Right Bundle Branch Block Morphology Research Articles

Conduction system pacing improved cardiac functions and functional capacity in heart failure with reduced ejection fraction and right bundle branch block

Abstract Conduction system pacing (CSP) is increasingly accepted as an alternative to biventricular pacing in heart failure (HF) patients with left bundle branch block (LBBB) and non-LBBB. However, its efficiency in right bundle branch block (RBBB) is ill-defined. Herein, we report on the clinical outcomes of CSP in HFrEF patients with wide QRS complex and RBBB morphology. His-bundle (HBP) or LBB-area pacing (LBBAP) was attempted as a primary strategy in patients with RBBB, QRS duration ≥130 ms and left ventricular ejection fraction (LV EF) <35% and NYHA class II to IV HF despite optimized medical treatment for at least 6 months. Data on functional status, NT-pro-BNP levels and echocardiographic parameters were collected during follow-up and expressed as mean ± SEM, Statistical significance was calculated with Student’s paired t-test and chi square distribution. CSP was performed in 12 RBBB-HF patients (age 64.3±2.9 years) with mean QRS duration of 150±4 msec and baseline LV EF of 25.4±2.3%. The aetiology of HF was ischaemic (6 patients) and non-ischaemic cardiomyopathy (6 patients). During the procedure, HBP was achieved in 7 and LBBAP in 5 patients, resulting in a significant reduction in the QRS-duration (115±2.6 msec, P<0.0001) as compared with baseline value. CSP improved LV function (LV EF= 31.8±2.8%, P=0.009) as well as NYHA functional class (25% of the patients with NYHA II and 75% with NYHA III before vs. 33% with NYHA I, 33% with NYHA II and 33% with NYHA III after CSP, P=0.048) as compared to what was obtained prior to the procedure. A numerical decrease was also found in NT-proBNP levels (4735±2606 ng/ml before CSP vs. 3972±1883 ng/ml after CSP) which did not reach the level of statistical significance (P=0.45). In conclusion, CSP improved both quality of life and LV function in HFrEF patients with RBBB. Our results support the use of CSP in HFrEF patients with QRS width>130msec and RBBB morphology.

Electrocardiographic predictors of left ventricular scar in athletes with right bundle branch block premature ventricular beats.

Right bundle branch block (RBBB) morphology non-sustained ventricular arrhythmias (VAs) have been associated with the presence of non-ischaemic left ventricular scar (NLVS) in athletes. The aim of this cross-sectional study was to identify clinical and electrocardiogram (ECG) predictors of the presence of NLVS in athletes with RBBB VAs. Sixty-four athletes [median age 39 (24-53) years, 79% males] with non-sustained RBBB VAs underwent cardiac magnetic resonance (CMR) with late gadolinium enhancement in order to exclude the presence of a concealed structural heart disease. Thirty-six athletes (56%) showed NLVS at CMR and were assigned to the NLVS positive group, whereas 28 athletes (44%) to the NLVS negative group. Family history of cardiomyopathy and seven different ECG variables were statistically more prevalent in the NLVS positive group. At univariate analysis, seven ECG variables (low QRS voltages in limb leads, negative T waves in inferior leads, negative T waves in limb leads I-aVL, negative T waves in precordial leads V4-V6, presence of left posterior fascicular block, presence of pathologic Q waves, and poor R-wave progression in right precordial leads) proved to be statistically associated with the finding of NLVS; these were grouped together in a score. A score ≥2 was proved to be the optimal cut-off point, identifying NLVS athletes in 92% of cases and showing the best accuracy (86% sensitivity and 100% specificity, respectively). However, a cut-off ≥1 correctly identified all patients with NLVS (absence of false negatives). In athletes with RBBB morphology non-sustained VAs, specific ECG abnormalities at 12-lead ECG can help in detecting subjects with NLVS at CMR.

Abstract 15885: A Masquerading Early Beat Induces Ventricular Fibrillation

Clinical Case: A 51 year old male with a history of hypertension, G6PD deficiency, thrombotic thrombocytopenic purpura, prior stroke, and morbid obesity presented with resuscitated out of hospital VF arrest. Electrolytes and ECG were normal. During his admission, the patient had two VF events that were induced by what appeared to be a short coupled right bundle branch block (RBBB) morphology PVC. He was brought to the electrophysiology lab for PVC ablation and ICD implantation. Baseline rhythm was sinus with what appeared to be both RBBB morphology PVCs and junctional extrasystoles. With both extrasystoles, the His potential preceded the QRS by 50 ms, and atrial activation in the His catheter and coronary sinus catheter was also earlier than the QRS. Activation mapping of the right bundle showed later activation than the His potential. This was all consistent with junctional premature complexes (JPC) with frequent RBBB aberrancy rather than fascicular PVCs. Slow pathway modification was performed to attempt to ablate the JPCs. After multiple ablations along the tricuspid annulus and back to the coronary sinus os that triggered slow junctional beats, the patient’s JPC burden was significantly reduced. An ICD was also implanted. The patient was discharged on flecainide. At 4 month follow up he had not had recurrence. Discussion: Early coupled PVCs are a well-known cause of ventricular fibrillation, but JPCs inducing VF have not been described previously. Placement of a coronary sinus and His catheter helped identify early that this was not simply a fascicular PVC. This case demonstrates the importance of keeping a broad differential diagnosis when starting any EP study. Ablating the slow pathway area can be effective to treat JPCs while preserving native AV conduction as demonstrated in this case.

PO-04-015 BIVENTRICULAR ARRHYTHMOGENIC CARDIOMYOPATHY ASSOCIATED WITH A NOVEL HETEROZYGOUS PLAKOPHILIN-2 EARLY TRUNCATING VARIANT

N/A N/A N/A A 31-year-old male patient suffered from palpitations, which occurred particularly during and shortly after physical activity. The patient was very athletic and took part in marathons. His family history was unremarkable. The electrocardiogram showed T wave inversions in V1-V3 (Figure 1A). During bicycle ergometry monomorphic premature ventricular complexes (PVC) and non-sustained ventricular tachycardia episodes (left-bundle branch block morphology, inferior axis) evolved (Figure 1B, black arrow). Of note, under maximal physical stress a second PVC with a right-bundle branch block morphology occurred (Figure 1B, red arrow) suggesting left ventricular (LV) involvement. Echocardiographic evaluation showed a dilated right ventricle (RV) with reduced systolic function, a subtricuspid aneurysm and multiple sacculations of the RV free wall (Figure 1C-D, white markers). Cardiac magnetic resonance imaging (MRI) confirmed the right ventricular findings (Figure 1E, red arrows). In addition, late gadolinium enhancement and fatty deposits were visible in the LV lateral wall (Figure 1F-G, yellow arrows and blue asterix). Genetic testing was performed using a panel covering 173 genes (Agilent, SureSelectQXTTarget Enrichment) and next generation sequencing (NGS) (Illumina MiSeq). It revealed a novel heterozygous nonsense variant in the plakophilin-2 (PKP2) gene (808C>T p. (Gln270Ter) in exon 3) that causes an early truncation, which was confirmed by Sanger sequencing. It was classified as pathogenic (class V). Cascade screening of the asymptomatic patient’s mother (64-y-old), father (70-y-old) and sister (33-y-old) showed that the patient's father and sister harbored the same PKP-2 variant. Both did not report a history of participating in competitive sports, and thorough cardiac evaluation of these two genotype positive family members showed normal findings. Previous studies have indicated that early truncation of the PKP2 C-terminus likely causes arrhythmogenic right ventricular cardiomyopathy (ARVC) irrespective of transcript position. Although desmosomal and non-desmosomal variants create certain genetic potential for the development of ARVC, exercise has an important role in determining the development, severity, and pattern of phenotypic expression. The fact that the only index patient, as a marathon runner, developed ARVC, suggests that the novel PKP2 variant poses a genetic risk, but is not sufficient for inducing an ARVC phenotype by itself.

Right ventricular cardiac resynchronization therapy in patients with right ventricular conduction delay and heart failure

Right ventricular cardiac resynchronization therapy in patients with right ventricular conduction delay and heart failure

Abstract 13416: Evaluation of Risk Factors for Pacemaker After Tavr Among Patients With a Pre-Existing Right Bundle Branch Block

Background : Pacemaker implantation (PMI) remains a common complication after TAVR. While a pre-existing right bundle branch block (RBBB) is consistently the strongest reported risk factor for PMI, most patients with a RBBB will not require PMI after TAVR. Objective : To identify factors associated with a higher risk of PMI after TAVR among patients with pre-existing RBBB. Methods : We identified all patients at a single institution undergoing first-time TAVR with a balloon-expandable prosthesis without a pre-existing pacemaker or ICD, and pre-existing RBBB (defined as RBBB morphology with QRS >=110ms) from December 2013 to December 2020 (n=219). We evaluated the univariate association for numerous clinical, EKG, imaging, and procedural characteristics with PMI. We included all factors with p=<0.10 in a logistic regression model to assess for independent associations with PMI in the original cohort and 1000 bootstrapped samples. Results : A history of syncope, body mass index, calcium channel blocker use, baseline PR interval, and prosthesis oversizing >16% were associated with PMI on univariate analysis. When included in a logistic regression model, syncope (OR 3.2, 95%CI: 1.1-8.8, p=0.027) and oversizing (OR 3.1, 95% CI: 1.4-6.8, p=0.005) remained independently associated with PMI. These findings were consistent in the bootstrapped samples. Those with both factors (n=4) had a PMI rate of 75% which was higher compared to those with one or neither (43% and 22%, respectively; p<0.001). Conclusion : Among those with pre-existing RBBB, a history of syncope and prosthesis oversizing >16% were independently associated with a higher risk of PMI. These findings warrant external validation.

Risk Stratification for Pacemaker Implantation after Transcatheter Aortic Valve Implantation in Patients with Right Bundle Branch Block.

Background: Permanent pacemaker implantation (PPI) after transcatheter valve implantation (TAVI) is a common complication. Pre-existing right bundle branch block (RBBB) is a strong risk factor for PPI after TAVI. However, a patient-specific approach for risk stratification in this subgroup has not yet been established. Methods: We investigated TAVI patients with pre-existing RBBB to stratify risk factors for PPI and 1-year-mortality by detailed analysis of ECG data, RBBB morphology and degree of calcification in the implantation area assessed by computed tomography angiography. Results: Between 2010 and 2018, 2129 patients underwent TAVI at our institution. Among these, 98 pacemaker-naïve patients with pre-existing RBBB underwent a TAVI procedure. PPI, because of relevant conduction disturbances (CD), was necessary in 43 (43.9%) patients. PPI was more frequently indicated in women vs. men (62.1% vs. 32.8%, p = 0.004) and in men treated with a self-expandable vs. a balloon-expandable valve (58.3% vs. 26.5%, p = 0.035). ECG data (heart rhythm, PQ, QRS, QT) and RBBB morphology had no influence on PPI rate, whereas risk for PPI increased with the degree of calcification in the left septal His-/left bundle branch-area to a 9.375-fold odds for the 3rd tertile of calcification (1.639–53.621; p = 0.012). Overall, 1-year-mortality was comparable among patients with or without PPI (14.0% vs. 16.4%; p = 0.697). Conclusions: Patients with RBBB undergoing TAVI have a high risk of PPI. Among this subgroup, female patients, male patients treated with self-expandable valve types, patients with high load/degree of non-coronary LVOT calcification and patients with atrial fibrillation need enhanced surveillance for CD after procedure.

What Is the Mechanism of This Cardiac Rhythm?

An 80-year-old man with syncope was admitted for evaluation. His clinical examination revealed nothing remarkable. He had no history of heart disease, his blood pressure and electrolyte levels were normal, and he was taking no medications known to cause bradyarrhythmia. Overnight telemetry revealed the electrocardiogram displayed below (Fig. 1).The rhythm strip suggests which diagnosis?D) Junctional escape and intermittent capture beatsThe telemetry strip displayed junctional rhythm, sinus capture after every second junctional rhythm, and right bundle branch block (RBBB) of the sinus-captured beat (Fig. 2). This rare phenomenon, wherein a sinus-captured beat occurs after 2 junctional escape beats, is termed escape-reentry-capture trigeminy.1In isorhythmic atrioventricular (AV) dissociation (Answer A), the atria and ventricles beat at the same rate but are dissociated from each other; here, however, the junctional beat with retrograde conduction to the atria rules out dissociation between competing rhythms. The lack of clear P waves preceding the QRS complexes and the absence of progressive PR prolongation makes Mobitz type I AV block (Answer B) unlikely. Premature ventricular contractions in trigeminy (Answer C) are unlikely because the wide complexes with RBBB morphology are preceded by a P wave, and the QRS pattern simulates a “typical” RBBB. The 2 junctional beats followed by P-wave capture makes premature atrial complexes in trigeminy (Answer E) unlikely.Escape-reentry-capture occurs in the presence of sinus nodal dysfunction (sick sinus syndrome) when the sinus impulse rate is slower than the junctional escape rate. The inverted P wave in Figure 2 (arrows) suggests that the first junctional beat was conducted retrograde to the atria, that the next junctional beat was not, and that the subsequent sinus beat was conducted with an RBBB. This aberrancy may be explained by the “long-short” sequence that prolongs the effective refractory period of the right bundle. Consequently, the sinus rate was apparently slow enough to be captured in a trigeminal pattern. Note also that the junctional rhythm did not affect the sinus rate. The patient was given a permanent pacemaker. This case illustrates the escape-reentry-capture phenomenon in a trigeminal pattern caused by sinus nodal dysfunction.Conflict of Interest Disclosure: NoneFunding/Support: None

671 First-in-man mapping and ablation of ventricular tachycardia using a novel ablation catheter with microelectrodes and thermocouples

Abstract Aims Catheter ablation (CA) is an important therapeutic option for patients with recurrent ventricular tachycardia (VT). Recently, a novel contact-force sensing catheter (QDOT, Biosense Webster) allowing radiofrequency ablation in a temperature-controlled fashion, equipped with microelectrodes and thermocouples has been developed and tested in very-high power short duration CA of atrial fibrillation. As of today, this catheter has never been used for VT ablation. To describe the safety and short-term clinical performance of the novel QDOT catheter for the ablation of recurrent VT/electrical storm. Methods and results Case 1: a 43-year-old male patient with prior anterior myocardial infarction (MI), left ventricular (LV) dysfunction with an apical aneurysm, and recurrent VT episodes was admitted to our hospital for CA of VT. The patient underwent high-density electroanatomical mapping of the left ventricle using a multipolar catheter (PentaRay, Biosense Webster), which showed an extensive apical dense scar region, corresponding to the ventricular aneurysm. When the QDOT catheter was advanced in that region, late/fragmented potentials were detected by microelectrodes as well as by conventional electrodes. During the procedure, a sustained VT with right bundle branch block (RBBB)-inferior axis morphology and transition in V2 could be induced. We recorder diastolic fragmented potentials inside the aneurysm, where the novel catheter previously showed late/fragmented potentials; radiofrequency energy delivery with conventional settings (40 W) in that area led to rapid arrhythmia termination (Figure A). At the end of the procedure, VTs were no more inducible. Case 2: a 79-year-old male patient with prior inferior MI, mild LV dysfunction with a 5 cm × 5 cm × 3 cm aneurysm of the basal-mid inferior wall, and two previous CAs for recurrent VT presented to our hospital for electrical storm due to multiple episodes of slow VT (cycle, 470 ms, RBBB morphology, inferior axis, transition in V6), which were refractory to antiarrhythmic drug treatment. We decided to perform redo CA using the QDOT catheter, which revealed long and fragmented low-amplitude diastolic potentials inside the LV aneurysm (Figure B). VT was rapidly terminated by means of radiofrequency energy delivery with usual settings (40 W) in this region, and was no more inducible afterwards. Conclusions The novel ablation catheter showed favourable manoeuverability in the ventricle, while also allowing a precise characterization of the tachycardia circuitry and of the arrhythmogenic myocardial substrate, which was enhanced by the availability of microelectrodes. We believe that this preliminary experience may pave the way for further assessments of this new technology in the so far unexplored ventricular milieu.

The Implantation of Left Bundle Branch Area Pacing in Patients with and without Bundle Branch Block.

To investigate the clinical safety and electrocardiogram (ECG) characteristics in patients with left bundle branch area pacing (LBBAP). Retrospective study. Department of Cardiology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, China, from May 2018 to January 2020. Patients scheduled for Left Bandle Branch Area Pacing (LBBAP), who were admitted due to bradycardia, had been prospectively recruited. The Medtronic 3830 pacing lead was first placed at the right ventricular (RV) side of the interventricular septum (IVS) with pacing parameters (pacing threshold, pacing impedance and sensing amplitude) and ECG characteristics [QRS morphology, paced QRS duration and stimulus to peak left ventricular activation time (Sti-LVAT)] measured, which was called the right ventricular septum pacing group (RVSP). Then the pacing lead was screwed towards the left ventricular (LV) side of the IVS; and the corresponding parameters and ECG characteristics were assessed, which was calledLBBAPgroup. RVSP caused left bundle block (LBBB) morphology on ECG, while pacing at left bundle area led to right bundle branch block (RBBB) morphology, without remarkable difference in pacing threshold and pacing impedance. The sensing amplitude during LBBAP was significantly higher compared with RVSP (p <0.05). QRS duration and Sti-LVAT were significantly shorter when paced on LBBAP compared with RVSP (p <0.05). Patients with LBBB morphology in intrinsic rhythm showed the greatest reduction in paced QRS duration and Sti-LVAT compared to patients with RBBB morphology or no bundle branch block morphology (p <0.001). There were no complications during pacemaker implantation and no adverse events observed during follow-up. The pacing parameters remained stable during the follow-up (9.2 ± 3.7 months). Compared with pacing on RVSP, patients with LBBAP showed RBBB morphology with significantly reduced QRS duration and LV Sti-LVAT under similar pacing parameters. LBBAP is safe and feasible and may be a promising strategy for patients with LBBB morphology who are indicated for ventricular pacing. Key Words: Physiological pacing, Left bundle branch pacing, Right ventricular pacing, Left bundle branch block, Pacemaker.

Right Bundle Branch Block Morphology After Right Ventricular Endocardial Pacing – When Should a Cardiologist Begin to Worry ?

Even though the left bundle branch block (LBBB) morphology in the surface electrocardiogram (ECG) is expected after right ventricular endocardial pacing, the right bundle branch block (RBBB) morphology may be paradoxically seen in around 8 to 10% of patients. The paced RBBB morphology should be given special attention in terms of safe RV pacing or septal and free wall perforation. Simple techniques such as moving the leads V1-2 to one interspace lower than standard (Klein maneuver) and combining frontal QRS axis between -30° to -90°, precordial transition point at or within V3, and absence of S wave in lead I as an algorithmic approach may correctly identify the pacemaker lead in right ventricle with high sensitivity, specificity, and positive predictive value.

Right bundle branch block ventricular tachycardia in arrhythmogenic right ventricular cardiomyopathy more commonly originates from the right ventricle: Criteria for identifying chamber of origin

Right bundle branch block (RBBB) ventricular tachycardia (VT) morphology is a criterion for left ventricular (LV) involvement in arrhythmogenic right ventricular cardiomyopathy (ARVC). The purpose of this study was to determine the frequency and chamber of origin of RBBB VT in patients with ARVC and VT. We studied 110 consecutive patients with VT who met the diagnostic International Task Force criteria for ARVC and underwent VT mapping/ablation. Patients with ≥1 RBBB VT were identified. Right ventricular (RV) origin of the RBBB VT was determined based on standard mapping criteria and elimination with ablation. Nineteen patients (17%) had 26 RBBB VTs. Eleven of these 19 patients (58%) had 16 RBBB VTs from the RV, and 9 patients (47%) had 10 RBBB VTs originating from the LV, with 1 patient demonstrating both. RBBB VT from RV most commonly (13/16 RBBB VTs) had an early precordial QRS transition (V2 or V3), with superiorly and typically leftward directed frontal plane axis, consistent with exit from dilated RV adjacent to inferior LV septum, whereas all 10 VTs from LV had RBBB morphology with positive R waves to V5 or V6 and rightward axis in 6 VTs characteristic of basal lateral origin. In patients with ARVC and VT presenting for VT ablation, RBBB VT occurs in 17% of cases, with most RBBB VTs (62%) originating from the RV and not indicative of LV origin. Precordial R-wave transition and frontal plane axis can be used to identify the anticipated chamber of origin of RBBB VT.

The characteristics of the electrocardiogram and the intracardiac electrogram in left bundle branch pacing.

Left bundle branch pacing (LBBP) has recently been reported to maintain left ventricular electrical synchrony with a low and stable threshold. However, the electrocardiogram (ECG) definitions of LBBP have not been well established. We report four cases to show the characteristics of the ECG and the intracardiac electrogram (EGM) in LBBP. Four patients, two with an atrioventricular block (AVB) and two with left bundle branch block (LBBB), were included in the study. LBBP was performed and the ECGs and EGMs were collected and compared at different pacing outputs. Selective LBBP (S-LBBP) was defined as only capturing the LBB with a typical RBBB morphology and a discrete component between the pacing stimulus and ventricular activation in the EGMs. While nonselective LBBP (NS-LBBP) captured both the LBB and the local myocardium, resulting in a narrow right bundle branch block (RBBB) morphology without the discrete component. The left bundle branch (LBB) potential was recorded in two cases during narrow QRS complex or LBBB correction by selective His bundle pacing and SLBBP (n = 3) was achieved. A constant and shortest stimulus to left ventricular activation time (LVAT) in LBBP was obtained at different pacing outputs. The ECG and EGM characteristics of LBBP can be summarized as: 1) RBBB pattern; 2) usually with the LBB potential; 3) SLBBP with specific ECG changes and a discrete component in EGM; and 4) with a constant and shortest stimulus to LVAT at different pacing outputs. Further studies are necessary to confirm these observations.

ECG morphology of premature ventricular contractions predicts the presence of myocardial fibrotic substrate on cardiac magnetic resonance imaging in patients undergoing ablation.

The most likely origin of premature ventricular contractions (PVCs) may be deduced from surface electrocardiogram (ECG) analysis while planning an electrophysiological study (EPS). Apart from purely benign forms of increased ventricular ectopy, myocardial substrate (e.g., regional fibrosis) may be present in certain cases, which will significantly impact the ablation approach. Cardiac magnetic resonance (CMR) imaging can reliably identify fibrotic target lesions and, hence, may assist in adequate patient selection and procedural planning. We analyzed 101 patients (59% males, mean age 57.15 ± 15.5 years, mean PVC count 19,801 ± 14,021 per 24 hours) referred for ablation of PVCs. The CMR (1.5T, Philips Ingenia, Best, The Netherlands) protocol included cine and three-dimensional-delayed enhancement imaging using standard cardiac geometries. On surface, ECG right bundle branch block (RBBB) morphology was present in 43% of patients. Twenty-one patients showed the fibrotic substrate on CMR. On univariate analysis, both RBBB morphology (P<0.001) and presence of multiple PVC morphologies (≥2) significantly predicted the presence of fibrotic substrate (P=0.01), which various baseline characteristics including left ventricular ejection fraction (45.7 ± 12.6% vs. 50.6 ± 11.0%, P=0.08) failed to do. CMR-identified fibrosis was associated with the site of origin of the clinical PVCs during EPS and was successfully treated by radiofrequency ablation in 93% (PVC reduction>95%). In patients with RBBB morphology and/or multiple PVC patterns, CMR imaging before ablation may be helpful due to the increased prevalence of fibrotic lesions with regard to patient stratification and periprocedural management.

To the Editor—Supernormal conduction or masked bundle branch block?

Carbone et al present an interesting case report in which both right bundle branch block (RBBB) and left bundle branch block (LBBB) aberrancy are seen during different initiations of an atrial tachycardia. They postulate that this is caused by phase 3–dependent block in the left bundle branch (LBB; long-short coupling interval) resulting in RBBB aberration with a prolonged PR interval, followed by intermittent supernormal conduction over the right bundle branch (RBB) resulting in LBBB aberration and a nearnormal PR interval. The existence of true supernormal conduction in the intact human heart has not been shown conclusively, however, and before invoking this phenomenon, alternative physiological mechanisms can be considered. In Figure 3, impulse 1 conducts with an LBBB morphology and a PR interval of 220 ms. Carbone et al propose that conduction is entirely blocked in the LBB at this time, when it may simply be significantly delayed by the premature atrial impulse. Impulse 2 (Figure 3) occurs slightly earlier and may block completely in the RBB and unmask the slowly conducting LBB, leading to a longer PR interval (340 ms) and an RBBB morphology. The principle of supernormal conduction does not need to be invoked because there is delayed conduction in the LBB with both impulse 1 and 2; it is simply masked by greater delay in the RBB after

A change in QRS morphology in right ventricular apical pacing: is it a red flag sign?

A 74-year-old man with symptomatic complete heart block underwent right ventricular apical permanent pacemaker implantation. The postoperative ECG showed, as expected, completely paced left bundle branch block QRS morphology. However,...

Electrocardiographic features and prevalence of bilateral bundle-branch delay.

Definitive diagnosis of bilateral bundle-branch delay/block may be made when catheter-induced right bundle-branch block (RBBB) develops in patients with baseline left bundle-branch (LBB) block. We hypothesized that a RBBB pattern with absent S waves in leads I and aVL will identify bilateral bundle-branch delay/block. Fifty patients developing transient RBBB pattern in lead V1 during right heart catheterization were studied. Patients were grouped according to whether the baseline ECG demonstrated a normal QRS, left fascicular blocks, or LBB block pattern. The RBBB morphologies in each group were compared. The prevalence of bilateral bundle-branch delay/block pattern was examined in our hospital ECG database. All patients with baseline normal QRS complexes (n=30) or left fascicular blocks (4 anterior, 5 posterior) developed a typical RBBB pattern. Among the 11 patients with a baseline LBB block pattern, 7 developed an atypical RBBB pattern with absent S waves in leads I and aVL and the remaining 4 demonstrated a typical RBBB. The absence of S waves in leads I and aVL during RBBB was 100% specific and 64% sensitive for the presence of pre-existing LBB block. Among the consecutive 2253 hospitalized patients with RBBB, 34 (1.5%) had the bilateral bundle-branch delay/block pattern. An ECG pattern of RBBB in lead V1 with absent S wave in leads I and aVL indicates concomitant LBB delay. Pure RBBB and bifascicular blocks are associated with S waves in leads I and aVL.

Does cardiac resynchronization therapy benefit patients with right bundle branch block: cardiac resynchronization therapy has a role in patients with right bundle branch block.

Does cardiac resynchronization therapy benefit patients with right bundle branch block: cardiac resynchronization therapy has a role in patients with right bundle branch block.

ECG Response: January 28, 2014

HomeCirculationVol. 129, No. 4ECG Response: January 28, 2014 Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBECG Response: January 28, 2014 Originally published28 Jan 2014https://doi.org/10.1161/CIRCULATIONAHA.113.008340Circulation. 2014;129:532–533IntroductionECG Challenge: A 64-year-old woman with a history of hypertension treated with a β-blocker and angiotensin-converting enzyme inhibitor presents to her primary care physician for a routine physical examination. She is asymptomatic, although she does state that she has intermittently felt her pulse and noted it to be irregular.Download figureDownload PowerPointThe rhythm is irregular, but there is a repeating pattern of long (↔) and short RR intervals (└┘). Therefore the rhythm is regularly irregular, with an average rate of 90 bpm. There appears to be group beating with 3 QRS complexes (triplet) and then a pause. There is no organized P wave before any of the QRS complexes, but there are rapid and regular atrial waveforms seen in leads II, III, and aVF (^). They are uniform in morphology, amplitude, and interval and have a rate of 300 bpm. They are negative in leads II and aVF. These are atrial flutter waves. As the atrial flutter waves are negative in leads II and aVF, this is typical (or isthmus dependent) atrial flutter. The regularly irregular rhythm is attributable to varying degrees of conduction through the AV node (ie, 2:1 alternating with 4:1 AV block [or conduction]). There are 2 different QRS complex morphologies noted. The first and third QRS complexes of the triplet (▼) are the same. They have a normal duration (0.08 sec), morphology, and axis between 0° and +90° (positive QRS complex in lead I and aVF). There are nonspecific ST-T wave changes in leads I, aVL, and V5 through V6. The QT/QTc intervals are normal (320/390 ms). The second or middle QRS complex of the triplet (+) has a prolonged duration (0.14 sec) and a right bundle-branch block (RBBB) morphology with an RSR in lead V1 and broad terminal S waves in leads I and V5 through V6. Although it might be considered that the RBBB is rate related, it can be seen that the RR interval between the first and second QRS complex (that has a RBBB morphology) is the same as the interval between the second and third QRS complex (└┘). Therefore, if this was a rate related RBBB both the second and third QRS complexes of the triplet would have a RBBB. However, only the middle QRS complex has the RBBB, and it is noted that it follows a long-short RR interval. Therefore, the RBBB aberrancy is the result of an Ashman’s phenomenon that is attributable to rate-related changes in His-Purkinje refractoriness, which are normal and physiological. When there is a slowing of the heart rate (long RR interval) His-Purkinje refractoriness increases, whereas with a faster heart rate (short RR interval) His-Purkinje refractoriness shortens. When there is an abrupt change in heart rate (ie, going from slow [long RR interval] to faster [short RR interval]), refractoriness may not adjust immediately and hence 1 or several QRS complexes may be conducted with a RBBB. Most often, the aberrated complex will have a RBBB as the refractoriness of the right bundle is slightly longer than that of the left bundle.Please go to the journal’s Facebook page for more ECG Challenges: http://goo.gl/cm4K7. Challenges are posted on Tuesdays, and Responses are posted on Wednesdays.FootnotesCorrespondence to Philip J. Podrid, MD, West Roxbury VA Hospital, Section of Cardiology, 1400 VFW Parkway, West Roxbury, MA 02132. E-mail [email protected] Previous Back to top Next FiguresReferencesRelatedDetails January 28, 2014Vol 129, Issue 4 Advertisement Article InformationMetrics © 2014 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.113.008340PMID: 24470475 Originally publishedJanuary 28, 2014 PDF download Advertisement SubjectsElectrocardiology (ECG)

Long-Term Effect of Continuing Sports Activity in Competitive Athletes With Frequent Ventricular Premature Complexes and Apparently Normal Heart

The long-term outcome of athletes with frequent ventricular premature complexes (VPCs) and apparently normal heart has not been fully clarified. To evaluate the clinical and prognostic significance of VPCs and the influence of continuing sports activity during follow-up, we studied 120 healthy athletes (96 men; median age 16 years) in whom frequent VPCs (>100 VPCs/24 hours) were discovered by chance during preparticipation screening. All athletes were followed up for a median of 84 months. During follow-up, 96 underwent serial 24-hour Holter recording and 62 underwent serial echocardiography. The median number of VPCs/24 hours on basal Holter was 3,760. During follow-up, 81 athletes continued sports activity, whereas 39 did not. No athlete died or developed overt heart disease. The median number of VPCs/24 hours decreased in both athletes who continued sports activity and those who did not (from 3,805 to 1,124, p <0.0001 and from 5,787 to 1,298, p <0.0001, respectively). During follow-up, left ventricular ejection fraction slightly decreased to <55% in 9 of 62 athletes who, in respect to the remaining 53, had more VPCs/24 hours both in the basal state (12,000 vs 3,880) and during follow-up (10,702 vs 1,368), and a longer follow-up (95 vs 36 months). In conclusion, (1) frequent VPCs in athletes without heart disease have a long-term benign prognostic significance, (2) sporting activity does not modify this benign outcome, (3) during follow-up, the burden of VPCs decreases whether or not subjects continue sports activity, and (4) in 14.5% of athletes, ejection fraction slightly decreases over time.