliest QRS complex of premature ventricular contractions (PVCs) to the distal right ventricular apical signal, (the QRS-RVA interval) and correlated this interval with origin of outflow tract PVCs as identified by the successful ablation during the procedure. Results Compared to PVCs originating from RVOT, the QRS-RVA interval was significantly longer in PVCs originating from LVOT (67.33±7.56 for LVOT PVCs vs. 37.11±4.34 for RVOT PVCs, p < 0.001). Receiver operating characteristic (ROC) analysis showed that a QRSRVA interval ≥47 ms has a sensitivity, specificity, positive and negative predictive values of 100%, 100%, 100%, 100% respectively, for prediction of an LVOT origin of PVCs Conclusion The QRS-RVA interval is a simple and accurate criterion for differentiating the origin of outflow tract arrhythmia during electrophysiology study, A QRS-RVA interval ≥47 ms suggests an LVOT origin of PVCs.

Efficacy and safety of left bundle branch area pacing versus right ventricular apex pacing in patients with atrioventricular block: study protocol for a randomised controlled trial

IntroductionLeft bundle branch area pacing (LBBaP) is a relatively new approach for physiologic pacing. A limited number of retrospective clinical studies, featuring small sample sizes, have shown that compared with right ventricular apex pacing (RVAP), the QRS duration of postoperative ECG in LBBaP patients is narrower and the cardiac systolic function is improved. However, there have been no randomised controlled trials (RCTs) evaluating the efficacy and safety of LBBaP in patients with atrioventricular block (AVB). Therefore, the current study intends to address the paucity in RCT data evaluating LBBaP versus RVAP in AVB patients.Analysis and methodsThis study is a single-centre, randomised controlled superiority trial to be conducted at the Cardiac Centre of Beijing Anzhen Hospital. From January 2021 to December 2023, 210 consecutive AVB patients meeting the inclusion criteria and receiving pacemaker implantation will be enrolled. Participants will be randomly divided into an experimental group (LBBaP) and a control group (RVAP) at a 1:1 ratio. The primary outcome is left ventricular ejection fraction (LVEF), which will be assessed by echocardiography. The secondary outcomes in this study are synchrony of left ventricular systole, NT-proBNP, LVEDD, the 6-min walk distance, quality of life (SF-36 scale), all-cause mortality, cardiovascular death events, rehospitalisation rate and major complication rate.Ethics and disseminationThis study was approved by the Medical Ethics Committee of Beijing Anzhen Hospital (No. 2020021X). The results of the trial will be presented at national and international conferences. We hypothesise that compared with RVAP, LBBaP will be superior for treating patients with AVB. This trial will provide evidence-based suggestion for the majority of electrophysiologists in pacing implantation.Trial registrationChiCTR2000034335.

Subacute right ventricle perforation: a pacemaker lead complication

Myocardial perforation is an uncommon but potentially life-threatening complication of pacemaker and implantable cardioverter-defibrillator. Myocardial perforation may be acute, subacute or chronic when it occurs within 24 hours of the device insertion; between 1 day and 30 days; and more than 30 days after implantation. This complication may occur in 1.7%–7% of patients. However, subacute myocardial perforation is rare and affects 0.5%–1.2% of patients. We report the case of an 85-year-old patient with a pacemaker failure 10 days after implantation due to a subacute myocardial perforation caused by an active fixation ventricular lead. Transthoracic echocardiography showed penetration of the ventricular lead through the right ventricular apex into the pericardium without any pericardial effusion. We confirmed myocardial perforation by a CT scan. We referred her to the surgery ward where she was successfully managed.

Abstract 14985: Presence of Repolarization Gradients Reverses Post-infarct Ventricular Tachycardia Exit and Entrance Sites in Personalized Digital Hearts

Introduction: Post-infarct ventricular tachycardias (VT) arise due to structural remodeling (scarring). Physiological repolarization gradients (apicobasal and transmural) exist in the human heart, but the effects on post-infarct VT dynamics are unknown. Hypothesis: We hypothesized that incorporation of repolarization gradients in personalized digital hearts of post-infarct patients impacts VT exit sites without altering the location of the VTs. Methods: 3D late-gadolinium enhanced CMR images were acquired from 7 post-infarct patients. Personalized image-based computational heart models (digital hearts) representing scar and infarct border zone distributions were constructed. Apicobasal (AB) and transmural (TM) repolarization gradients were incorporated using a validated method (Fig A). VTs were induced at baseline (no repolarization gradient) via rapid pacing in the right ventricular apex, using two pacing cycle lengths, mimicking non-invasive programmed stimulation. Pacing protocols that induced baseline VTs were repeated under AB and TM conditions. Results: Ten VTs were induced in baseline digital hearts. 8 AB VTs and 8 TM VTs were induced; the remaining 2 VTs for both AB and TM digital hearts could not be induced. 5/8 induced AB VTs had VT exit sites matching baseline VT exit sites; the remaining 3/8 AB VTs had reversed VT exit and entrance sites from the corresponding baseline VTs (Fig B, VT 1 & 2). 4/8 induced TM VTs had exit sites that matched those at baseline; the remaining TM VTs had exit and entrance sites reversed from those of baseline VTs (Fig B, VT 1, 2 & 3). All 8 AB VTs and 8 TM VTs had the same location as corresponding baseline VTs. Conclusion: AB and TM repolarization gradients can act to reverse VT entrance and exit sites without changing VT location. Thus, incorporation of physiological repolarization gradients into personalized digital hearts may not impact VT ablation targeting but may affect accurate prediction of VT exit or entrance sites.

P706 LMCA and LAD coronary ectasia in an asymptomatic young patient reassessment with multimodality imaging after 17 years

A 25 years old male patient was referred to an advanced center because of 2/6-degree systolo-diastolic murmur heard at meso-cardiac area during his pre-military routine examination. ECG revealed T wave inversions at standard D1 to D3 and precordial V1 to V4 leads, treadmill was non-diagnostic for ischemia. In his transthoracic echocardiogram, measurement of heart chambers and wall thicknesses were within normal range with normal wall motion of the left ventricle, EF was 55%. 2D and color-Doppler echocardiography revealed a cystic structure with venous flow in it at the right ventricular apex, and created a suspicion of a fistula. Myocardial perfusion scintigraphy showed ischemia at the apical sections of the septal wall. He underwent coronary angiography, LMCA and proximal LAD were ectatic, LAD ectasia was in consistent with the first septal branch, circumflex (Cx) and right coronary artery (RCA) angiograms were normal. LAD flow was examined and no fistula was detected. Right and left ventriculography revealed normal ventricular functions, oxygen saturations were 70.9% in pulmonary artery, 70.4% in right ventricle, 72.9% in right atrium, and 97.4% in the aorta. Pulmonary capillary wedge pressure was 10 mmHg, pulmonary artery pressure 10/26/5 mmHg, right ventricular pressure 13/6 mmHg, left ventricular pressure 120/0/8 mmHg. Further investigations for etiology and congenital malformations were planned and the patient was discharged with oral anticoagulant therapy. The patient had no contact with the outpatient clinic for 17 years. At the 17th year of the diagnosis he was called and reevaluated. He was still asymptomatic and oscultation findings were the same. Transthoracic 2D and 3D and color-Doppler echocardiography revealed the same cystic structure at the right ventricular apex, but this time with no-flow. Coronary CT angiography was performed, LMCA was ectatic and the diameter was 8.1 mm, proximal LAD was ectatic and the diameter was 6 mm, ectasia was in continuous with the first septal branch. The ectatic septal branch was at the apical level of the right ventricle, appearing like a cystic structure with a diameter of 2.8 cm, and the lack of contrast enhancement was thougt to be in consistent with thrombus formation. Cx and RCA artery calibrations were found to be normal. In order to confirm the diagnosis of thrombus formation, MR angiography was performed. Perfusion MRI showed no evidence of thrombus in the ectatic septal branch. Abstract P706 Figure.