Atypical Left Bundle Branch Block Research Articles

Impact of non-typical LBBB on CRT response

Abstract Introduction Cardiac resynchronization therapy (CRT) benefits have been established in patients with heart failure and reduced left ventricular ejection fraction (HFrEF) who have a broad QRS and remain symptomatic despite optimized medical therapy. Responders typically are female, with LBBB and broader QRS. It remains uncertain to what extent do patients with non-LBBB QRS complex morphology respond to CRT and also if there are differences among various types of intraventricular conduction delays. Purpose To evaluate the impact of non-typical left bundle branch block (LBBB) on reverser remodeling and clinical events. Methods Single center, observational, retrospective study including patients (pts) who implanted CRT in the context of HFrEF, from 2015 to 2020. Evaluation of QRS morphology analysis was conducted. CRT response was defined by a reduction of LVESV≥15% or an increase in LVEF≥10%. Predictors of CRT response were evaluated with Chi-square and Mann- Whitney analysis. Impact on reverse remodeling and clinical outcomes was performed with Kaplan-Meyer analysis. Results A total of 361 pts were included for analysis, of which 184 had non-typical LBBB. Pts had a mean age of 71±9years old, the majority of pts were female (61%), and almost half were ischemic (47.8%). EGC evaluation prior to CRT implantation, revealed an atypical LBBB in 83 (45.1%) pts, typical RBBB in 23 (12.5%) pts, atypical RBBB 94.(9%) pts and nonspecific intraventricular conduction delay in 69 (37.5%) pts. During a mean time of follow-up of 2.9 ±2.4years, 33 pts (18%) had hospitalizations due to HF and 68 (37%) died. In this cohort, 78 pts (42.4%) were deemed as responders, who presented a better clinical outcome when compared to non-responders (p < 0.001, HR 2.629 [95% CI 1.635-4.225]. There was no difference among the four types of intraventricular conduction analyzed in respect to degree of CRT response – figure 1. Regarding clinical events during follow-up, there was once again no significant difference among the different patterns of non-typical LBBB– figure 2. In this subset population we found no independent predictors of CRT response, although non-responders were significantly older than responders (72±8 vs 69±10 years-old (p=0.016). Conclusion Although pts with non-typical LBBB morphology display a lower therapy response to CRT than reported for LBBB pts, the rate of response is not negligible and represents a protective factor for clinical outcomes. Different types of intraventricular conduction delay present no difference regarding long- term prognosis or reverse remodeling.Survival according to CRT response

Non-specific intraventricular conduction delay or atypical LBBB - How to predict acute coronary occlusion?

We describe two patient cases with acute coronary syndrome (ACS) and broad QRS in the acute phase electrocardiogram (ECG). The patients' ECG findings resembled left bundle branch block (LBBB), but with atypical features. Broad QRS not fulfilling the criteria for LBBB or right bundle branch block (RBBB) is diagnosed as non-specific intraventricular conduction delay (NSIVCD). The case report deals with the challenges of predicting acute coronary occlusion in patients with NSIVCD in their acute phase ECG. In one of the cases, the ECG changed from typical LBBB to NSIVCD or atypical LBBB with the development of systolic dysfunction and clinical heart failure.

Impact of paced left ventricular dyssynchrony on left ventricular reverse remodeling after cardiac resynchronization therapy.

We investigated whether pacing-induced electrical dyssynchrony at the time of cardiac resynchronization therapy (CRT) device implantation was associated with chronic CRT response. We included a total of 69 consecutive heart failure patients who received a CRT device. Left (LVp-RVs) and right (RVp-LVs) pacing-induced interlead delays were measured intraoperatively and used to determine if there was paced left ventricular (LV) dyssynchrony, defined as present when LVp-RVs is larger than RVp-LVs. CRT response was defined as a reduction in LV end-systolic volume ≥15%, 6 months after implantation. Paced left ventricular dyssynchrony (PLVD) was associated with ischemic cardiomyopathy (ICM) (χ2 : 8; P = .005) but not with QRS morphology nor with pacing lead positions. In a univariate analysis, PLVD (odds ratio [OR], 6.53; 95% confidence interval [CI], 2.2-18.9; P = .001), atypical left bundle branch block (LBBB) (OR, 3.3; 95% CI, 1.2-9.4; P = .022), and ICM (OR, 5.2; 95% CI, 1.6-17; P = .006) were associated with nonresponse. In a multivariate analysis, both PLVD (OR, 9.74; 95% CI, 2.8-33.9; P < .0001) and atypical LBBB (OR, 5.6; 95% CI, 1.5-20.3; P = .009) were independently associated with nonresponse. Adding PLVD to a model based on QRS morphology provided a significant and meaningful incremental value to predict LV reverse remodeling after CRT (χ2 to enter: 8; P < .005). Computer simulations corroborate these findings by showing that, while intrinsic electrical dyssynchrony is a prerequisite, the level of pacing-induced dyssynchrony modulates acute CRT response. In addition to the intrinsic electrical substrate, PLVD is strongly associated with less LV reverse remodeling, demonstrating that measuring the electrical substrate during pacing has additional value for prediction of CRT response in an already well-selected patient population.

Do all intra-ventricular conduction defect ECG patterns respond equally to CRT?

Response to cardiac resynchronization therapy (CRT) is well-established in patients with typical left bundle branch block (LBBB) but modest or even negative in those with intraventricular conduction delay (IVCD). However, IVCD pattern is heterogeneous, and it is possible that QRS patterns may also respond to CRT. Consecutive baseline ECGs of 239 patients implanted between 2007 and 2010 with CRT were analyzed. ECGs were classified into the following three groups: (a) typical LBBB (TLBBB) according to accepted guidelines (n= 67); (b) IVCD with LBBB pattern criteria in V1, 1, and aVL but with QS or rS in V5-V6 which we defined as atypical LBBB (ALBBB) (n= 74); and (c) all other IVCD (OIVCD) patterns (n= 98). Endpoints were 2years mortality and echocardiographic response, defined as a decrease of ≥ 10% in indexed LVESV or an increase of ≥ 5% in left ventricular ejection fraction at 1year of follow-up. Baseline clinical characteristics were similar among all the three groups. Rates of echocardiographic response were lower among those with OIVCD compared to those with LBBB and ALBBB (50% vs. 75% and 72%, respectively, p= 0.01 for both comparisons). A multivariable model showed a lower likelihood of echocardiographic response in OIVCD [HR = 0.40; (0.16-0.98)] and a similar likelihood in ALBBBB [HR = 0.98; (0.40-2.40)] compared to TLBBB. Cumulative 2-year survival was 88% in ALBBB, 86% in TLBBB, and 76% in OIVCD (p value = 0.011). Patients with ALBBB may have a favorable echocardiographic response to CRT and display similar survival rates to typical LBBB. This subgroup of IVCD should be considered for CRT. Atypical left bundle branch morphology defined as QS or rS in lead V1, broad R waves in lead I, and aVL but with QS or rS in V5-V6 is associated with favorable echocardiographic response to CRT and displays similar survival rates to typical LBBB patients.

Endocardial ablation of ventricular ectopic beats arising from the basal inferoseptal process of the left ventricle

Idiopathic ventricular ectopy (VE) shows predilection to sites within the left ventricular (LV) base such as the outflow tract/aortic sinuses, LV summit, and areas adjacent to the aortomitral continuity. We characterize VE arising from the inferior septum of the LV base that was successfully managed by LV endocardial ablation from the inferoseptal recess of the LV. The purpose of this study was to determine the incidence, electrocardiographic (ECG) findings, electrophysiological findings, and anatomical features associated with VE arising from the basal inferoseptal process of the LV (ISP-LV) ablated using an LV endocardial approach via the inferoseptal recess of the LV. A total of 425 consecutive patients undergoing VE ablation between January 1, 2012 and December 31, 2016 at 3 centers were evaluated. Demographic characteristics, ECG findings, and procedural data were analyzed for patients with ISP-LV VEs. Seven (1.5%) had a site of origin from the ISP-LV. Common ECG findings were a right bundle branch block concordant pattern or an atypical left bundle branch block early transition pattern, suggestive of a basal origin with a left superior axis, a biphasic QRS complex in lead aVR, and a small s wave in lead V6. Earliest activation was seen in an area below the outflow tract accessed from the inferoseptal recess inferior to the His bundle. In 3 cases, transient junctional rhythm was seen during ablation. All cases were ablated successfully with no complications. VE arising from the ISP-LV represents a distinct subset of idiopathic arrhythmia and can be successfully treated by endocardial catheter ablation from the inferoseptal recess. They share common surface ECG and electrophysiological findings with special anatomical features that need recognition for successful catheter ablation.

Bundle branch reentry VT : Diagnosis, mapping, and ablation

Macroreentry in the His-Purkinje system can result in sustained ventricular tachycardia (VT) termed bundle branch reentry VT. Bundle branch reentry is usually associated with His-Purkinje disease and depressed left ventricular function. In the case of typical bundle branch reentry, the right bundle is activated in the anterograde direction and ventricular depolarization begins at the distal end of the right bundle on the ventricular septum generating atypical left bundle branch block QRS morphology. However, atypical surface ECGs can also be found in patients with severe left ventricular dysfunction and involvement of the right ventricle complicating the diagnosis of bundle branch reentry VT. It is important to diagnose bundle branch reentry VT because patients with bundle branch reentry VT may suffer from ahigh rate of serial implantable cardioverter defibrillator (ICD) interventions based on VT recurrences due to immediate reinitiation of the arrhythmia. Ablation of the right bundle branch easily cures bundle branch reentry VT and can prevent frequent ICD interventions. After ablation of bundle branch reentry VT, mortality remains high due to the severe left ventricular dysfunction in many patients, and the patients are candidates for cardiac resynchronization therapy (CRT-D).

High degree right bundle branch block with left anterior hemiblock and lateral fibrosis resembling an atypical left bundle branch block in the limb leads

High degree right bundle branch block with left anterior hemiblock and lateral fibrosis resembling an atypical left bundle branch block in the limb leads

Acute myocardial infarction and electrically induced left bundle branch block: is a diagnosis possible?

An 86-year-old man was hospitalised for congestive heart failure. He had severe aortic stenosis, had previously undergone implantation of a single-chamber pacemaker and was in permanent atrial fibrillation. ECG at...

Alternating bizarrely–shaped broad QRS complex tachycardia. What is the mechanism?

Answer to the rhythm puzzle Figure 1 is an atrial flutter with 1:1 conduction and atypical left bundle branch block (LBBB) as a result of flecainide use. Figure 2 is still an atrial flutter but with 2:1 conduction and no functional aberration. A total atrioventricular block was achieved after the administration of intravenous adenosine, revealing the flutter waves as shown in Fig. 3. Fig. 1 Broad QRS complex tachycardia with obvious QRS alternans Fig. 2 ECG after spontaneous stabilisation of the tachycardia Fig. 3 Rhythm strip showing flutter waves after achieving total atrioventricular block using intravenous adenosine Antiarrhythmic drugs, especially those that slow conduction such as class Ic drugs, may cause proarrhythmia represented by monomorphic ventricular tachycardia (VT). On the other hand, these drugs may cause bizarre aberrant conduction during supraventricular tachycardia which may mimics VT [1]. The QRS complex during aberration is characterised by a QRS duration between 180 and 240 ms and bizarre right bundle branch block (RBBB) with a right or northwest axis, or atypical LBBB with left axis, mimicking VT [2]. The explanation of the occurrence of this bizarrely shaped BBB during treatment with class Ic antiarrhythmic drugs, particularly flecainide, is as yet uncertain. A possible explanation is the occurrence of use-dependent conduction delay especially in the myocardium beyond the block [2]. In contrast, conduction is relatively unhampered in areas activated by way of the His-Purkinje system, preserving the initial part of the QRS complex. That conduction delay due to flecainide is more pronounced in the ventricular myocardium than in the His-Purkinje system has been suggested by animal experiments [2]. In contrast to the situation during a straightforward BBB, this may result in an exaggerated asynchrony of activation of the various parts of the heart, giving rise to a bizarre type of BBB [2]. Electrical alternans is usually seen in (narrow complex) circus movement tachycardia. Beat-to-beat variations can occur during tachycardia whether ventricular or supraventricular because of an alternating discrete conduction disturbance with beat-to-beat variation in the width and shape of the QRS complexes, as in this case [3].

Novel mechanism of postinfarction ventricular tachycardia originating in surviving left posterior Purkinje fibers

Other than bundle branch reentry and interfascicular reentry, monomorphic postmyocardial infarction (post-MI) reentrant ventricular tachycardia (VT) including the His-Purkinje system has not been reported. Verapamil-sensitive idiopathic left VT includes the left posterior Purkinje fibers but develops in patients without structural heart disease. The purpose of this study was to describe a novel mechanism of reentrant VT arising from the left posterior Purkinje fibers in patients with a prior MI. The study consisted of four patients with a prior MI and symptomatic heart failure who underwent electrophysiologic study and catheter ablation for VT showing right bundle branch block (n = 3) or atypical left bundle branch block (n = 1) morphology with superior axis. In two patients, the VT frequently emerged during the acute phase of MI and required emergency catheter ablation. Clinical VT was reproducibly induced by programmed stimulation. In three patients, both diastolic and presystolic Purkinje potentials were sequentially recorded along the left ventricular posterior septum during the VT, whereas in the fourth patient, only presystolic Purkinje potentials were observed. During entrainment pacing from the right atrium, diastolic Purkinje potentials were captured orthodromically and demonstrated decremental conduction properties, whereas presystolic Purkinje potentials were captured antidromically and appeared between the His and QRS complex. Radiofrequency energy delivered at the site exhibiting a Purkinje-QRS interval of 58 +/- 26 ms successfully eliminated the VTs without provoking any conduction disturbances. Reentrant monomorphic VT originating from the left posterior Purkinje fibers, which is analogous to idiopathic left VT, can develop in the acute or chronic phase of MI. Catheter ablation is highly effective in eliminating this VT without affecting left ventricular conduction.

Atypical Left Bundle Branch Block in Dilative “Burned‐Out” Phase of Hypertrophic Cardiomyopathy

We present the case of a 70-year-old man admitted in congestive heart failure. The patient was diagnosed 22 years ago of hypertrophic cardiomyopathy (HC). ECG showed a very peculiar and pathological form of left bundle branch block (LBBB). 2D-echocardiogram revealed a dilated left ventricle (LV) and ejection fraction of 25%. LV remodeling represents an important component of the pathophysiology of HC and, paradoxically, some patients develop LV wall thinning, systolic dysfunction, and congestive heart failure (in the absence of coronary artery disease). This evolution is designated as "end-stage" or "burned-out"phase. We present this rare LBBB and his pathological evolution along the time as unique manifestation of this "burned-out" phase. The mechanism of this wall thinning remains unclear but changes in ECG may alert us about it.

Successful Radiofrequency Catheter Ablation of Epicardial Left Ventricular Outflow Tract Tachycardia from the Anterior Interventricular Coronary Vein

We report a case of idiopathic left ventricular outflow tract (LVOT) tachycardia that was eliminated by a radiofrequency application from the anterior interventricular coronary vein (AIV). The ECG exhibited QRS complexes with an inferior axis and atypical left bundle branch block pattern with an early transition of the precordial R waves at V3. Several radiofrequency applications from the coronary cusps and endocardial LVOT were not effective. Radiofrequency applications in the AIV, where the activation preceded the onset of the QRS by 30 msec, successfully eliminated the tachycardia. The AIV may be an optional site for radiofrequency ablation of idiopathic epicardial LVOT tachycardia.

Left ventricular epicardial outflow tract tachycardia: a new distinct subgroup of outflow tract tachycardia.

The present study investigated the incidence and ECG characteristics of ventricular tachycardias (VTs) originating from the left ventricular (LV) epicardium. Thirty-one consecutive patients with VT or premature ventricular contraction originating from the outflow tract (OT-VT) underwent catheter ablation. Twenty-one OT-VTs were ablated from the endocardium in the right ventricular (RV) OT and 3 were ablated from the endocardium in the LVOT. In the remaining 7 patients, 4 (13%) OT-VTs were LV epicardial in origin, and 1 of these was ablated from the left sinus of Valsalva. The ECG characteristics of OT-VT of epicardial origin included prominent tall R-waves in the inferior leads, an R-wave in V1 and an S-wave in V2, precordial R-wave transition in V2-4, a deep QS-wave in aVL, and no S-wave in V6. In addition, there was an atypical left bundle branch block morphology with an inferior axis. These findings were observed during pacing from several sites in the LV epicardium. Furthermore, pacing from the left sinus of Valsalva caused a relatively tall R in V1, deep S-wave in V2 and a tall R-wave with a shallow S-wave in V3, as well as tall R-waves in the inferior leads, which represented intermediate characteristics between RV endocardial OT-VT and LV endocardial OT-VT. In conclusion, OT-VT originating from the LV epicardium is not uncommon and has characteristic ECG findings. Some of them can be ablated from the left sinus of Valsalva.

Evaluation of Criteria for Diagnosis of Myocardial Infarction: Study of 256 Patients with Intermittent Left Bundle Branch Block

In an attempt to elucidate the specificity and sensitivity of atypical findings during left bundle branch block (LBBB) with respect to myocardial infarction (MI), we analyzed ECGs from patients with intermittent LBBB obtained by mail solicitation of cardiologists. The group consisted of 256 patient files fulfilling the following criteria: 1) complete LBBB present on one or more 12-lead ECGs, and 2) at leat one 12-lead ECG taken subsequent to a LBBB tracing exhibiting absence of LBBB (non-LBBB). The sensitivity of atypical LBBB for predicting presence of MI was 0.41, the specificity 0.64, and the accuracy 0.59. No specific atypical finding was significantly better than any other in predicting MI. We conclude that atypical findings present during LBBB are of little value in predicting the presence of MI (as diagnosed by significant Q waves present during non-LBBB conduction).