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Discordant vs. concordant left bundle branch block: A potential clinical significance
Discordant Vs. Concordant Left Bundle Branch Block: A Potential Clinical Significance Jalkh Khalil, Abi Saleh Bernard, Khoury Maurice, Yousef Zaheer, Refaat Marwan, Rebeiz Abdallah, Alam Samir, Skouri Hadi PII: DOI: Reference:
S0022-0736(15)00288-5 doi: 10.1016/j.jelectrocard.2015.08.031 YJELC 52128
To appear in:
Journal of Electrocardiology
Please cite this article as: Khalil Jalkh, Bernard Abi Saleh, Maurice Khoury, Zaheer Yousef, Marwan Refaat, Abdallah Rebeiz, Samir Alam, Hadi Skouri, Discordant Vs. Concordant Left Bundle Branch Block: A Potential Clinical Significance, Journal of Electrocardiology (2015), doi: 10.1016/j.jelectrocard.2015.08.031
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Discordant Vs. Concordant Left Bundle Branch Block:
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A Potential Clinical Significance
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Jalkh,Khalil¹^; Abi Saleh,Bernard¹^;Khoury,Maurice¹;; Yousef,Zaheer²;Refaat, Marwan¹;Rebeiz,Abdallah¹;Alam,Samir¹;Skouri,Hadi¹*
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¹ American University of Beirut Medical Center; Lebanon ² Cardiff Hospital; England ^ Co- first authors * Corresponding Author: Contacts: Email: [email protected]; Work Phone: +961-1-374374 Office extension: 1-5309; Fax: +9611370814 Abstract:
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Aim:
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LBBB in heart failure patients has prognostic significance. Subtypes of LBBB (concordant and discordant) have not been considered when considering management. The aim of this study is to explore the clinical difference between the two subtypes.
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Methods:
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216 patients with LBBB were included and categorized into concordant (LBBBC) and discordant (LBBBD) groups.
Of the 216 patients (age 69.13 ±11.7; 56% male 44% female), 133 (61.5%) were LBBBD and 83 (38.5%) were LBBBC. LBBBD patients presented with lower LVEF (mean 36% vs 51%; P<0.001), wider QRS (mean 160ms vs 151ms; 2 2 P<0.001), larger LA (mean 45 cm vs 40 cm ; P<0.001), moderate to severe mitral and tricuspid regurgitation (17% vs 3%; P<0.05, 10% vs 1%; P<0.05 respectively), CKD (41% vs 18%; P<0.001), COPD (4.6% vs 0%; P<0.01), CAD (67% vs 36%; P<0.001), and CABG (39% vs 16%; P<0.001). Conclusion: LBBBD is significantly associated with worse cardiac function and clinical characteristics.
Keywords: Heart failure, Left bundle branch block, CRT, Dyssynchrony.
ACCEPTED MANUSCRIPT Introduction:
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Defects in left ventricular function due to abnormal activation patterns have been well-documented. In 1974, Abbassi et. al described the paradoxical movement of the interventricular septum in left bundle branch block (LBBB) (1). Later, Van Oosterhout et. al described the effect of asynchronous electrical activation of the ventricles on workload differences that may possibly result in ventricular dilation or hypertrophy (2). The prevalence of LBBB strongly correlates with age and the presence of cardiovascular disease. LBBB usually indicates an underlying progressive degenerative disease of the ventricular myocardium (3, 4). In HF patients the prevalence of LBBB st reported to be approximately 11-25%(5-7). Since the beginning of the 21 century, Heart Failure (HF) has become a pandemic. Despite the progress in the pharmacological management, hospitalization rates and mortality are still high. In addition most of HF patients remain symptomatic imposing significant socioeconomic burden. LBBB and QRS duration have been linked to HF as their presence increases the risk of mortality and disease progression (8). This has led to the emergence of an appealing intervention that corrects the mechanical left ventricular dyssynchrony due to the presence of LBBB through changing the sequence of electrical activation (9-11). Cardiac resynchronization therapy (CRT) as a means of optimizing synchrony has shown to have great impact on HF patient’s symptoms, re-hospitalization rates, mortality, and affected reverse remodeling and was successful in 70% of patients leaving around 30% failure rate (9, 10, 12). The significant failure led physicians to regain interest in LBBB diagnostic criteria and different morphological patterns (13, 14). One of the old definitions of LBBB has looked at two different subtypes (15) and these subtypes (Concordant vs. Discordant) have been revisited lately and proved to be clinically different with potential future clinical implications (13). The aim of this study is to determine the prevalence of the two subtypes while screening for LBBB with the new criteria, assess whether there exists a correlation between the two different morphological subtypes and various clinical scenarios or categories of cardiac diseases, and determine whether it can provide us with any potential prognostic implications especially HF- related.
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Design and Methods: Patient Population:
LBBB diagnosis:
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This is a retrospective single center study. All patients more than 18 years of age with a LBBB on an ECG done at the American University of Beirut Medical center (AUBMC) and stored in the ECG department from April 2004 till December 2012 were included. Patients were excluded if they have paced rhythm, had an acute coronary syndrome within the last 6 months, had inter-operator variability in ECG diagnosis, and had missing clinical and echocardiographic data from the medical record.
LBBB was diagnosed during the above mentioned period using the old criteria: QRS interval >120 ms; slurred/notched wide and predominant R waves in leads I, aVL, V5, and V6; slurred/notched and broad S waves in V1 and V2 with absent or small R waves; mid-conduction delay defined as notching or a plateau in the mid-QRS wave; ventricular activation time >50 ms at the onset of the QRS interval; M-shaped QRS variants with occasionally wide R waves in V5 and V6; no initial Q wave over the left precordium; and absence of pre-excitation (16). These patients’ ECGs were further analyzed by applying the new criteria suggested by Strauss et. al (14) that consist of: QRS duration 140 ms (men) or 130 ms (women) or wider, QS or rS in leads V1 and V2, and mid-QRS notching or slurring in 2 of leads V1, V2, V5, V6, I, and aVL. Applying the new criteria has yielded to further classification of the LBBB into two categories: True LBBB as per the new (Strauss) definition and a category labeled as non-specific intra ventricular conduction delays (IVCDs) for ECGs that did not comply with the new definition nor with the definition of RBBB (QRS duration greater than or equal to 120 ms in adults, rsr′, rsR′, or rSR′ in leads V1 or V2; S wave of greater duration than R wave or greater than 40 ms in leads I and V6 in adults; normal R peak time in leads V5 and V6 but greater than 50 ms in lead V1 (16)).
ACCEPTED MANUSCRIPT LBBB were further subdivided into two subtypes: concordant LBBB ( LBBBC ) where the ECGs have their T-wave orientation concordant with QRS complex in leads I, V5 and V6and discordant LBBB ( LBBB D ) where the ECGs have their T-wave orientation discordant with the QRS complex in leads I, V5, and V6 (See fig. 1), (see fig 2.)(15).
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Data Collection:
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An extensive chart review was performed with data collection on demographics, cardiac risk factors, comorbidities, cardiac interventional data, electrocardiographic data including rhythm and QRS duration, and echocardiographic data. Electrographic recordings and echocardiographic data were first screened by a cardiology fellow and then independently re-examined by an electrophysiology specialist and a heart failure specialist. Echocardiographic parameters were measured in the AUBMC core laboratory. Left ventricular volumes were measured by Simpson’s method of discs in the apical 4 and 2 chamber views and averaged. Left ventricular ejection fractions were calculated according to standard methods. Left atrial volumes were measured using Simpson’s method of discs in the apical 4 and 2 chamber views and averaged. Valvular abnormalities and its grades as well as assessment of systolic pulmonary artery pressure were collected too. The study protocol was approved by the Institutional Review Board at AUBMC.
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Statistical Methods:
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Statistical analysis was performed using IBM’s Statistical Package for the Social Sciences (SPSS) version 20.0. Continuous variables are presented as mean +/- standard deviation. Categorical data are presented as percentages. Comparison between categorical variables has been performed using Chi-squared test. Comparison between continuous variables has been performed using Bonferroni’s t-test. A two tailed P value < 0.05 was considered as statistically significant.
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Results:
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From April 2004 till December 2012, 394 patients with LBBB as ECG diagnosis were initially included in the study. Complete files were only available for 283 out of the 394 initial patients. Of the 283 patients, 11 were excluded because there was inter-operator variability in ECG interpretation. Out of the eleven patients, three exhibited change from discordant to concordant in a period of less than 6 months. 272 patients were left with complete files and agreed upon ECGs for the study analysis. Of the 272 patients, 56 (20.5%) showed non-specific IVCD and 216 (79.5%) showed LBBB on ECG. Patients’ demographic, clinical, electrocardiographic and echocardiographic characteristics for LBBB and IVCD groups are shown in table 1. There were no significant findings when comparing those with a LBBB pattern to those with non-specific IVCD with the exception of CKD which had been more prevalent in the IVCD population (p=0.01). Of the 216 patients, 83 (38.4%) showed a concordant pattern and 133 (61.6%) showed a discordant pattern. LBBB subtype patients’ demographic, clinical, electrocardiographic and echocardiographic characteristics are reported in table 2. Patients with LBBBD were more often male (P<0.01), had a higher prevalence of COPD (P=0.01), CKD (P<0.01), PVD (p=0.04), ischemic heart disease (P<0.01), more often had underwent CABG (p<0.01), showed worse LVEF (p<0.01), higher incidence of mitral stenosis (p=0.024),higher incidence of significant valvular regurgitation: moderate to severe mitral regurgitation (17% vs 3%; P<0.05) and moderate to severe tricuspid regurgitation (10% vs 1%; P<0.05), larger LVEDD (p<0.01), and higher PASP (P=0.008). No differences were observed concerning ICD. CRTD were more implanted in the discordant group. Gender difference in the distribution of discordant pattern may have been due to the higher prevalence of males with ischemic heart disease in our study and thus might have been a confounding factor. Ischemic heart disease can be associated with a more diseased conduction system causing the LBBB D pattern.
ACCEPTED MANUSCRIPT Discussion:
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Left bundle branch block (LBBB) is a relatively common pattern seen on the electrocardiogram (ECG) and is increasingly recognized for its profound hemodynamic effects on the heart. Several epidemiologic studies have been conducted to establish the prevalence of LBBB in the general population and it was reported to fall in the range of 0.1–0.8% based on variations in the population size and sampling criteria (17-21). Moreover, it was shown that the prevalence strongly correlates with age and with the presence of cardiovascular disease (3, 22). Isolated LBBB occurring in the setting of young, clinically healthy men conveys a benign prognosis (20). However, in older patients, LBBB usually indicates an underlying progressive degenerative disease of the ventricular myocardium. As for the prevalence of LBBB among heart failure population varied and has been reported to range from 11% to 25% (6, 7). Newby et al. reported that the incidence of LBBB in acute myocardial infarction requiring thrombolytic therapy was 7% (23). After coronary bypass grafting (CABG) or valvular surgery the incidence of developing new LBBB ranged between 2 - 4 % (24, 25).
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LBBB is known to impair the mechanical function of the left ventricle secondary to asynchronous myocardial activation, which sequentially, may trigger ventricular remodeling. Thus, it inversely affects the perfusion, systolic/diastolic performance and hemodynamics of the heart (26-28). This is further emphasized by Zannad et al. who proposed the following sequence for the development of HF in patients with LBBB: intra-ventricular asynchrony–reduced pump function–neurohormonal activation–asymmetric hypertrophy–dilatation (5).
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One of the earliest studies to demonstrate a clear association between LBBB and cardiovascular diseases was the Framingham Heart study which concluded that subjects with acquired LBBB were more likely to have or to subsequently develop advanced cardiovascular manifestations (such as hypertension and ischemic heart disease), and exhibit increased cardiovascular morbidity and mortality with a 50 % ten-year mortality associated with new LBBB (22). The presence of LBBB is considered an unfavorable prognostic marker in the setting of acute/chronic HF, coronary artery disease (CAD) and myocardial infarction (MI).
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In heart failure patients, the presence of ventricular dyssynchrony further depresses left ventricular function by placing it at an additional mechanical disadvantage. This dyssynchrony has been shown to hasten disease progression in heart failure. The more pronounced the dyssynchrony as evidenced by a wider QRS complex the more the mortality in patients with HF (29-31). Based on the mentioned data, it became conceivable that patients with LV dysfunction and dyssynchronized ventricular activation would benefit from biventricular pacing that attempt to restore synchronous contraction to maintain optimal atrial–ventricular (AV) synchrony and prolong the time available for myocardial perfusion. This idea was tested in a case report which proved efficacy and drove further studies in the field (32). Cardiac resynchronization therapy (CRT) was shown to improve symptoms, exercise capacity, quality of life, LVEF, survival, and decreased hospitalizations in patients with advanced HF (NYHA class III or IV with LVEF <35 %. The wider the QRS complex, the more the dysynchrony and the more the CRT benefit (33). The most recent HF guidelines recommended CRT in HF patients with LBBB and QRS duration ≥150 ms as class Ia indication and QRS between 120-150ms as a class Ib indication (34, 35). LBBB pattern has been further classified since late 1950s into two morphological variants: “Homophasic” (concordant: LBBBC) and “Heterophasic” (discordant: LBBBD) based on the associated T wave direction in leads I, V5 and V6 (15). LBBB with positive T waves is considered LBBBC, whereas, LBBB with negative T waves is considered LBBBD. Padeletti et al. recently assessed the prevalence and clinical significance of homophasic and heterophasic LBBB in a prospective cohort of 897 HF patients of which 26% had LBBB. Results revealed that the prevalence of LBBBD was greater than that of LBBBC, with percentages of 69 % and 31% respectively. Regarding the clinical
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characteristics of patients with LBBBD, they were indicative of greater severity of the disease since these patients were older, and had a worse renal function. They also had worse left ventricular ejection fraction, higher left vetricular end-diastolic/end-systolic volumes and enhanced neurohormonal activation secondary to higher levels of BNP, NT-proBNP, norepinephrine, and elevated renin activity. Moreoever, the results demonstrated that LBBBD in systolic HF is associated with a worse prognosis secondary to the enhanced neurohormonal activation as compared to cLBBB. Thus, they suggested that the difference between LBBBC and LBBBD could be used as a predictive tool for the composite endpoint of sudden death and life-threatening ventricular tachyarrhythmias and could be a useful low-cost tool in the clinical assessment and prognostic stratification of HF patients (13).
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Our study has revealed that 20% of patients labeled with LBBB according to the old criteria are no more diagnosed with LBBB when the new strict Strauss criteria were applied. Strauss criteria were suggested after several studies has shown that around one third of patients are mislabeled as LBBB which may be affecting response to CRT therapy (36). This will lead to multiple unanswered questions. Is there a difference in the natural history and clinical characteristics of this group of patients compared to the LBBB group? Are they at an increased risk of arrhythmias, lower LVEF and would they respond differently to CRT? In our study there was no difference between IVCD and LBBB except presence of CKD was more prevalent in the IVCD group. Re-analysis of the previous published trials according to the new LBBB criteria would better define the IVCD group, its natural history and its clinical characteristics. As well, new larger prospective trials are needed to look at the clinical, echocardiograpghic and mortality data for the IVCD group in comparison to the revised LBBB group.
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Second, there is a significant difference between the two coexisting subtypes of LBBB. In our study, we confirmed the presence of two distinct LBBB patterns and assigned potential clinical significance to each subtype. A discordant T-wave in leads I, V5 and V6 in a left bundle branch block patients was associated with a lower LVEF, larger LA size, larger end diastolic diameter, wider QRS complex, ischemic heart disease, and chronic kidney disease. These results were consistent with Padeletti et. al’s findings who analyzed systolic heart failure patients (13). Moreover, previous published studies on CRT had never been analyzed by the two different subtypes. This brings us to the conclusion that there may be different clinical implications in the two subtypes of LBBB. Larger trials are needed to determine and confirm this difference on several levels.
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The two subtypes differ in their T wave morphology. Our current understanding of T-wave morphology is explained by a model proposing the presence of a different trans-mural repolarization sequence within the ventricular wall where the epicardium recovers before the endocardium (37) . A disruption in the endocardium may result in further delay or abolishment of repolarization which may cause the T-wave to invert. This model may explain the results encountered in our study. Elements that may cause endomyocardial damage such as those seen in ischemic heart disease, dilated cardiomyopathy, higher LV filling volumes and pressures with significant LV remodeling. These may be manifested by slowing of conduction and subsequent QRS widening that have had their T-wave pattern inverted. Moreover, follow up studies should determine if there exist any change from one subtype to the other and whether this change can imply prognostic evidence or response/failure to therapy. In our study 3 patients exhibited change from discordant to concordant in a period of less than 6 months and this change could be related to optimization of medical management or improvement in clinical and echocardiographic findings. That warrants further investigation on a broader aspect. This study has several limitations that include its design as a retrospective study with a large number of incomplete charts which reduced effective number of the study population. There is a low number of CRT implantation despite recommendations due to unavailability of financial coverage in our country for this type of intervention. Data on
ACCEPTED MANUSCRIPT mortality was not available on most of these patients due to unavailability on means to follow-up in a significant portion of patients. Despite all these limitations, this study showed significant difference between two subtypes of LBBB that may hold future clinical implications.
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In conclusion, LBBBD is associated with more comorbidities and worse cardiac characteristics when compared to LBBBC. This difference may hold therapeutic and prognostic implications especially in LBBB HF population. Further studies are needed in this regard to better characterize the two subtypes.
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26. Grines CL, Bashore TM, Boudoulas H, Olson S, Shafer P, Wooley CF. Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony. Circulation. 1989 Apr;79(4):845-53. PubMed PMID: 2924415. Epub 1989/04/01. eng. 27. Ozdemir K, Altunkeser BB, Danis G, Ozdemir A, Uluca Y, Tokac M, Telli HH, Gok H. Effect of the isolated left bundle branch block on systolic and diastolic functions of left ventricle. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography. 2001 Nov;14(11):1075-9. PubMed PMID: 11696831. Epub 2001/11/07. eng. 28. Lee SJ, McCulloch C, Mangat I, Foster E, De Marco T, Saxon LA. Isolated bundle branch block and left ventricular dysfunction. Journal of cardiac failure. 2003 Apr;9(2):87-92. PubMed PMID: 12751128. Epub 2003/05/17. eng. 29. Askenazi J, Alexander JH, Koenigsberg DI, Belic N, Lesch M. Alteration of left ventricular performance by left bundle branch block simulated with atrioventricular sequential pacing. The American journal of cardiology. 1984 Jan 1;53(1):99-104. PubMed PMID: 6691284. Epub 1984/01/01. eng. 30. Xiao HB, Lee CH, Gibson DG. Effect of left bundle branch block on diastolic function in dilated cardiomyopathy. British heart journal. 1991 Dec;66(6):443-7. PubMed PMID: 1772710. Pubmed Central PMCID: PMC1024819. Epub 1991/12/01. eng. 31. Mann DL. Mechanisms and models in heart failure: A combinatorial approach. Circulation. 1999 Aug 31;100(9):999-1008. PubMed PMID: 10468532. Epub 1999/09/01. eng. 32. Cazeau S, Ritter P, Bakdach S, Lazarus A, Limousin M, Henao L, Mundler O, Daubert JC, Mugica J. Four chamber pacing in dilated cardiomyopathy. Pacing and clinical electrophysiology : PACE. 1994 Nov;17(11 Pt 2):1974-9. PubMed PMID: 7845801. Epub 1994/11/01. eng. 33. Gold MR, Thebault C, Linde C, Abraham WT, Gerritse B, Ghio S, St John Sutton M, Daubert JC. Effect of QRS duration and morphology on cardiac resynchronization therapy outcomes in mild heart failure: results from the Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) study. Circulation. 2012 Aug 14;126(7):822-9. PubMed PMID: 22781424. English. 34. Brignole M, Auricchio A, Baron-Esquivias G, Bordachar P, Boriani G, Breithardt OA, Cleland J, Deharo JC, Delgado V, Elliott PM, Gorenek B, Israel CW, Leclercq C, Linde C, Mont L, Padeletti L, Sutton R, Vardas PE, Zamorano JL, Achenbach S, Baumgartner H, Bax JJ, Bueno H, Dean V, Deaton C, Erol C, Fagard R, Ferrari R, Hasdai D, Hoes AW, Kirchhof P, Knuuti J, Kolh P, Lancellotti P, Linhart A, Nihoyannopoulos P, Piepoli MF, Ponikowski P, Sirnes PA, Tamargo JL, Tendera M, Torbicki A, Wijns W, Windecker S, Kirchhof P, Blomstrom-Lundqvist C, Badano LP, Aliyev F, Bansch D, Baumgartner H, Bsata W, Buser P, Charron P, Daubert JC, Dobreanu D, Faerestrand S, Hasdai D, Hoes AW, Le Heuzey JY, Mavrakis H, McDonagh T, Merino JL, Nawar MM, Nielsen JC, Pieske B, Poposka L, Ruschitzka F, Tendera M, Van Gelder IC, Wilson CM. 2013 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy: the Task Force on cardiac pacing and resynchronization therapy of the European Society of Cardiology (ESC). Developed in collaboration with the European Heart Rhythm Association (EHRA). European heart journal. 2013 Aug;34(29):2281-329. PubMed PMID: 23801822. Epub 2013/06/27. eng. 35. McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Bohm M, Dickstein K, Falk V, Filippatos G, Fonseca C, Gomez-Sanchez MA, Jaarsma T, Kober L, Lip GY, Maggioni AP, Parkhomenko A, Pieske BM, Popescu BA, Ronnevik PK, Rutten FH, Schwitter J, Seferovic P, Stepinska J, Trindade PT, Voors AA, Zannad F, Zeiher A. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. European heart journal. 2012 Jul;33(14):1787-847. PubMed PMID: 22611136. Epub 2012/05/23. eng.
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36. Strauss DG. Differentiation between left bundle branch block and left ventricular hypertrophy: implications for cardiac resynchronization therapy. Journal of electrocardiology.45(6):635-9. PubMed PMID: 23022304. 37. Wagner GS, Marriott HJL. Marriott's practical electrocardiography. 9th ed. Baltimore: Williams & Wilkins; 1994. xiv, 434 p. p.
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Fig. 1 LBBB subtypes.
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Fig 2. Inclusion criteria
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Table 1: Demographic, clinical, electrocardiographic, and echocardiographic characteristics between LBBB and IVCD groups.
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Variable All IVCD LBBB P (IVCD vs LBBB) n 272 56 216 Age 69.63 ± 11.72 71.55 ± 11.70 69.13 ± 11.70 .168 Gender (M/F) 54.41% / 45.59% 48.21% / 51.79% 56.01% / 43.99% .296 BMI 28.49 ± 5.53 29.00 ± 5.70 28.35 ± 5.48 .502 HTN 84.56% 83.93% 84.72% .884 DM II 41.91% 50.00% 39.81% .169 Dyslipidemic 58.46% 58.93% 58.33% .936 COPD 4.78% 5.36% 4.63% .820 ESRD 2.94% 1.79% 3.24% .566 CKD 35.29% 50.00% 31.48% .010 CVA 6.25% 8.93% 5.56% .353 PVD 5.88% 8.93% 5.09% .277 CAD 56.25% 58.93% 55.56% .650 CABG 31.25% 32.14% 31.02% .871 PCI 25.37% 26.79% 25.00% .784 Valve replacement 11.40% 12.50% 11.11% .804 Pacemaker 4.04% 7.14% 3.24% .187 ICD 3.31% 5.36% 2.78% .336 CRTD 8.46% 7.14% 8.80% .692 QRS 155.55 ± 23.57 150.03 ± 27.13 156.98 ±22.40 .490 LVEF 0.42 ± .16 0.42 ± .16 .42 ± .16 .952 LVEDD 52.88 ± 8.77 52.98 ± 8.77 52.84 ± 9.99 .921 LA size 43.87 ± 7.18 44.94 ± 6.95 43.58 ± 7.23 .236 Mild MR 44.49% 51.79% 42.59% .213 Moderate MR 12.50% 8.93% 13.43% .580 Severe MR 6.25% 3.57% 6.94% .566 Mild MS 2.57% 5.36% 1.85% .213 Moderate MS 1.10% 0.00% 1.39% .580 Severe MS 0.37% 0.00% 0.46% .560 Mild AR 32.72% 33.93% 32.41% .299 Moderate AR 1.84% 3.57% 1.39% .570 Severe AR 0.74% 1.79% 0.46% .437 Mild AS 2.57% 5.36% 1.85% .299 Moderate AS 4.04% 5.36% 3.70% .570 Severe AS 3.68% 5.36% 3.24% .437 Mild TR 53.68% 50.00% 54.62% .536 Moderate TR 8.09% 5.35% 8.79% .400 Severe TR 2.21% 1.78% 2.31% .810 PASP 40.99 ± 13.82 43.42 ± 16.57 40.49 ± 13.16 .302 (BMI: body mass index, HTN: hypertension, DM II: type 2 diabetes mellitus, COPD: chronic obstructive pulmonary disease, ESRD: end stage renal disease, CKD: chronic kidney disease, CVA: cerebrovascular accident, PVD: peripheral vascular disease, CAD: coronary artery disease, CABG: coronary artery bypass graft, PCI: percutaneous coronary intervention, CRTD: cardiac resynchronization therapy with defibrillator, ICD: internal cardiac defibrillator, LVEF: left ventricular ejection fraction, LA: left atrium, MR: mitral regurgitation, MS: mitral stenosis, AR: aortic regurgitation, AS: aortic stenosis, TR: tricuspid regurgitation, TS: tricuspid stenosis, PASP: pulmonary artery systolic pressure) Values are mean ± standard deviation for continuous normally distributed variables and as median (25th to 75th percentile) for continuous nonnormally distributed variables.
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Table 2: Demographic, clinical, electrocardiographic and echocardiographic characteristics between LBBBD and LBBBC groups.
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Variable All LBBBC LBBBD P (LBBBC vs LBBBD) n 216 83 133 Age 69.13 ± 11.70 69.70 ± 12.20 68.77 ± 11.41 0.570 Gender (M/F) 56.01% / 43.99% 33.73% / 66.27% 69.92% / 30.08% <.001 BMI 28.35 ± 5.48 29.21 ± 5.96 27.81 ± 5.11 .121 HTN 84.72% 80.72% 87.22% .197 DM II 39.81% 34.94% 42.86% .332 Dyslipidemic 58.33% 54.22% 60.90% .248 COPD 4.63% 0.00% 7.52% .011 ESRD 3.24% 1.20% 4.51% .182 CKD 31.48% 15.66% 41.35% <.001 CVA 5.56% 2.41% 7.52% .111 PVD 5.09% 1.20% 7.52% .040 CAD 55.56% 36.14% 67.67% <.001 CABG 31.02% 16.87% 39.85% <.001 PCI 25.00% 19.28% 28.57% .125 Valve replacement 11.11% 6.02% 14.29% .270 Pacemaker 3.24% 3.61% 3.01% .806 ICD 2.78% 0.00% 4.51% .050 CRTD 8.80% 3.61% 12.03% .034 QRS 156.98 ± 22.40 151.42 ± 20.39 160.45 ± 22.97 .004 LVEF 0.42 ± .16 0.51 ± .14 0.36 ± .15 <.001 LVEDD 52.84 ± 9.99 49.64 ± 8.93 55.20 ± 10.11 <.001 LA size 43.58 ± 7.23 40.61 ± 6.29 45.66 ± 7.14 <.001 Mild MR 42.59% 43.37% 42.11% .949 Moderate MR 13.43% 4.82% 18.80% .024 Severe MR 6.94% 3.61% 9.02% .225 Mild MS 1.85% 1.20% 2.26% .949 Moderate MS 1.39% 1.20% 1.50% .024 Severe MS 0.46% 0.00% 0.75% .225 Mild AR 32.41% 31.33% 33.08% .956 Moderate AR 1.39% 1.20% 1.50% .578 Severe AR 0.46% 0.00% 0.75% .296 Mild AS 1.85% 2.41% 1.50% .956 Moderate AS 3.70% 2.41% 4.51% .578 Severe AS 3.24% 1.20% 4.51% .296 Mild TR 54.63% 61.45% 50.38% .112 Moderate TR 8.80% 2.41% 12.78% .009 Severe TR 2.31% 0.00% 3.76% .074 PASP 40.49 ± 13.16 36.8 ± 9.51 42.75 ± 14.55 .008 (BMI: body mass index, HTN: hypertension, DM II: type 2 diabetes mellitus, COPD: chronic obstructive pulmonary disease, ESRD: end stage renal disease, CKD: chronic kidney disease, CVA: cerebrovascular accident, PVD: peripheral vascular disease, CAD: coronary artery disease, CABG: coronary artery bypass graft, PCI: percutaneous coronary intervention, CRTD: cardiac resynchronization therapy with defibrillator, ICD: internal cardiac defibrillator, LVEF: left ventricular ejection fraction, LA: left atrium, MR: mitral regurgitation, MS: mitral stenosis, AR: aortic regurgitation, AS: aortic stenosis, TR: tricuspid regurgitation, TS: tricuspid stenosis, PASP: pulmonary artery systolic pressure) Values are mean ± standard deviation for continuous normally distributed variables and as median (25th to 75th percentile) for continuous non-normally distributed variables.
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Left bundle branch block can be further classified into discordant and concordant. These subtypes carry clinical significance. Discordant pattern in patients with LBBB is associated with lower LVEF, wider QRS, larger LA size, moderate to severe mitral and tricuspid regurgitation, CKD, CAD, and had more frequently underwent CABG. Discordant pattern in patients with LBBB show more prominent bi-ventricular dyssynchrony which raises the hypothesis of it being used to better predict response to CRT.
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Highlights:
S0022-0736(15)00288-5 doi: 10.1016/j.jelectrocard.2015.08.031 YJELC 52128
To appear in:
Journal of Electrocardiology
Please cite this article as: Khalil Jalkh, Bernard Abi Saleh, Maurice Khoury, Zaheer Yousef, Marwan Refaat, Abdallah Rebeiz, Samir Alam, Hadi Skouri, Discordant Vs. Concordant Left Bundle Branch Block: A Potential Clinical Significance, Journal of Electrocardiology (2015), doi: 10.1016/j.jelectrocard.2015.08.031
This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Discordant Vs. Concordant Left Bundle Branch Block:
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A Potential Clinical Significance
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Jalkh,Khalil¹^; Abi Saleh,Bernard¹^;Khoury,Maurice¹;; Yousef,Zaheer²;Refaat, Marwan¹;Rebeiz,Abdallah¹;Alam,Samir¹;Skouri,Hadi¹*
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¹ American University of Beirut Medical Center; Lebanon ² Cardiff Hospital; England ^ Co- first authors * Corresponding Author: Contacts: Email: [email protected]; Work Phone: +961-1-374374 Office extension: 1-5309; Fax: +9611370814 Abstract:
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Aim:
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LBBB in heart failure patients has prognostic significance. Subtypes of LBBB (concordant and discordant) have not been considered when considering management. The aim of this study is to explore the clinical difference between the two subtypes.
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Methods:
Results:
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216 patients with LBBB were included and categorized into concordant (LBBBC) and discordant (LBBBD) groups.
Of the 216 patients (age 69.13 ±11.7; 56% male 44% female), 133 (61.5%) were LBBBD and 83 (38.5%) were LBBBC. LBBBD patients presented with lower LVEF (mean 36% vs 51%; P<0.001), wider QRS (mean 160ms vs 151ms; 2 2 P<0.001), larger LA (mean 45 cm vs 40 cm ; P<0.001), moderate to severe mitral and tricuspid regurgitation (17% vs 3%; P<0.05, 10% vs 1%; P<0.05 respectively), CKD (41% vs 18%; P<0.001), COPD (4.6% vs 0%; P<0.01), CAD (67% vs 36%; P<0.001), and CABG (39% vs 16%; P<0.001). Conclusion: LBBBD is significantly associated with worse cardiac function and clinical characteristics.
Keywords: Heart failure, Left bundle branch block, CRT, Dyssynchrony.
ACCEPTED MANUSCRIPT Introduction:
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Defects in left ventricular function due to abnormal activation patterns have been well-documented. In 1974, Abbassi et. al described the paradoxical movement of the interventricular septum in left bundle branch block (LBBB) (1). Later, Van Oosterhout et. al described the effect of asynchronous electrical activation of the ventricles on workload differences that may possibly result in ventricular dilation or hypertrophy (2). The prevalence of LBBB strongly correlates with age and the presence of cardiovascular disease. LBBB usually indicates an underlying progressive degenerative disease of the ventricular myocardium (3, 4). In HF patients the prevalence of LBBB st reported to be approximately 11-25%(5-7). Since the beginning of the 21 century, Heart Failure (HF) has become a pandemic. Despite the progress in the pharmacological management, hospitalization rates and mortality are still high. In addition most of HF patients remain symptomatic imposing significant socioeconomic burden. LBBB and QRS duration have been linked to HF as their presence increases the risk of mortality and disease progression (8). This has led to the emergence of an appealing intervention that corrects the mechanical left ventricular dyssynchrony due to the presence of LBBB through changing the sequence of electrical activation (9-11). Cardiac resynchronization therapy (CRT) as a means of optimizing synchrony has shown to have great impact on HF patient’s symptoms, re-hospitalization rates, mortality, and affected reverse remodeling and was successful in 70% of patients leaving around 30% failure rate (9, 10, 12). The significant failure led physicians to regain interest in LBBB diagnostic criteria and different morphological patterns (13, 14). One of the old definitions of LBBB has looked at two different subtypes (15) and these subtypes (Concordant vs. Discordant) have been revisited lately and proved to be clinically different with potential future clinical implications (13). The aim of this study is to determine the prevalence of the two subtypes while screening for LBBB with the new criteria, assess whether there exists a correlation between the two different morphological subtypes and various clinical scenarios or categories of cardiac diseases, and determine whether it can provide us with any potential prognostic implications especially HF- related.
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Design and Methods: Patient Population:
LBBB diagnosis:
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This is a retrospective single center study. All patients more than 18 years of age with a LBBB on an ECG done at the American University of Beirut Medical center (AUBMC) and stored in the ECG department from April 2004 till December 2012 were included. Patients were excluded if they have paced rhythm, had an acute coronary syndrome within the last 6 months, had inter-operator variability in ECG diagnosis, and had missing clinical and echocardiographic data from the medical record.
LBBB was diagnosed during the above mentioned period using the old criteria: QRS interval >120 ms; slurred/notched wide and predominant R waves in leads I, aVL, V5, and V6; slurred/notched and broad S waves in V1 and V2 with absent or small R waves; mid-conduction delay defined as notching or a plateau in the mid-QRS wave; ventricular activation time >50 ms at the onset of the QRS interval; M-shaped QRS variants with occasionally wide R waves in V5 and V6; no initial Q wave over the left precordium; and absence of pre-excitation (16). These patients’ ECGs were further analyzed by applying the new criteria suggested by Strauss et. al (14) that consist of: QRS duration 140 ms (men) or 130 ms (women) or wider, QS or rS in leads V1 and V2, and mid-QRS notching or slurring in 2 of leads V1, V2, V5, V6, I, and aVL. Applying the new criteria has yielded to further classification of the LBBB into two categories: True LBBB as per the new (Strauss) definition and a category labeled as non-specific intra ventricular conduction delays (IVCDs) for ECGs that did not comply with the new definition nor with the definition of RBBB (QRS duration greater than or equal to 120 ms in adults, rsr′, rsR′, or rSR′ in leads V1 or V2; S wave of greater duration than R wave or greater than 40 ms in leads I and V6 in adults; normal R peak time in leads V5 and V6 but greater than 50 ms in lead V1 (16)).
ACCEPTED MANUSCRIPT LBBB were further subdivided into two subtypes: concordant LBBB ( LBBBC ) where the ECGs have their T-wave orientation concordant with QRS complex in leads I, V5 and V6and discordant LBBB ( LBBB D ) where the ECGs have their T-wave orientation discordant with the QRS complex in leads I, V5, and V6 (See fig. 1), (see fig 2.)(15).
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Data Collection:
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An extensive chart review was performed with data collection on demographics, cardiac risk factors, comorbidities, cardiac interventional data, electrocardiographic data including rhythm and QRS duration, and echocardiographic data. Electrographic recordings and echocardiographic data were first screened by a cardiology fellow and then independently re-examined by an electrophysiology specialist and a heart failure specialist. Echocardiographic parameters were measured in the AUBMC core laboratory. Left ventricular volumes were measured by Simpson’s method of discs in the apical 4 and 2 chamber views and averaged. Left ventricular ejection fractions were calculated according to standard methods. Left atrial volumes were measured using Simpson’s method of discs in the apical 4 and 2 chamber views and averaged. Valvular abnormalities and its grades as well as assessment of systolic pulmonary artery pressure were collected too. The study protocol was approved by the Institutional Review Board at AUBMC.
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Statistical Methods:
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Statistical analysis was performed using IBM’s Statistical Package for the Social Sciences (SPSS) version 20.0. Continuous variables are presented as mean +/- standard deviation. Categorical data are presented as percentages. Comparison between categorical variables has been performed using Chi-squared test. Comparison between continuous variables has been performed using Bonferroni’s t-test. A two tailed P value < 0.05 was considered as statistically significant.
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Results:
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From April 2004 till December 2012, 394 patients with LBBB as ECG diagnosis were initially included in the study. Complete files were only available for 283 out of the 394 initial patients. Of the 283 patients, 11 were excluded because there was inter-operator variability in ECG interpretation. Out of the eleven patients, three exhibited change from discordant to concordant in a period of less than 6 months. 272 patients were left with complete files and agreed upon ECGs for the study analysis. Of the 272 patients, 56 (20.5%) showed non-specific IVCD and 216 (79.5%) showed LBBB on ECG. Patients’ demographic, clinical, electrocardiographic and echocardiographic characteristics for LBBB and IVCD groups are shown in table 1. There were no significant findings when comparing those with a LBBB pattern to those with non-specific IVCD with the exception of CKD which had been more prevalent in the IVCD population (p=0.01). Of the 216 patients, 83 (38.4%) showed a concordant pattern and 133 (61.6%) showed a discordant pattern. LBBB subtype patients’ demographic, clinical, electrocardiographic and echocardiographic characteristics are reported in table 2. Patients with LBBBD were more often male (P<0.01), had a higher prevalence of COPD (P=0.01), CKD (P<0.01), PVD (p=0.04), ischemic heart disease (P<0.01), more often had underwent CABG (p<0.01), showed worse LVEF (p<0.01), higher incidence of mitral stenosis (p=0.024),higher incidence of significant valvular regurgitation: moderate to severe mitral regurgitation (17% vs 3%; P<0.05) and moderate to severe tricuspid regurgitation (10% vs 1%; P<0.05), larger LVEDD (p<0.01), and higher PASP (P=0.008). No differences were observed concerning ICD. CRTD were more implanted in the discordant group. Gender difference in the distribution of discordant pattern may have been due to the higher prevalence of males with ischemic heart disease in our study and thus might have been a confounding factor. Ischemic heart disease can be associated with a more diseased conduction system causing the LBBB D pattern.
ACCEPTED MANUSCRIPT Discussion:
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Left bundle branch block (LBBB) is a relatively common pattern seen on the electrocardiogram (ECG) and is increasingly recognized for its profound hemodynamic effects on the heart. Several epidemiologic studies have been conducted to establish the prevalence of LBBB in the general population and it was reported to fall in the range of 0.1–0.8% based on variations in the population size and sampling criteria (17-21). Moreover, it was shown that the prevalence strongly correlates with age and with the presence of cardiovascular disease (3, 22). Isolated LBBB occurring in the setting of young, clinically healthy men conveys a benign prognosis (20). However, in older patients, LBBB usually indicates an underlying progressive degenerative disease of the ventricular myocardium. As for the prevalence of LBBB among heart failure population varied and has been reported to range from 11% to 25% (6, 7). Newby et al. reported that the incidence of LBBB in acute myocardial infarction requiring thrombolytic therapy was 7% (23). After coronary bypass grafting (CABG) or valvular surgery the incidence of developing new LBBB ranged between 2 - 4 % (24, 25).
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LBBB is known to impair the mechanical function of the left ventricle secondary to asynchronous myocardial activation, which sequentially, may trigger ventricular remodeling. Thus, it inversely affects the perfusion, systolic/diastolic performance and hemodynamics of the heart (26-28). This is further emphasized by Zannad et al. who proposed the following sequence for the development of HF in patients with LBBB: intra-ventricular asynchrony–reduced pump function–neurohormonal activation–asymmetric hypertrophy–dilatation (5).
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One of the earliest studies to demonstrate a clear association between LBBB and cardiovascular diseases was the Framingham Heart study which concluded that subjects with acquired LBBB were more likely to have or to subsequently develop advanced cardiovascular manifestations (such as hypertension and ischemic heart disease), and exhibit increased cardiovascular morbidity and mortality with a 50 % ten-year mortality associated with new LBBB (22). The presence of LBBB is considered an unfavorable prognostic marker in the setting of acute/chronic HF, coronary artery disease (CAD) and myocardial infarction (MI).
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In heart failure patients, the presence of ventricular dyssynchrony further depresses left ventricular function by placing it at an additional mechanical disadvantage. This dyssynchrony has been shown to hasten disease progression in heart failure. The more pronounced the dyssynchrony as evidenced by a wider QRS complex the more the mortality in patients with HF (29-31). Based on the mentioned data, it became conceivable that patients with LV dysfunction and dyssynchronized ventricular activation would benefit from biventricular pacing that attempt to restore synchronous contraction to maintain optimal atrial–ventricular (AV) synchrony and prolong the time available for myocardial perfusion. This idea was tested in a case report which proved efficacy and drove further studies in the field (32). Cardiac resynchronization therapy (CRT) was shown to improve symptoms, exercise capacity, quality of life, LVEF, survival, and decreased hospitalizations in patients with advanced HF (NYHA class III or IV with LVEF <35 %. The wider the QRS complex, the more the dysynchrony and the more the CRT benefit (33). The most recent HF guidelines recommended CRT in HF patients with LBBB and QRS duration ≥150 ms as class Ia indication and QRS between 120-150ms as a class Ib indication (34, 35). LBBB pattern has been further classified since late 1950s into two morphological variants: “Homophasic” (concordant: LBBBC) and “Heterophasic” (discordant: LBBBD) based on the associated T wave direction in leads I, V5 and V6 (15). LBBB with positive T waves is considered LBBBC, whereas, LBBB with negative T waves is considered LBBBD. Padeletti et al. recently assessed the prevalence and clinical significance of homophasic and heterophasic LBBB in a prospective cohort of 897 HF patients of which 26% had LBBB. Results revealed that the prevalence of LBBBD was greater than that of LBBBC, with percentages of 69 % and 31% respectively. Regarding the clinical
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characteristics of patients with LBBBD, they were indicative of greater severity of the disease since these patients were older, and had a worse renal function. They also had worse left ventricular ejection fraction, higher left vetricular end-diastolic/end-systolic volumes and enhanced neurohormonal activation secondary to higher levels of BNP, NT-proBNP, norepinephrine, and elevated renin activity. Moreoever, the results demonstrated that LBBBD in systolic HF is associated with a worse prognosis secondary to the enhanced neurohormonal activation as compared to cLBBB. Thus, they suggested that the difference between LBBBC and LBBBD could be used as a predictive tool for the composite endpoint of sudden death and life-threatening ventricular tachyarrhythmias and could be a useful low-cost tool in the clinical assessment and prognostic stratification of HF patients (13).
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Our study has revealed that 20% of patients labeled with LBBB according to the old criteria are no more diagnosed with LBBB when the new strict Strauss criteria were applied. Strauss criteria were suggested after several studies has shown that around one third of patients are mislabeled as LBBB which may be affecting response to CRT therapy (36). This will lead to multiple unanswered questions. Is there a difference in the natural history and clinical characteristics of this group of patients compared to the LBBB group? Are they at an increased risk of arrhythmias, lower LVEF and would they respond differently to CRT? In our study there was no difference between IVCD and LBBB except presence of CKD was more prevalent in the IVCD group. Re-analysis of the previous published trials according to the new LBBB criteria would better define the IVCD group, its natural history and its clinical characteristics. As well, new larger prospective trials are needed to look at the clinical, echocardiograpghic and mortality data for the IVCD group in comparison to the revised LBBB group.
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Second, there is a significant difference between the two coexisting subtypes of LBBB. In our study, we confirmed the presence of two distinct LBBB patterns and assigned potential clinical significance to each subtype. A discordant T-wave in leads I, V5 and V6 in a left bundle branch block patients was associated with a lower LVEF, larger LA size, larger end diastolic diameter, wider QRS complex, ischemic heart disease, and chronic kidney disease. These results were consistent with Padeletti et. al’s findings who analyzed systolic heart failure patients (13). Moreover, previous published studies on CRT had never been analyzed by the two different subtypes. This brings us to the conclusion that there may be different clinical implications in the two subtypes of LBBB. Larger trials are needed to determine and confirm this difference on several levels.
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The two subtypes differ in their T wave morphology. Our current understanding of T-wave morphology is explained by a model proposing the presence of a different trans-mural repolarization sequence within the ventricular wall where the epicardium recovers before the endocardium (37) . A disruption in the endocardium may result in further delay or abolishment of repolarization which may cause the T-wave to invert. This model may explain the results encountered in our study. Elements that may cause endomyocardial damage such as those seen in ischemic heart disease, dilated cardiomyopathy, higher LV filling volumes and pressures with significant LV remodeling. These may be manifested by slowing of conduction and subsequent QRS widening that have had their T-wave pattern inverted. Moreover, follow up studies should determine if there exist any change from one subtype to the other and whether this change can imply prognostic evidence or response/failure to therapy. In our study 3 patients exhibited change from discordant to concordant in a period of less than 6 months and this change could be related to optimization of medical management or improvement in clinical and echocardiographic findings. That warrants further investigation on a broader aspect. This study has several limitations that include its design as a retrospective study with a large number of incomplete charts which reduced effective number of the study population. There is a low number of CRT implantation despite recommendations due to unavailability of financial coverage in our country for this type of intervention. Data on
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In conclusion, LBBBD is associated with more comorbidities and worse cardiac characteristics when compared to LBBBC. This difference may hold therapeutic and prognostic implications especially in LBBB HF population. Further studies are needed in this regard to better characterize the two subtypes.
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36. Strauss DG. Differentiation between left bundle branch block and left ventricular hypertrophy: implications for cardiac resynchronization therapy. Journal of electrocardiology.45(6):635-9. PubMed PMID: 23022304. 37. Wagner GS, Marriott HJL. Marriott's practical electrocardiography. 9th ed. Baltimore: Williams & Wilkins; 1994. xiv, 434 p. p.
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Fig. 1 LBBB subtypes.
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Fig 2. Inclusion criteria
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Table 1: Demographic, clinical, electrocardiographic, and echocardiographic characteristics between LBBB and IVCD groups.
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Variable All IVCD LBBB P (IVCD vs LBBB) n 272 56 216 Age 69.63 ± 11.72 71.55 ± 11.70 69.13 ± 11.70 .168 Gender (M/F) 54.41% / 45.59% 48.21% / 51.79% 56.01% / 43.99% .296 BMI 28.49 ± 5.53 29.00 ± 5.70 28.35 ± 5.48 .502 HTN 84.56% 83.93% 84.72% .884 DM II 41.91% 50.00% 39.81% .169 Dyslipidemic 58.46% 58.93% 58.33% .936 COPD 4.78% 5.36% 4.63% .820 ESRD 2.94% 1.79% 3.24% .566 CKD 35.29% 50.00% 31.48% .010 CVA 6.25% 8.93% 5.56% .353 PVD 5.88% 8.93% 5.09% .277 CAD 56.25% 58.93% 55.56% .650 CABG 31.25% 32.14% 31.02% .871 PCI 25.37% 26.79% 25.00% .784 Valve replacement 11.40% 12.50% 11.11% .804 Pacemaker 4.04% 7.14% 3.24% .187 ICD 3.31% 5.36% 2.78% .336 CRTD 8.46% 7.14% 8.80% .692 QRS 155.55 ± 23.57 150.03 ± 27.13 156.98 ±22.40 .490 LVEF 0.42 ± .16 0.42 ± .16 .42 ± .16 .952 LVEDD 52.88 ± 8.77 52.98 ± 8.77 52.84 ± 9.99 .921 LA size 43.87 ± 7.18 44.94 ± 6.95 43.58 ± 7.23 .236 Mild MR 44.49% 51.79% 42.59% .213 Moderate MR 12.50% 8.93% 13.43% .580 Severe MR 6.25% 3.57% 6.94% .566 Mild MS 2.57% 5.36% 1.85% .213 Moderate MS 1.10% 0.00% 1.39% .580 Severe MS 0.37% 0.00% 0.46% .560 Mild AR 32.72% 33.93% 32.41% .299 Moderate AR 1.84% 3.57% 1.39% .570 Severe AR 0.74% 1.79% 0.46% .437 Mild AS 2.57% 5.36% 1.85% .299 Moderate AS 4.04% 5.36% 3.70% .570 Severe AS 3.68% 5.36% 3.24% .437 Mild TR 53.68% 50.00% 54.62% .536 Moderate TR 8.09% 5.35% 8.79% .400 Severe TR 2.21% 1.78% 2.31% .810 PASP 40.99 ± 13.82 43.42 ± 16.57 40.49 ± 13.16 .302 (BMI: body mass index, HTN: hypertension, DM II: type 2 diabetes mellitus, COPD: chronic obstructive pulmonary disease, ESRD: end stage renal disease, CKD: chronic kidney disease, CVA: cerebrovascular accident, PVD: peripheral vascular disease, CAD: coronary artery disease, CABG: coronary artery bypass graft, PCI: percutaneous coronary intervention, CRTD: cardiac resynchronization therapy with defibrillator, ICD: internal cardiac defibrillator, LVEF: left ventricular ejection fraction, LA: left atrium, MR: mitral regurgitation, MS: mitral stenosis, AR: aortic regurgitation, AS: aortic stenosis, TR: tricuspid regurgitation, TS: tricuspid stenosis, PASP: pulmonary artery systolic pressure) Values are mean ± standard deviation for continuous normally distributed variables and as median (25th to 75th percentile) for continuous nonnormally distributed variables.
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Table 2: Demographic, clinical, electrocardiographic and echocardiographic characteristics between LBBBD and LBBBC groups.
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Variable All LBBBC LBBBD P (LBBBC vs LBBBD) n 216 83 133 Age 69.13 ± 11.70 69.70 ± 12.20 68.77 ± 11.41 0.570 Gender (M/F) 56.01% / 43.99% 33.73% / 66.27% 69.92% / 30.08% <.001 BMI 28.35 ± 5.48 29.21 ± 5.96 27.81 ± 5.11 .121 HTN 84.72% 80.72% 87.22% .197 DM II 39.81% 34.94% 42.86% .332 Dyslipidemic 58.33% 54.22% 60.90% .248 COPD 4.63% 0.00% 7.52% .011 ESRD 3.24% 1.20% 4.51% .182 CKD 31.48% 15.66% 41.35% <.001 CVA 5.56% 2.41% 7.52% .111 PVD 5.09% 1.20% 7.52% .040 CAD 55.56% 36.14% 67.67% <.001 CABG 31.02% 16.87% 39.85% <.001 PCI 25.00% 19.28% 28.57% .125 Valve replacement 11.11% 6.02% 14.29% .270 Pacemaker 3.24% 3.61% 3.01% .806 ICD 2.78% 0.00% 4.51% .050 CRTD 8.80% 3.61% 12.03% .034 QRS 156.98 ± 22.40 151.42 ± 20.39 160.45 ± 22.97 .004 LVEF 0.42 ± .16 0.51 ± .14 0.36 ± .15 <.001 LVEDD 52.84 ± 9.99 49.64 ± 8.93 55.20 ± 10.11 <.001 LA size 43.58 ± 7.23 40.61 ± 6.29 45.66 ± 7.14 <.001 Mild MR 42.59% 43.37% 42.11% .949 Moderate MR 13.43% 4.82% 18.80% .024 Severe MR 6.94% 3.61% 9.02% .225 Mild MS 1.85% 1.20% 2.26% .949 Moderate MS 1.39% 1.20% 1.50% .024 Severe MS 0.46% 0.00% 0.75% .225 Mild AR 32.41% 31.33% 33.08% .956 Moderate AR 1.39% 1.20% 1.50% .578 Severe AR 0.46% 0.00% 0.75% .296 Mild AS 1.85% 2.41% 1.50% .956 Moderate AS 3.70% 2.41% 4.51% .578 Severe AS 3.24% 1.20% 4.51% .296 Mild TR 54.63% 61.45% 50.38% .112 Moderate TR 8.80% 2.41% 12.78% .009 Severe TR 2.31% 0.00% 3.76% .074 PASP 40.49 ± 13.16 36.8 ± 9.51 42.75 ± 14.55 .008 (BMI: body mass index, HTN: hypertension, DM II: type 2 diabetes mellitus, COPD: chronic obstructive pulmonary disease, ESRD: end stage renal disease, CKD: chronic kidney disease, CVA: cerebrovascular accident, PVD: peripheral vascular disease, CAD: coronary artery disease, CABG: coronary artery bypass graft, PCI: percutaneous coronary intervention, CRTD: cardiac resynchronization therapy with defibrillator, ICD: internal cardiac defibrillator, LVEF: left ventricular ejection fraction, LA: left atrium, MR: mitral regurgitation, MS: mitral stenosis, AR: aortic regurgitation, AS: aortic stenosis, TR: tricuspid regurgitation, TS: tricuspid stenosis, PASP: pulmonary artery systolic pressure) Values are mean ± standard deviation for continuous normally distributed variables and as median (25th to 75th percentile) for continuous non-normally distributed variables.
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Left bundle branch block can be further classified into discordant and concordant. These subtypes carry clinical significance. Discordant pattern in patients with LBBB is associated with lower LVEF, wider QRS, larger LA size, moderate to severe mitral and tricuspid regurgitation, CKD, CAD, and had more frequently underwent CABG. Discordant pattern in patients with LBBB show more prominent bi-ventricular dyssynchrony which raises the hypothesis of it being used to better predict response to CRT.
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