Impact of Left and Right Bundle Branch Block on Left Ventricular Systolic Function and Myocardial Mechanics Assessed by Speckle‐Tracking Echocardiography and Cardiac Magnetic Resonance Feature Tracking: A Systematic Review and Meta‐Analysis

ABSTRACT

Background

Bundle branch conduction abnormalities are associated with ventricular dyssynchrony, impaired myocardial mechanics, and progressive systolic dysfunction. Advanced deformation imaging techniques, including speckle‐tracking echocardiography (STE) and cardiac magnetic resonance feature tracking (CMR‐FT), may identify subclinical ventricular dysfunction beyond conventional left ventricular ejection fraction (LVEF). We performed a systematic review and meta‐analysis to evaluate conventional systolic function and myocardial deformation abnormalities associated with left bundle branch block (LBBB) and right bundle branch block (RBBB).

Methods

PubMed, Scopus, and EMBASE databases were systematically searched for observational studies evaluating ventricular systolic function and myocardial deformation parameters in patients with LBBB and/or RBBB using STE and/or CMR‐FT. Comparative meta‐analyses were performed using standardized mean differences (SMDs) with 95% confidence intervals (CIs). Separate analyses were conducted for LVEF and left ventricular global longitudinal strain (LV‐GLS).

Results

Sixteen studies were included in the systematic review, whereas eight were eligible for quantitative meta‐analysis. Compared with healthy controls, patients with LBBB demonstrated significantly reduced LVEF (SMD −0.404, 95% CI −0.553 to −0.255; p < 0.001) and impaired LV‐GLS (SMD −0.345, 95% CI −0.535 to −0.156; p < 0.001). In contrast, isolated RBBB was not associated with significant overall differences in either LVEF (SMD 0.051, 95% CI −0.146 to 0.247; p = 0.613) or LV‐GLS (SMD 0.064, 95% CI −0.134 to 0.262; p = 0.527). Direct comparisons demonstrated significantly greater impairment of both LVEF (SMD −0.361, 95% CI −0.519 to −0.202; p < 0.001) and LV‐GLS (SMD −0.436, 95% CI −0.595 to −0.276; p < 0.001) in LBBB than in RBBB. STE‐based studies generally demonstrated larger effect sizes and greater heterogeneity than CMR‐FT investigations.

Conclusions

Bundle branch conduction abnormalities, particularly LBBB, are closely associated with impaired left ventricular systolic performance and myocardial mechanics. LV‐GLS abnormalities appeared consistently more pronounced than LVEF abnormalities across several comparisons, suggesting that myocardial deformation imaging may be more sensitive to the mechanical consequences of conduction abnormalities at a population level. Given the observational nature of the included studies, the substantial clinical and methodological heterogeneity across populations, the limited evidence available for RBBB, and the potential influence of residual confounding factors such as age and underlying structural heart disease, these findings should be considered hypothesis‐generating and warrant confirmation in larger prospective studies.

Schematic representation of the principal findings of the present systematic review and meta‐analysis evaluating the impact of bundle branch block on left ventricular systolic function and myocardial mechanics. LBBB is associated with marked electromechanical dyssynchrony, resulting in significant impairment of both LVEF and LV‐GLS compared with healthy controls. In contrast, isolated RBBB exerts a less pronounced effect on ventricular mechanics, with no significant overall differences in LVEF or LV‐GLS. Across 16 studies included in the systematic review and eight studies included in the quantitative meta‐analysis, advanced myocardial deformation imaging by STE and CMR‐FT provided complementary information beyond conventional systolic function assessment. These findings support the role of multimodality strain imaging for the identification of electromechanical dysfunction, phenotypic characterization, risk stratification, and potentially the selection and monitoring of patients undergoing CRT. CMR‐FT, cardiac magnetic resonance feature tracking; CRT, cardiac resynchronization therapy; LBBB, left bundle branch block; LV‐GLS, left ventricular global longitudinal strain; LVEF, left ventricular ejection fraction; RBBB, right bundle branch block; SMD, standardized mean difference; STE, speckle‐tracking echocardiography.

1. Introduction

Left bundle branch block (LBBB) and right bundle branch block (RBBB) are common intraventricular conduction abnormalities associated with significant alterations in ventricular activation, myocardial mechanics, and clinical outcomes [1, 2, 3]. Although conventional electrocardiographic assessment remains the cornerstone for the diagnosis of bundle branch block patterns, increasing evidence suggests that electrical dyssynchrony does not necessarily correspond to the extent of underlying mechanical dysfunction [4, 5]. In this context, advanced cardiac imaging modalities, particularly speckle‐tracking echocardiography (STE) and cardiac magnetic resonance feature tracking (CMR‐FT), have emerged as valuable tools for the comprehensive assessment of myocardial deformation and ventricular dyssynchrony [6].

Myocardial strain imaging allows the early identification of subtle systolic dysfunction, even in patients with preserved left ventricular ejection fraction (LVEF), providing incremental diagnostic and prognostic information beyond conventional echocardiographic parameters [7, 8, 9, 10]. In patients with LBBB, impaired left ventricular global longitudinal strain (LV‐GLS), abnormal septal deformation patterns, reduced myocardial work efficiency, and electromechanical dyssynchrony have been associated with adverse ventricular remodeling, heart failure (HF) progression, and poorer response to cardiac resynchronization therapy (CRT) [11, 12, 13]. Conversely, RBBB has traditionally received less attention in clinical research, despite growing evidence suggesting a relevant impact on right ventricular mechanics, interventricular coupling, myocardial fibrosis burden, and long‐term outcomes in selected populations [14, 15, 16].

In recent years, both STE and CMR‐FT have been increasingly applied to characterize myocardial mechanics in patients with conduction abnormalities across different clinical settings, including HF, dilated cardiomyopathy, post‐transcatheter aortic valve replacement (TAVR), and apparently isolated bundle branch block without overt structural heart disease. However, available studies remain heterogeneous in terms of imaging methodology, study design, analyzed strain parameters, patient populations, and reported clinical endpoints. Furthermore, the relative contribution of left‐ versus right‐sided conduction delay to ventricular remodeling and prognostic stratification remains incompletely understood.

Accordingly, the present systematic review and meta‐analysis aimed to comprehensively evaluate the available evidence regarding myocardial deformation abnormalities assessed by STE and CMR‐FT in patients with LBBB and RBBB. Specifically, we sought to summarize the clinical and imaging characteristics of the included studies, assess the association between conduction abnormalities and myocardial strain impairment, and explore the prognostic implications of deformation imaging parameters across different bundle branch block phenotypes.

2. Materials and Methods

The present systematic review and meta‐analysis was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) recommendations [17]. The PRISMA checklist is provided in the Supporting Information (Supporting Information File S1). The study protocol was prospectively registered in the International Platform of Registered Systematic Review and Meta‐analysis Protocols (INPLASY) (registration number: INPLASY202650169; registration date: May 29, 2026) (Supporting Information File S2). The review was registered at the stage of “completed but not published,” as permitted by INPLASY registration policies. Importantly, the registered protocol accurately reflected the methodology ultimately implemented in the study, and no modifications to the review objectives, eligibility criteria, outcomes, or statistical analysis plan were made after registration.

2.1. Search Strategy

A comprehensive literature search was independently performed by two investigators to identify studies evaluating myocardial mechanics, cardiac function, and deformation imaging abnormalities in patients with LBBB and/or RBBB using STE and/or CMR‐FT.

Electronic databases including PubMed, Scopus, and EMBASE were systematically searched from database inception to May 2026. The search strategy combined Medical Subject Headings (MeSH) terms and free‐text keywords related to conduction abnormalities, ventricular dyssynchrony, myocardial deformation, and cardiac mechanics. Search terms included combinations of “left bundle branch block”, “right bundle branch block”, “LBBB”, “RBBB”, “bundle branch block”, “conduction abnormalities”, “intraventricular conduction delay”, “cardiac mechanics”, “cardiac function”, “myocardial deformation”, “global longitudinal strain”, “GLS”, “global circumferential strain”, “GCS”, “global radial strain”, “GRS”, “right ventricular strain”, “mechanical dyssynchrony”, “speckle tracking echocardiography”, “2D‐STE”, “3D‐STE”, “cardiac magnetic resonance”, “CMR”, “feature tracking”, “CMR‐FT”, “left ventricular ejection fraction”, and “right ventricular ejection fraction”.

No restrictions regarding publication year, geographic region, or language were applied. Additional potentially eligible studies were identified through manual screening of the reference lists of included articles and relevant review papers. Any disagreement during study selection was resolved by discussion and consensus, with involvement of a third reviewer when necessary.

2.2. Eligibility Criteria

Studies were considered eligible if they had an observational design, including prospective cohorts, retrospective cohorts, or cross‐sectional investigations, and evaluated myocardial deformation parameters and/or ventricular systolic function in adult patients with LBBB and/or RBBB using STE and/or CMR‐FT techniques.

Eligible studies were required to report extractable quantitative imaging data regarding at least one of the following parameters: LVEF, LV‐GLS, left ventricular global circumferential strain (LV‐GCS), left ventricular global radial strain (LV‐GRS), right ventricular global longitudinal strain (RV‐GLS), right ventricular free‐wall longitudinal strain (RV‐FWLS), right ventricular ejection fraction (RVEF), or other deformation‐derived markers of ventricular mechanics and dyssynchrony.

Studies including healthy control groups were considered eligible for quantitative meta‐analysis. Investigations lacking a control population were retained for the systematic review and descriptive pooled analyses but were excluded from comparative meta‐analytic synthesis.

Both echocardiographic and CMR‐derived deformation analyses were considered eligible because the primary objective of the study was to comprehensively evaluate myocardial mechanics across different imaging modalities. Studies performed in pediatric populations, animal models, or experimental settings were excluded. Similarly, conference abstracts, editorials, reviews, case reports, expert opinions, and studies without sufficient quantitative imaging data were not considered eligible.

2.3. Study Selection, Data Collection, and Variable Extraction

Two investigators independently screened all retrieved studies by title and abstract, followed by full‐text evaluation according to predefined inclusion and exclusion criteria. Disagreements regarding study eligibility were resolved through consensus discussion.

Data extraction was independently performed using a standardized collection form specifically developed for the present review. Extracted variables included first author, publication year, country, study design, imaging modality, software vendor, study population, sample size, and sex distribution.

Clinical variables included age, cardiovascular risk factors, atrial fibrillation prevalence, heart rate, blood pressure values, New York Heart Association (NYHA) class, renal function, natriuretic peptide levels, and ongoing medical therapies whenever available.

Conventional imaging parameters were systematically collected to characterize cardiac structure and function. These included left ventricular dimensions and volumes, LVEF, left atrial dimensions, E/A ratio, E/e′ ratio, systolic pulmonary artery pressure (sPAP), tricuspid annular plane systolic excursion (TAPSE), right ventricular dimensions, and ventricular volumetric parameters.

Deformation‐derived imaging variables obtained by STE and/or CMR‐FT were additionally extracted, including LV‐GLS, LV‐GCS, LV‐GRS, RV‐GLS, RV‐FWLS, septal deformation patterns, myocardial work indices, mechanical dispersion, ventricular dyssynchrony parameters, late gadolinium enhancement (LGE), and extracellular volume fraction (ECV) whenever available.

Clinical endpoints including cardiovascular mortality, heart failure hospitalization, arrhythmic events, CRT response, ventricular remodeling, valve intervention outcomes, and composite major adverse cardiovascular events were systematically recorded.

For consistency and interpretability, strain parameters originally expressed as negative percentages were uniformly reported as absolute positive values throughout pooled analyses and tables without altering relative intergroup differences or statistical significance.

2.4. Methodological Quality Assessment and Risk‐of‐Bias Evaluation

Methodological quality and risk of bias were independently assessed by two investigators using the National Institutes of Health (NIH) Quality Assessment Tool for Observational Cohort and Cross‐Sectional Studies [18].

This tool evaluates several methodological domains including study population definition, participant selection, exposure and outcome assessment, statistical methodology, confounding adjustment, reproducibility of measurements, and adequacy of follow‐up.

Each study was evaluated across 14 predefined domains and classified as “Yes”, “No”, “Cannot Determine”, “Not Reported”, or “Not Applicable”. Overall study quality was categorized as good, fair, or poor according to the number of fulfilled criteria and the clinical relevance of methodological limitations. Disagreements between reviewers were resolved through joint reassessment until consensus was achieved.

2.5. Statistical Analysis

To provide an overall descriptive characterization of the included populations, pooled study‐level estimates were calculated using weighted descriptive statistics. Continuous variables were summarized as weighted means with weighted interquartile ranges (IQRs), using study sample size as a weighting factor. Since most studies reported data as mean ± standard deviation, approximate pooled distributions were derived assuming near‐normal distribution. These pooled estimates were intended for descriptive purposes rather than formal patient‐level inferential analyses. Accordingly, exploratory p values should be interpreted cautiously.

The primary quantitative analyses aimed to evaluate differences in ventricular systolic function and myocardial deformation parameters among LBBB, RBBB, and control populations. Separate meta‐analyses were performed for LVEF and LV‐GLS. Specifically, six independent comparative meta‐analyses were conducted: (1) LVEF in LBBB versus controls, (2) LVEF in RBBB versus controls, (3) LVEF in LBBB versus RBBB, (4) LV‐GLS in LBBB versus controls, (5) LV‐GLS in RBBB versus controls, and (6) LV‐GLS in LBBB versus RBBB.

For each meta‐analysis, studies were a priori stratified according to the technique used for myocardial functional assessment, namely STE and CMR‐FT. Separate pooled effect estimates (subtotal analyses) were first calculated within each subgroup. Subsequently, an overall pooled estimate was derived by combining all eligible studies irrespective of assessment technique. This hierarchical approach allowed assessment of both modality‐specific effects and overall differences between study populations, while also permitting formal evaluation of between‐subgroup heterogeneity according to imaging technique. Importantly, STE‐ and CMR‐FT–specific pooled estimates were considered the primary analyses, whereas overall pooled estimates were interpreted as exploratory multimodality summaries providing an integrated overview of the available evidence. Because STE and CMR‐FT differ substantially in image acquisition, temporal resolution, tracking methodology, and post‐processing algorithms, potential differences in effect size between modalities were formally evaluated through subgroup analyses and Q‐between statistics and were taken into account when interpreting pooled results.

Given the relatively small number of eligible studies and the substantial methodological diversity across the available literature, particular attention was devoted to the assessment and interpretation of heterogeneity. The included studies differed considerably with respect to clinical setting, encompassing isolated bundle branch block, non‐ischemic cardiomyopathy, heart failure populations, post‐transcatheter aortic valve replacement (TAVR) cohorts, and asymptomatic subjects. In addition, myocardial deformation was assessed using different imaging approaches, including two‐dimensional (2D) speckle tracking echocardiography (2D‐STE), three‐dimensional speckle‐tracking echocardiography (3D‐STE), and CMR‐FT. Most STE studies used vendor‐specific software with semi‐automated endocardial border tracking followed by manual adjustment when required, whereas CMR‐FT studies relied on dedicated feature‐tracking algorithms applied to cine magnetic resonance images. These methodological differences represent potential contributors to between‐study and between‐modality heterogeneity and should be considered when interpreting pooled estimates.

Comparative pooled analyses were conducted using standardized mean differences (SMDs) with corresponding 95% confidence intervals (CIs). Fixed‐effects or random‐effects models were selected according to the degree of between‐study heterogeneity. Specifically, fixed‐effects models were applied in the presence of negligible heterogeneity (I ² = 0%), whereas random‐effects models based on the DerSimonian–Laird method were used when heterogeneity was moderate or high.

Statistical heterogeneity was assessed using Cochran's Q statistic and quantified using the I ² index. Heterogeneity was evaluated both within individual imaging modality subgroups (STE and CMR‐FT) and across the pooled model. The Q‐between statistic was used to formally evaluate whether the magnitude of the observed effect differed according to imaging technique. Evidence of between‐subgroup heterogeneity was considered when interpreting pooled multimodality estimates. Because only a limited number of studies were available for several comparisons, particularly those involving RBBB and CMR‐FT, the ability to comprehensively explore sources of heterogeneity was necessarily restricted. Notably, only one CMR‐FT study was available for some RBBB‐related analyses, precluding robust modality‐specific quantitative comparisons in these subsets. I ² values of approximately 25%, 50%, and 75% were considered indicative of low, moderate, and high heterogeneity, respectively.

Sensitivity analyses using a leave‐one‐out approach were performed whenever appropriate to evaluate the influence of individual studies on the overall pooled estimates and to assess the stability of the observed results.

Publication bias and small‐study effects were explored through visual inspection of funnel plots and Egger's regression asymmetry test when technically feasible. However, because all quantitative syntheses included substantially fewer than the generally recommended minimum of 10 studies, formal assessment of publication bias was considered severely underpowered and should be interpreted with extreme caution. Accordingly, funnel plots and Egger's regression results were interpreted descriptively rather than as reliable indicators of publication bias. Funnel plots and meta‐regression analyses were not performed in meta‐analyses including only two studies because of the limited statistical reliability and interpretability of these approaches in very small datasets.

Exploration of potential sources of heterogeneity through random‐effects meta‐regression was undertaken only when the number of included studies was considered sufficient and clinically meaningful heterogeneity was present. Prespecified moderators included age, sex distribution, imaging modality, and software vendor whenever relevant data were available. Because substantial clinical and methodological heterogeneity was anticipated across studies—including differences in patient populations, imaging techniques (2D‐STE, 3D‐STE, and CMR‐FT), software platforms, and strain analysis methodologies—meta‐regression findings were considered exploratory and intended primarily to identify potential contributors to between‐study variability rather than to establish causal relationships.

All statistical analyses were performed using Comprehensive Meta‐Analysis software (version 3.0; Biostat, Englewood, NJ, USA). All statistical tests were two‐sided, and a p value <0.05 was considered statistically significant.

2.6. Artificial Intelligence–Supported Language Editing

During the preparation of this manuscript, the authors used ChatGPT (OpenAI, GPT‐5.5) exclusively to assist with English language editing, including improvements in grammar, syntax, readability, and overall linguistic clarity. The artificial intelligence tool was not used to generate scientific ideas or hypotheses, perform the literature search, select or screen studies, extract data, conduct statistical analyses, interpret the results, or formulate the scientific conclusions. All scientific content, methodological decisions, data analyses, and conclusions were conceived, critically evaluated, verified, and approved solely by the authors, who take full responsibility for the accuracy and integrity of the manuscript.

3. Results

3.1. Literature Search and Study Selection

The systematic literature search identified a total of 641 records from PubMed, Scopus, and EMBASE databases. After removal of 31 duplicate articles, 610 records underwent title and abstract screening. Of these, 574 studies were excluded according to the predefined exclusion criteria.

Subsequently, 36 full‐text articles were assessed for eligibility. Among them, 20 studies were excluded because of incomplete STE and/or CMR‐FT data or lack of extractable deformation imaging parameters. Ultimately, 16 studies [19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34] fulfilled the inclusion criteria and were incorporated into the systematic review. Among these, eight studies including an appropriate control population [20, 22, 23, 24, 28, 30, 32, 34] were eligible for quantitative meta‐analysis, whereas eight studies were excluded from comparative pooled analyses because of the absence of a control group [19, 21, 25, 26, 27, 29, 31, 33].

The overall study selection process is summarized in Figure 1 according to PRISMA recommendations.

FIGURE 1.

PRISMA flow diagram illustrating the identification, screening, eligibility assessment, and inclusion process of studies evaluating ventricular systolic function and myocardial deformation abnormalities in patients with bundle branch block using STE and/or CMR‐FT. CMR‐FT, cardiac magnetic resonance feature tracking; PRISMA, Preferred Reporting Items for Systematic Reviews and Meta‐Analyses; STE, speckle‐tracking echocardiography.

3.2. Characteristics of the Included Studies

A total of 16 studies published between 2014 and 2025 were included in the present systematic review, comprising patients with LBBB, RBBB, intraventricular conduction abnormalities, and healthy control populations. Detailed study characteristics are shown in Table 1 [19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34].

TABLE 1.

Main methodological and clinical characteristics of the included studies [19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34] according to imaging modality, software platform, and study population.

Study (publication year), country	Method	Software	Size (% males)	Study population
Maréchaux S. (2014), France [19]	2D‐STE	GE	101 (68.0%)	Ambulatory patients with stable heart failure, LVEF ≤35%, NYHA class II–IV, and LBBB referred for CRT implantation
Dobson L.E. (2017), United Kingdom [20]	CMR‐FT	Circle Cardiovascular Imaging	24 (54.0%)	New‐onset post‐TAVR LBBB
Hwang I.C. (2018), South Korea [21]	2D‐STE	GE	269 (46.8%)	Patients with LBBB without prior cardiac surgery, atrial fibrillation, and poor image quality
Wang Y. (2018), China [22]	2D‐STE	GE	40 (42.5%)	Asymptomatic patients with isolated complete LBBB and preserved LVEF, without structural heart disease
Nakazawa N. (2020), Japan [23]	3D‐STE	Canon Medical Systems	26 (54.0%)	Mixed congenital and acquired heart disease population
Burke G.M. (2021), USA [24]	2D‐STE	GE	11 (64.0%)	TAVR‐induced LBBB
Kim H.M. (2023), South Korea [25]	2D‐STE and 3D‐STE	GE	290 (45.2%)	Patients with LBBB without CRT, poor image quality and without follow‐up <3 months
Layec J. (2023), France [26]	2D‐STE with myocardial work analysis	GE	121 (70.0%)	HFrEF patients with unfavorable electrical characteristics undergoing CRT
Yuan Y. (2023), China [27]	CMR‐FT	Circle Cardiovascular Imaging	87 (67.8%)	Dilated cardiomyopathy patients undergoing CMR
Naseer N.K. (2024), India [28]	3D‐STE	GE	50 (42.0%)	Patients with non‐ischemic LBBB
Pastorini G. (2024), Italy [29]	2D‐STE	GE	78 (59.0%)	Outpatients with complete LBBB and atypical chest pain, without known coronary artery disease
Chen M. (2024), China [30]	2D‐STE	GE	44 (38.6%)	Isolated complete RBBB, patients with isolated complete LBBB, and healthy controls without structural heart disease
Margulescu A.D. (2024), United Kingdom [31]	2D‐STE	NS	38 (42.1%)	New‐onset LBBB post TAVR
Seçkin Göbüt Ö. (2025), Turkey [32]	2D‐STE	GE	39 (50.0%)	Patients with idiopathic RBBB vs. healthy controls
Atabekov T. (2025), Russia [33]	2D‐STE	Philips	54 (66.6%)	Patients with heart failure, NYHA class II–III, sinus rhythm, reduced LVEF ≤35%, and Strauss LBBB criteria undergoing CRT‐D implantation
Zhou D. (2025), China [34]	CMR‐FT	Circle Cardiovascular Imaging	483 (67.9%)	Nonischemic HFrEF and prolonged QRS duration vs. 200 HFrEF controls with normal QRS duration

Abbreviations: CMR, cardiac magnetic resonance; CMR‐FT, cardiac magnetic resonance feature tracking; CRT, cardiac resynchronization therapy; CRT‐D, cardiac resynchronization therapy‐defibrillator; GE, General Electric; HFrEF, heart failure with reduced ejection fraction; LBBB, left bundle branch block; LVEF, left ventricular ejection fraction; NS, not specified; NYHA, New York Heart Association; QRS, QRS complex duration on electrocardiogram; RBBB, right bundle branch block; STE, speckle‐tracking echocardiography; TAVR, transcatheter aortic valve replacement; 2D‐STE, two‐dimensional speckle‐tracking echocardiography; 3D‐STE, three‐dimensional speckle‐tracking echocardiography.

The included investigations were conducted across multiple geographic regions, including Europe, Asia, North America, and Russia, with relevant contributions originating from France, China, South Korea, the United Kingdom, Italy, Turkey, India, Japan, and the United States. Most studies adopted a prospective observational design, whereas a smaller proportion consisted of retrospective or cross‐sectional analyses. The majority of investigations represented single‐center experiences, while only a limited number of studies included larger multicenter cohorts.

STE represented the predominant imaging modality used for myocardial deformation assessment across the included studies. Most echocardiographic investigations employed 2D‐STE techniques, whereas selected studies additionally incorporated 3D‐STE analysis and myocardial work assessment. CMR‐FT was used in selected cohorts, mainly to evaluate ventricular mechanics, myocardial remodeling, and tissue characterization in patients with conduction abnormalities.

Substantial methodological heterogeneity was observed regarding software vendors and post‐processing platforms. GE‐based echocardiographic systems represented the most frequently used imaging platform, whereas Philips, Canon Medical Systems, and Circle Cardiovascular Imaging software were also employed in selected studies. This variability likely reflects the progressive technological evolution of myocardial deformation imaging over the last decade.

The study populations were clinically heterogeneous and included ambulatory HF patients with reduced LVEF undergoing CRT implantation, patients with isolated complete LBBB or idiopathic RBBB without overt structural heart disease, post‐TAVR conduction abnormalities, and dilated cardiomyopathy cohorts undergoing advanced CMR evaluation.

Chronologically, the included literature demonstrates the progressive transition from early exploratory strain imaging studies mainly focused on LV longitudinal mechanics toward more comprehensive multimodality investigations integrating biventricular deformation analysis, myocardial work assessment, electromechanical dyssynchrony characterization, tissue characterization, and prognostic stratification.

3.3. Demographic and Clinical Characteristics of the Study Populations

The overall demographic profile and clinical characteristics of LBBB, RBBB, and control populations are presented in Table 2.

TABLE 2.

Weighted demographic and clinical characteristics of LBBB, RBBB, and control populations included in the systematic review. Data are presented as weighted means with weighted interquartile ranges (IQRs), using the sample size of each study as weighting factor. The “Number of studies” column indicates the number of investigations reporting each variable. Weighted estimates were calculated at the study level and are intended to provide a descriptive characterization of the included populations rather than formal patient‐level pooled analyses. Exploratory p values were derived from study‐level comparisons among LBBB, RBBB, and control groups using the Kruskal–Wallis test and should therefore be interpreted cautiously, as they do not account for within‐study variability and were not adjusted for multiple comparisons. NA indicates that insufficient data were available for pooled estimation.

Parameter	Number of studies	LBBB weighted mean (IQR)	RBBB weighted mean (IQR)	Controls weighted mean (IQR)	p value
% Males	16	57.4 (45.2–67.9)	68.3 (52.3–77.2)	58.1 (41.0–77.5)	0.074
Mean age (yrs)	16	62.6 (52.9–69.5)	50.2 (50.0–51.8)	50.1 (46.1–56.5)	0.036
Hypertension (%)	12	47.5 (34.0–60.0)	22.3 (23.9–23.9)	40.7 (36.5–36.5)	0.067
Smoking (%)	5	28.9 (22.5–39.1)	33.8 (18.2–59.3)	14.0 (14.3–17.5)	0.139
Diabetes (%)	12	23.5 (14.3–32.0)	18.0 (17.9–17.9)	15.7 (15.5–15.5)	0.177
Dyslipidemia (%)	5	30.0 (21.3–33.0)	19.2 (18.5–18.5)	21.5 (21.5–21.5)	0.257
Obesity (%)	2	4.4 (3.3–3.3)	NA	NA	NA
CAD (%)	11	20.3 (0.0–35.0)	0.0 (0.0–0.0)	34.2 (27.0–37.5)	0.381
Carotid atherosclerosis (&)	1	41.0 (41.0–41.0)	NA	NA	NA
AF (%)	6	16.9 (10.1–14.0)	21.7 (21.7–21.7)	21.8 (21.5–21.5)	0.580
Creatinine (mg/dl)	3	1.0 (1.0–1.0)	1.0 (1.0–1.0)	1.1 (1.1–1.1)	0.667
eGFR	3	69.8 (65.0–74.3)	NA	NA	NA
CKD (%)	4	20.4 (19.3–22.0)	NA	NA	NA
NT‐proBNP (pg/mL)	4	937.5 (455.0–1000.0)	1236.6 (1260.0–1260.0)	20.0 (20.0–20.0)	0.297
HR (bpm)	7	75.8 (74.0–79.5)	74.8 (69.0–77.6)	78.1 (67.1–83.9)	0.836
QRS duration (msec)	9	152.3 (148.5–158.2)	146.7 (149.4–149.4)	99.3 (97.5–97.6)	0.002
DBP (mmHg)	4	72.9 (69.0–76.9)	72.2 (70.8–78.4)	72.5 (69.6–80.6)	0.845
NYHA IV (%)	3	29.9 (17.0–55.0)	21.8 (15.8–15.8)	NA	0.564
Antiplatelets (%)	5	38.1 (29.5–53.7)	NA	NA	NA
Anticoagulants (%)	2	34.7 (33.3–36.8)	NA	NA	NA
BB (%)	10	72.6 (43.6–98.3)	93.4 (95.7–95.7)	55.0 (55.0–55.0)	0.563
Loop Diuretics (%)	8	65.4 (48.1–91.7)	NA	NA	NA
MRA (%)	4	77.8 (54.0–91.3)	79.1 (83.7–83.7)	NA	0.643
Digoxin (%)	1	81.6 (81.6–81.6)	76.2 (76.2–76.2)	NA	0.317
Nitrates (%)	1	2.8 (2.8–2.8)	NA	NA	NA
Statins (%)	5	44.5 (12.8–82.0)	NA	64.0 (64.0–64.0)	0.770
CRT (%)	4	53.2 (10.8–100.0)	NA	NA	NA

Abbreviations: ACEI, angiotensin‐converting enzyme inhibitors; AF, atrial fibrillation; ARB, angiotensin receptor blockers; ARNI, angiotensin receptor–Neprilysin inhibitors; BB, beta‐blockers; CAD, coronary artery disease; CKD, chronic kidney disease; CRT, cardiac resynchronization therapy; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; HR, heart rate; IQR, interquartile range; LBBB, left bundle branch block; MRA, mineralocorticoid receptor antagonists; NA, not available; NT‐proBNP, N‐terminal pro‐B‐type natriuretic peptide; NYHA, New York Heart Association; QRS, QRS complex duration; RBBB, right bundle branch block; SBP, systolic blood pressure; SGLT2i, sodium–Glucose cotransporter‐2 inhibitors.

Overall, LBBB populations consisted predominantly of older patients with a high prevalence of cardiovascular comorbidities and HF‐related clinical characteristics. Weighted mean age was 62.6 years in LBBB cohorts, compared with approximately 50 years in both RBBB and control groups. Male sex predominated across all study populations, particularly among RBBB cohorts.

Hypertension, diabetes mellitus, dyslipidemia, smoking history, atrial fibrillation, and coronary artery disease (CAD) were variably represented across the included studies, reflecting the heterogeneous clinical settings of the analyzed populations. Notably, CAD prevalence was numerically higher among control cohorts included in selected HF and TAVR‐related investigations, whereas isolated conduction abnormality cohorts generally excluded overt structural heart disease.

LBBB patients demonstrated markedly prolonged QRS duration compared with controls, consistent with advanced intraventricular conduction delay and electromechanical dyssynchrony. Among studies using STE, the weighted mean QRS duration was 153.7 ms in LBBB cohorts compared with 99.8 ms in control populations. Only one study employing CMR‐FT reported QRS duration data, showing similarly prolonged QRS durations in LBBB patients (158.2 ms) relative to controls (97.5 ms) [34]. However, the limited availability of CMR‐FT data precluded formal comparisons between imaging modalities.

In addition, natriuretic peptide levels were generally elevated among conduction abnormality cohorts, particularly in studies including HF populations.

Pharmacological treatment data reflected contemporary HF management in the studies enrolling HFrEF populations, with frequent use of beta‐blockers, loop diuretics, mineralocorticoid receptor antagonists, anticoagulants, antiplatelet agents, and CRT implantation. Conversely, studies focused on isolated LBBB or idiopathic RBBB cohorts included patients with fewer cardiovascular comorbidities and lower treatment burden.

3.4. Conventional Echocardiographic, STE, and CMR‐FT Findings

Table 3 summarizes the pooled structural, functional, and myocardial deformation imaging findings across LBBB, RBBB, and control populations.

TABLE 3.

Weighted conventional echocardiographic, speckle‐tracking echocardiography, and cardiac magnetic resonance feature‐tracking parameters across LBBB, RBBB, and control populations. Data are presented as weighted means with weighted interquartile ranges (IQRs), using the sample size of each study as weighting factor. The “Number of studies” column indicates the number of investigations reporting each imaging parameter. Weighted estimates were calculated at the study level and are intended to provide a descriptive summary of structural, functional, and myocardial deformation characteristics across LBBB, RBBB, and control populations rather than formal patient‐level pooled analyses. Exploratory p values were derived from study‐level comparisons among groups using the Kruskal–Wallis test and should therefore be interpreted cautiously, as they do not account for within‐study variability and were not adjusted for multiple comparisons. NA indicates that insufficient data were available for pooled estimation.

Parameter	Number of studies	LBBB weighted mean (IQR)	RBBB weighted mean (IQR)	Controls weighted mean (IQR)	p value
IVS (mm)	1	9.8 (9.8–9.8)	9.0 (9.0–9.0)	9.0 (9.0–9.0)	0.368
PW (mm)	1	10.1 (10.1–10.1)	8.0 (8.0–8.0)	8.0 (8.0–8.0)	0.368
LVEDD (mm)	7	54.4 (51.1–52.5)	46.6 (43.0–49.7)	43.5 (41.3–45.8)	0.010
LVESD (mm)	5	42.4 (37.7–39.7)	26.0 (26.0–26.0)	24.5 (24.1–25.0)	0.070
LVEDV (mL)	10	214.6 (109.4–349.0)	216.0 (141.6–278.0)	105.2 (81.4–138.5)	0.157
LVESV (mL)	10	153.7 (67.6–271.0)	150.0 (87.7–206.0)	50.1 (34.0–70.4)	0.169
LVEF (%)	14	36.9 (24.2–47.1)	40.3 (27.6–61.2)	62.6 (59.0–65.2)	0.004
LVSV (mL)	3	76.0 (76.0–76.0)	71.0 (71.0–71.0)	67.9 (52.1–94.3)	0.953
E/A	5	0.8 (0.7–0.8)	1.3 (1.0–1.4)	1.4 (1.3–1.5)	0.163
E/e'	5	13.9 (13.7–14.3)	8.9 (6.3–10.9)	7.6 (7.5–8.9)	0.014
LA (mm)	3	38.5 (37.7–37.7)	NA	30.0 (30.0–30.0)	0.180
RVIT (mm)	2	28.6 (25.1–32.9)	35.4 (29.0–41.1)	30.5 (30.0–31.0)	0.867
TAPSE (mm)	3	19.8 (19.0–21.6)	16.8 (15.2–20.0)	20.2 (16.6–22.0)	0.260
RVEF (%)	2	38.7 (38.7–38.7)	33.7 (34.4–34.4)	36.0 (36.0–36.0)	0.259
sPAP (mmHg)	4	29.4 (28.6–29.2)	32.2 (22.3–47.0)	31.2 (20.6–44.0)	0.920
LV‐GLS (%)	12	10.9 (6.2–13.5)	11.2 (7.3–18.0)	20.4 (17.7–21.8)	0.014
LV‐GCS (%)	5	9.2 (6.5–12.8)	7.9 (7.9–7.9)	15.1 (15.1–15.1)	0.243
LV‐GRS (%)	3	14.3 (8.9–23.2)	10.5 (10.5–10.5)	31.6 (31.6–31.6)	0.344
RV‐GLS (%)	2	23.3 (23.3–23.3)	21.1 (18.5–24.0)	26.2 (25.7–26.9)	0.223
RV‐FWLS (%)	1	12.1 (12.1–12.1)	25.4 (25.4–25.4)	28.6 (28.6–28.6)	0.368
LGE (%)	1	60.0 (60.0–60.0)	70.7 (70.7–70.7)	NA	0.317
ECV (%)	1	33.4 (33.4–33.4)	35.1 (35.1–35.1)	NA	0.317

Abbreviations: ECV, extracellular volume fraction; IQR, interquartile range; IVS, interventricular septal thickness; LA, left atrial diameter; LGE, late gadolinium enhancement; LVEDD, left ventricular end‐diastolic diameter; LVEDV, left ventricular end‐diastolic volume; LVEF, left ventricular ejection fraction; LVESD, left ventricular end‐systolic diameter; LVESV, left ventricular end‐systolic volume; LV‐GCS, left ventricular global circumferential strain; LV‐GLS, left ventricular global longitudinal strain; LV‐GRS, left ventricular global radial strain; LVSV, left ventricular stroke volume; NA, not available; PW, posterior wall thickness; RBBB, right bundle branch block; RVEF, right ventricular ejection fraction; RV‐FWLS, right ventricular free‐wall longitudinal strain; RV‐GLS, right ventricular global longitudinal strain; RVIT, right ventricular inferior wall thickness; sPAP, systolic pulmonary artery pressure; TAPSE, tricuspid annular plane systolic excursion.

Overall, patients with conduction abnormalities demonstrated evidence of ventricular remodeling, impaired systolic performance, abnormal diastolic function, and marked subclinical myocardial deformation abnormalities compared with healthy controls.

LBBB populations showed significantly larger LV dimensions and volumes, together with substantially reduced LVEF values compared with controls. In addition, E/e′ ratio values were significantly increased among LBBB cohorts, suggesting elevated LV filling pressures and more advanced diastolic dysfunction.

Myocardial deformation imaging demonstrated pronounced impairment of ventricular mechanics in patients with conduction abnormalities. In particular, LV‐GLS values were markedly reduced in both LBBB and RBBB populations compared with controls, indicating significant alteration of longitudinal myocardial function despite the heterogeneous clinical characteristics of the included cohorts. Similarly, LV‐GCS and LV‐GRS values tended to be numerically lower among conduction abnormality populations, although these findings were more heterogeneous across studies.

Right ventricular assessment demonstrated mildly reduced TAPSE, RV‐GLS, and RV‐FWLS values among RBBB cohorts compared with controls, supporting the potential impact of right‐sided conduction delay on RV mechanics and ventricular coupling. In contrast, sPAP values appeared relatively comparable across groups, although considerable interstudy variability was observed.

CMR‐derived analyses additionally suggested the presence of myocardial tissue abnormalities and ventricular remodeling in selected populations with conduction abnormalities. LGE and ECV values tended to be increased in patients with prolonged QRS duration and heart failure with reduced ejection fraction (HFrEF), supporting the possible contribution of diffuse myocardial fibrosis and adverse remodeling to mechanical dysfunction and dyssynchrony.

3.5. Clinical Outcomes and Determinants of Prognosis

Clinical outcomes, follow‐up duration, event rates, and the principal prognostic determinants identified across the included studies are provided separately for studies including patients with LBBB and RBBB in Tables 4 and 5, respectively.

TABLE 4.

Clinical outcomes, follow‐up duration, event rates, and main prognostic predictors in studies including patients with left bundle branch block [19, 20, 21, 22, 24, 25, 26, 27, 28, 29, 30, 31, 33, 34]. The table summarizes follow‐up duration, reported clinical endpoints, event rates, and principal prognostic predictors identified in studies including patients with left bundle branch block (LBBB). Follow‐up duration is expressed in months. Event rates are reported as percentages whenever available. Predictors are presented as reported by the original studies and may include hazard ratios (HRs), odds ratios (ORs), imaging‐derived parameters, or qualitative prognostic determinants. Because of substantial heterogeneity in study design, patient populations, endpoint definitions, and follow‐up duration, no quantitative pooling of outcomes was performed. NR indicates not reported; “/” indicates that follow‐up duration was not applicable or not available.

LBBB Study name	Size	Follow‐up (months)	Endpoint	Events rate (%)	Predictors
Maréchaux S. [19]	101	18	Cardiac death or hospitalization for heart failure after CRT; echocardiographic CRT response	13	Septal deformation pattern 1 or 2 strongly predictive of CRT response
Dobson L.E. [20]	24	6	Change in LVEF and GLS after TAVR	NR	TAVR‐induced LBBB is associated with less favorable cardiac reverse remodeling
Hwang I.C. [21]	269	27.5	Composite of cardiovascular mortality and hospitalization for heart failure	20.4	GLS (HR 0.21)
Wang Y. [22]	40	23	Relative reduction in LV GLS >15% from baseline to 2‐year follow‐up	36.1	Septal flash (OR 1.27)
Burke G.M. [24]	11	1	Electrocardiographic and echocardiographic changes after TAVR	NR	TAVR‐induced GLS deterioration in patients with new‐onset LBBB
Kim H.M. [25]	290	29.1	Follow‐up LVEF <40%	0.262	2D‐GLS (OR 0.65), 3D‐GLS (OR 0.72), 3D‐GCS (OR 0.61)
Layec J. [26]	121	46	Composite of all‐cause death or heart failure hospitalization after CRT	0.41	CRT response predictors: septal deformation pattern 1 or 2 (OR 10.05), GWW ≥200 mmHg% (OR 4.17), ischemic etiology (OR 0.25)
Yuan Y. [27]	87	58	Composite endpoint: cardiovascular death, heart transplantation, malignant arrhythmias, ICD/CRT‐D appropriate shocks	0.379	LBBB independently associated with adverse outcome (HR 2.025)
Naseer N.K. [28]	50	12	Composite of cardiovascular mortality and/or hospitalization for heart failure	Composite endpoint: 22%; CV mortality: 4%; HF hospitalization: 18%	GLS <13.5%, GCS <12.5%, GRS <14.5% associated with composite outcome
Pastorini G. [29]	78	33	Composite of cardiovascular death or acute heart failure	CV death: 1.3%; urgent outpatient HF visits: 17.9%; HF hospitalization: 15.4%	LVEF (HR 0.89), Diastolic dysfunction grade ≥2 (HR 3.30), GLS (HR 0.70), Agatston score (HR 1.01), Syntax score (HR 1.16)
Chen M. [30]	44	/	Impaired RV and LV systolic/diastolic function and ventricular dyssynchrony in isolated CRBBB vs. CLBBB and healthy controls	NR	RV‐GLS independently associated with RV mechanical dispersion; LV‐GLS independently associated with RV‐GLS
Margulescu A.D. [31]	38	18	Progression of LV dysfunction and mechanical dyssynchrony after TAVR‐related N‐LBBB	Mortality at follow‐up: new‐onset LBBB 29.4%; chronic LBBB 17.6%	N‐LBBB after TAVR results in an immediate reduction of cardiac function
Atabekov T. [33]	54	6	CRT super‐response defined as NYHA class improvement ≥1 plus either LVEF increase ≥15% or LVESV reduction ≥30%	72.2	GLS (OR 0.43), S‐wave amplitude in lead V2 (OR 8.53), interventricular dyssynchrony (OR 1.03)
Zhou D. [34]	483	/	Presence and characterization of conduction delay (LBBB vs. RBBB vs. IVCD) in nonischemic HFrEF	LBBB: 44.4%; RBBB: 16.9%; IVCD: 20.2% of the whole cohort	More impaired left ventricular torsion and strains than those with RBBB

Abbreviations: CRT, cardiac resynchronization therapy; CRT‐D, cardiac resynchronization therapy‐defibrillator; CV, cardiovascular; GCS, global circumferential strain; GLS, global longitudinal strain; GWW, global wasted work; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; HR, hazard ratio; ICD, implantable cardioverter‐defibrillator; IVCD, intraventricular conduction delay; LBBB, left bundle branch block; LVEF, left ventricular ejection fraction; LVESV, left ventricular end‐systolic volume; LV‐GLS, left ventricular global longitudinal strain; N‐LBBB, new‐onset left bundle branch block; NR, not reported; NYHA, New York Heart Association; OR, odds ratio; RBBB, right bundle branch block; RV‐GLS, right ventricular global longitudinal strain; TAVR, transcatheter aortic valve replacement.

TABLE 5.

Clinical outcomes, follow‐up duration, event rates, and main prognostic predictors in studies including patients with right bundle branch block [23, 27, 30, 32, 34]. The table summarizes follow‐up duration, reported clinical endpoints, event rates, and principal prognostic predictors identified in studies including patients with right bundle branch block (RBBB). Follow‐up duration is expressed in months. Event rates are reported as percentages whenever available. Predictors are presented as reported by the original studies and may include imaging‐derived parameters or qualitative prognostic determinants. Because of substantial heterogeneity in study design, patient populations, endpoint definitions, and follow‐up duration, no quantitative pooling of outcomes was performed. NR indicates not reported; “/” indicates that follow‐up duration was not applicable or not available.

RBBB Study name	Size	Follow‐up (months)	Endpoint	Events rate (%)	Predictors
Nakazawa N. [23]	26	/	RV enlargement and systolic dysfunction associated with CRBBB and RV mechanical dyssynchrony	NR	RBBB was associated with delayed RV mechanical activation, larger RV volumes, and reduced RV systolic function
Yuan Y. [27]	27	58	Composite endpoint: cardiovascular death, heart transplantation, malignant arrhythmias, ICD/CRT‐D appropriate shocks	18.5	RBBB not independently associated with outcome
Chen M. [30]	44	/	Impaired RV and LV systolic/diastolic function and ventricular dyssynchrony in isolated CRBBB vs. CLBBB and healthy controls	NR	RV‐GLS independently associated with RV mechanical dispersion; LV‐GLS independently associated with RV‐GLS
Seçkin Göbüt Ö. [32]	39	/	To assess ventricular mechanics in idiopathic RBBB patients	NR	RBBB significantly affects the longitudinal strain
Zhou D. [34]	184	/	Presence and characterization of conduction delay (LBBB vs. RBBB vs. IVCD) in nonischemic HFrEF	LBBB: 44.4%; RBBB: 16.9%; IVCD: 20.2% of the whole cohort	Larger LGE percentage and ECV than those with LBBB

Abbreviations: CLBBB, complete left bundle branch block; CRBBB, complete right bundle branch block; CRT‐D, cardiac resynchronization therapy‐defibrillator; ECV, extracellular volume fraction; HFrEF, heart failure with reduced ejection fraction; ICD, implantable cardioverter‐defibrillator; IVCD, intraventricular conduction delay; LBBB, left bundle branch block; LGE, late gadolinium enhancement; LV, left ventricular; LV‐GLS, left ventricular global longitudinal strain; NR, not reported; RBBB, right bundle branch block; RV, right ventricular; RV‐GLS, right ventricular global longitudinal strain.

Follow‐up duration varied substantially among studies, ranging from short‐term post‐procedural evaluations to extended longitudinal follow‐up in HF and cardiomyopathy cohorts. Event rates were similarly heterogeneous, reflecting differences in study design, patient selection, and clinical settings.

Studies including LBBB patients (Table 4) predominantly evaluated hard clinical outcomes, including cardiovascular mortality, HF hospitalization, ventricular remodeling, CRT response, and composite cardiovascular endpoints. In these populations, advanced myocardial deformation parameters, particularly LV‐GLS, septal deformation patterns, myocardial work indices, and markers of electromechanical dyssynchrony, consistently emerged as important determinants of prognosis.

Conversely, studies including RBBB patients (Table 5) more frequently focused on ventricular mechanics, RV remodeling, and myocardial deformation abnormalities rather than major adverse clinical events. Accordingly, prognostic analyses in RBBB cohorts were less frequently reported, and available evidence mainly highlighted the association between RBBB, impaired RV mechanics, ventricular dyssynchrony, and subclinical myocardial dysfunction.

The most frequently reported endpoints included arrhythmic events and atrial fibrillation, all‐cause or cardiovascular mortality, HF progression and hospitalization, major adverse cardiovascular events, and valve‐related interventions. Figure 2 illustrates the comparative distribution of the main clinical outcomes across LBBB and RBBB studies, highlighting the predominance of HF‐, arrhythmia‐, and mortality‐related endpoints among LBBB populations. In contrast, RBBB investigations more frequently focused on ventricular mechanics and subclinical myocardial dysfunction rather than hard clinical outcomes.

FIGURE 2.

Comparative distribution of clinical outcomes across LBBB and RBBB studies. Comparative distribution of the principal clinical outcomes reported among studies including patients with LBBB and RBBB. Bars represent the number of studies reporting each outcome category. LBBB studies predominantly evaluated arrhythmias/atrial fibrillation, mortality, heart failure progression, hospitalization, and valve‐related interventions, whereas RBBB studies more frequently focused on ventricular mechanics and subclinical myocardial dysfunction. AF, atrial fibrillation; LBBB, left bundle branch block; MACE, major adverse cardiovascular events; MI, myocardial infarction; RBBB, right bundle branch block.

Across the included studies, myocardial deformation imaging parameters consistently emerged as important determinants of prognosis. Reduced LV‐GLS values, abnormal septal deformation patterns, impaired myocardial work efficiency, and advanced electromechanical dyssynchrony were frequently associated with adverse ventricular remodeling, poorer CRT response, HF progression, and unfavorable long‐term outcomes.

Several studies additionally demonstrated the incremental prognostic value of advanced deformation imaging beyond conventional echocardiographic parameters and QRS duration alone. In particular, strain‐derived indices appeared capable of identifying subclinical myocardial dysfunction and heterogeneous mechanical activation patterns not fully captured by standard electrical or volumetric assessment.

Among CRT populations, markers of mechanical dyssynchrony, septal strain abnormalities, and myocardial work redistribution were strongly associated with CRT response and reverse remodeling. Conversely, in isolated LBBB or idiopathic RBBB cohorts without overt structural heart disease, deformation imaging abnormalities mainly reflected early subclinical impairment of ventricular mechanics.

3.5.1. Meta‐Analysis of Differences in Left Ventricular Ejection Fraction Between LBBB Patients and Controls

The results of the meta‐analysis evaluating differences in LVEF between patients with LBBB and control subjects without LBBB are illustrated in the forest plot (Figure 3).

FIGURE 3.

Forest plot showing pooled SMDs in LVEF between patients with LBBB and control subjects. Separate analyses are reported according to imaging modality (STE and CMR‐FT), together with subgroup and overall pooled estimates. Negative SMD values indicate lower LVEF in patients with LBBB. CI, confidence interval; CMR‐FT, cardiac magnetic resonance feature tracking; LBBB, left bundle branch block; LVEF, left ventricular ejection fraction; SMD, standardized mean difference; STE, speckle‐tracking echocardiography.

Using a random‐effects model because of the substantial overall heterogeneity, pooled analysis demonstrated significantly lower LVEF values among patients with LBBB compared with controls, with an overall SMD of −0.404 (95% CI −0.553 to −0.255; p < 0.001). These findings support the concept that LBBB is associated with impaired conventional systolic function and adverse ventricular mechanics.

Subgroup analyses according to imaging modality revealed important differences between STE‐ and CMR‐FT–derived measurements. Among STE studies, pooled analysis demonstrated markedly reduced LVEF values in LBBB patients compared with controls (SMD −1.261, 95% CI −1.688 to −0.835; p < 0.001), with moderate‐to‐high heterogeneity (I ² = 61.0%). Conversely, CMR‐FT studies demonstrated a smaller but still statistically significant reduction in LVEF associated with LBBB (SMD −0.285, 95% CI −0.444 to −0.126; p < 0.001), with no significant heterogeneity observed within this subgroup (I ² = 0.0%). The between‐subgroup difference was statistically significant (Q_between = 17.640, p < 0.001), suggesting that imaging modality substantially influenced the magnitude of observed systolic functional impairment.

Overall between‐study heterogeneity was considerable, with an I ² value of 90.6% (Q = 53.223, p < 0.001), supporting the use of random‐effects modeling for the primary pooled analysis. The fixed‐effect model similarly demonstrated significantly reduced LVEF values in LBBB patients (SMD −0.572, 95% CI −0.707 to −0.437; p < 0.001), confirming the consistency of the overall findings despite methodological heterogeneity.

Potential publication bias was evaluated through visual inspection of the funnel plot (Figure 4) and Egger's regression test. Visual analysis demonstrated a relatively symmetrical distribution of studies around the pooled effect estimate, although mild asymmetry was observed among smaller investigations characterized by larger negative effect sizes. Egger's regression intercept was −3.830 (SE 2.073), with a non‐significant two‐tailed p value of 0.138, indicating no statistically significant evidence of publication bias or small‐study effects despite the limited number of included studies.

FIGURE 4.

Funnel plot displaying the relationship between study precision (standard error) and effect size (standardized mean difference) for studies comparing LVEF between patients with LBBB and controls. LBBB, left bundle branch block; LVEF, left ventricular ejection fraction; SMD, standardized mean difference.

The results of the exploratory random‐effects meta‐regression analyses performed to investigate potential sources of heterogeneity are summarized in Table 6. Because of the relatively small number of studies included in this meta‐analysis, exploratory meta‐regression analyses were performed cautiously using two separate random‐effects models in order to minimize model overfitting and instability. The first model mainly explored demographic and clinical variables, whereas the second model evaluated imaging‐ and methodology‐related parameters. As shown in Table 6, none of the investigated covariates, including mean age, systolic blood pressure, heart rate, body mass index, diabetes prevalence, and male sex distribution, demonstrated a statistically significant association with pooled effect size. Although a borderline trend was observed for male sex distribution (p = 0.092), no moderator reached conventional statistical significance. Exploratory analyses nevertheless suggested that differences in imaging modality, baseline ventricular remodeling severity, and HF burden may partially contribute to the observed heterogeneity across studies. Given the limited statistical power related to the small sample of included studies, these findings should be considered hypothesis‐generating rather than definitive.

TABLE 6.

Exploratory random‐effects meta‐regression analyses investigating potential sources of heterogeneity in the meta‐analysis of LVEF differences between LBBB patients and controls. Model 1 evaluated demographic and hemodynamic variables, whereas Model 2 assessed selected clinical characteristics. Regression coefficients represent the estimated change in pooled standardized mean difference (SMD) associated with a one‐unit increase in the corresponding covariate. Given the limited number of available studies, all meta‐regression analyses should be considered exploratory and hypothesis‐generating.

Covariate	Coefficient	Standard error	95% Lower	95% Upper	p value
Model 1
Intercept	−7.827	16.735	−40.627	24.973	0.640
Mean age (yrs)	0.011	0.036	−0.059	0.081	0.765
SBP (mmHg)	−0.002	0.081	−0.160	0.157	0.985
HR (bpm)	0.088	0.126	−0.160	0.335	0.487

Model 2
Intercept	−8.741	13.359	−34.925	17.442	0.513
BMI (Kg/m2)	0.262	0.518	−0.752	1.277	0.613
Diabetes (%)	−0.020	0.022	−0.063	0.023	0.370
% Males	0.036	0.022	−0.006	0.079	0.092

Abbreviations: BMI, body mass index; HR, heart rate; LBBB, left bundle branch block; LVEF, left ventricular ejection fraction; SBP, systolic blood pressure; SMD, standardized mean difference.

Sensitivity analyses using a leave‐one‐out approach confirmed the robustness of the pooled estimates. Sequential exclusion of individual studies resulted in only modest fluctuations in pooled SMD values, which consistently remained statistically significant throughout all iterations. Recalculated pooled effect sizes ranged approximately between −0.746 and −1.090 following sequential study removal, with corresponding p values persistently remaining below the threshold for statistical significance. These findings support the stability and reproducibility of the observed association between LBBB and reduced LVEF.

3.5.2. Meta‐Analysis of Differences in Left Ventricular Ejection Fraction Between RBBB Patients and Controls

The results of the meta‐analysis evaluating differences in LVEF between patients with RBBB and control subjects without RBBB are illustrated in the forest plot (Figure 5).

FIGURE 5.

Forest plot showing pooled SMDs in LVEF between patients with RBBB and control subjects. Subgroup analyses according to imaging modality (STE and CMR‐FT) and the overall pooled estimate are reported. Negative SMD values indicate lower LVEF in patients with RBBB. CI, confidence interval; CMR‐FT, cardiac magnetic resonance feature tracking; LVEF, left ventricular ejection fraction; RBBB, right bundle branch block; SMD, standardized mean difference; STE, speckle‐tracking echocardiography.

Using a random‐effects model because of the substantial overall heterogeneity, pooled analysis demonstrated no statistically significant overall difference in LVEF between RBBB patients and controls, with an overall SMD of 0.051 (95% CI −0.146 to 0.247; p = 0.613). These findings suggest that conventional systolic function assessed by LVEF may remain relatively preserved in RBBB populations despite the presence of electrical conduction abnormalities.

Subgroup analyses according to imaging modality revealed heterogeneous findings between STE‐ and CMR‐FT–derived measurements. Among STE studies, pooled analysis demonstrated a non‐significant trend toward lower LVEF values in RBBB patients compared with controls (SMD −0.505, 95% CI −1.498 to 0.488; p = 0.319), with very high heterogeneity (I ² = 91.9%). Conversely, the single available CMR‐FT study demonstrated no significant difference in LVEF between RBBB and control subjects (SMD 0.073, 95% CI −0.127 to 0.274; p = 0.473), with no within‐subgroup heterogeneity observed.

Overall between‐study heterogeneity was considerable, with an I ² value of 91.9% (Q = 37.320, p < 0.001), indicating marked variability across the included investigations. In contrast to the LBBB analysis, the fixed‐effect model demonstrated only a borderline non‐significant reduction in LVEF among RBBB patients (SMD −0.137, 95% CI −0.300 to 0.026; p = 0.101), further supporting the absence of a consistent detrimental effect of RBBB on conventional systolic performance.

Potential publication bias was evaluated using funnel plot inspection (Figure 6) and Egger's regression test. Visual inspection of the funnel plot demonstrated a relatively symmetrical distribution of studies around the pooled effect estimate despite the limited number of included investigations. Egger's regression intercept was −3.802 (SE 4.430), with a non‐significant two‐tailed p value of 0.481, indicating no statistically significant evidence of publication bias or small‐study effects.

FIGURE 6.

Funnel plot illustrating study precision versus effect size for studies evaluating differences in LVEF between patients with RBBB and controls. LVEF, left ventricular ejection fraction; RBBB, right bundle branch block; SMD, standardized mean difference.

Because only three studies were available for quantitative synthesis, meta‐regression analyses were not performed according to the predefined methodological criteria. Consequently, potential sources of heterogeneity could not be formally investigated. The substantial between‐study variability observed may reflect differences in patient characteristics, underlying cardiac disease burden, imaging modality, and methodological approaches across the included investigations.

Sensitivity analyses using a leave‐one‐out approach demonstrated moderate instability of pooled estimates. Sequential exclusion of individual studies resulted in substantial fluctuations in pooled SMD values, with recalculated effect sizes ranging approximately between −0.553 and 0.020. Importantly, pooled results remained consistently non‐significant throughout all iterations, confirming the absence of a robust association between isolated RBBB and reduced LVEF compared with controls.

3.5.3. Meta‐Analysis of Differences in Left Ventricular Ejection Fraction Between LBBB and RBBB Patients

The results of the meta‐analysis evaluating differences in LVEF between patients with LBBB and RBBB are illustrated in the forest plot (Figure 7).

FIGURE 7.

Forest plot showing pooled SMDs in LVEF between patients with LBBB and RBBB. Analyses are stratified according to imaging modality (STE and CMR‐FT). Negative SMD values indicate lower LVEF among patients with LBBB. CI, confidence interval; CMR‐FT, cardiac magnetic resonance feature tracking; LBBB, left bundle branch block; LVEF, left ventricular ejection fraction; RBBB, right bundle branch block; SMD, standardized mean difference; STE, speckle‐tracking echocardiography.

Because no significant between‐study heterogeneity was observed, pooled analyses were performed using a fixed‐effects model. Overall pooled analysis demonstrated significantly lower LVEF values in patients with LBBB compared with those with RBBB, with an overall SMD of −0.361 (95% CI −0.519 to −0.202; p < 0.001). These findings support the concept that LBBB is associated with a more pronounced impairment of conventional systolic function than RBBB.

Subgroup analyses according to imaging modality demonstrated largely consistent findings between STE‐ and CMR‐FT–derived measurements. The STE subgroup demonstrated a non‐significant trend toward lower LVEF values in LBBB patients compared with RBBB patients (SMD −0.354, 95% CI −0.776 to 0.067; p = 0.099). In contrast, the CMR‐FT subgroup demonstrated significantly lower LVEF values in LBBB populations (SMD −0.362, 95% CI −0.533 to −0.191; p < 0.001). No statistically significant between‐subgroup heterogeneity was observed (Q_between = 0.001, p = 0.975), suggesting substantial consistency between echocardiographic and CMR‐derived findings.

Overall heterogeneity was negligible, with an I ² value of 0.0% (Q = 0.001, p = 0.975), indicating excellent consistency across the included studies and supporting the robustness of the pooled effect estimate.

Given the very limited number of included studies (n = 2), funnel plot analysis, Egger's regression testing, and meta‐regression analyses were not performed because of the limited statistical reliability and interpretability of these approaches in extremely small datasets.

Sensitivity analyses using a leave‐one‐out approach demonstrated excellent stability of pooled estimates. Sequential exclusion of individual studies resulted in only minimal fluctuations in pooled SMD values, which remained directionally consistent throughout all iterations. Removal of the CMR‐FT study maintained a trend toward lower LVEF values in LBBB patients (SMD −0.354, p = 0.099), whereas exclusion of the STE study preserved a statistically significant reduction in LVEF among LBBB populations (SMD −0.362, p < 0.001). Overall, these findings support the reproducibility and methodological consistency of the observed association between LBBB and greater systolic dysfunction compared with RBBB.

3.5.4. Meta‐Analysis of Differences in Left Ventricular Global Longitudinal Strain Between LBBB Patients and Healthy Controls

The results of the meta‐analysis evaluating differences in LV‐GLS between patients with LBBB and healthy control subjects are illustrated in the forest plot (Figure 8).

FIGURE 8.

Forest plot showing pooled SMDs in LV‐GLS between patients with LBBB and healthy controls. Separate subgroup analyses according to STE and CMR‐FT are presented. Negative SMD values indicate more impaired LV longitudinal mechanics in patients with LBBB. CI, confidence interval; CMR‐FT, cardiac magnetic resonance feature tracking; LBBB, left bundle branch block; LV‐GLS, left ventricular global longitudinal strain; SMD, standardized mean difference; STE, speckle‐tracking echocardiography.

Using a random‐effects model because of the substantial between‐study heterogeneity, pooled analysis demonstrated significantly impaired LV‐GLS values in patients with LBBB compared with controls, with an overall SMD of −0.345 (95% CI −0.535 to −0.156; p < 0.001). These findings indicate the presence of significant subclinical and overt impairment of LV longitudinal mechanics among LBBB populations.

Subgroup analyses according to imaging modality demonstrated important differences between STE‐ and CMR‐FT–derived measurements. Among STE studies, pooled analysis demonstrated markedly impaired LV‐GLS values in LBBB patients compared with controls (SMD −1.538, 95% CI −2.550 to −0.527; p = 0.003). In contrast, CMR‐FT studies demonstrated a smaller but still statistically significant reduction in LV‐GLS values among LBBB patients (SMD −0.302, 95% CI −0.495 to −0.109; p = 0.002). Between‐subgroup heterogeneity was statistically significant (Q_between = 5.537, p = 0.019), suggesting that imaging modality substantially influenced the magnitude of the observed deformation abnormalities.

Overall between‐study heterogeneity was considerable, with an I ² value of 94.5% (Q = 90.678, p < 0.001). Heterogeneity was particularly pronounced among STE investigations (I ² = 92.2%), whereas CMR‐FT studies demonstrated substantially lower heterogeneity (I ² = 7.3%). These findings likely reflect differences in study populations, acquisition protocols, software vendors, and myocardial strain analysis methodologies across echocardiographic studies.

Potential publication bias was evaluated using funnel plot inspection (Figure 9). Visual assessment demonstrated a relatively asymmetric distribution of studies around the pooled effect estimate, with smaller studies tending to report larger negative effect sizes. However, interpretation should remain cautious because of the limited number of included studies.

FIGURE 9.

Funnel plot illustrating the distribution of studies evaluating LV‐GLS differences between patients with LBBB and controls according to study precision and effect size. LBBB, left bundle branch block; LV‐GLS, left ventricular global longitudinal strain; SMD, standardized mean difference.

Egger's regression testing was additionally performed and did not demonstrate statistically significant evidence of publication bias, although the relatively small number of studies limited the statistical power of this analysis.

The results of the exploratory random‐effects meta‐regression analyses performed to investigate potential sources of heterogeneity are summarized in Table 7. Because of the relatively limited number of included investigations and the substantial heterogeneity observed across studies, meta‐regression analyses were considered exploratory and interpreted cautiously. As shown in Table 7, none of the evaluated demographic, clinical, or hemodynamic covariates demonstrated a statistically significant association with pooled LV‐GLS effect sizes. Mean age, body mass index, heart rate, and systolic blood pressure were not significant moderators of the observed association between LBBB and impaired LV longitudinal mechanics. A borderline trend was observed for heart rate in Model 1 (p = 0.081), although statistical significance was not reached. Overall, the findings suggest that the impairment in LV longitudinal mechanics observed among LBBB patients was relatively consistent across studies and unlikely to be explained solely by demographic or basic hemodynamic differences.

TABLE 7.

Exploratory random‐effects meta‐regression analyses investigating potential sources of heterogeneity in the meta‐analysis of LV‐GLS differences between LBBB patients and healthy controls. Model 1 evaluated demographic and hemodynamic variables, whereas Model 2 assessed anthropometric and additional hemodynamic characteristics. Regression coefficients represent the estimated change in pooled standardized mean difference (SMD) associated with a one‐unit increase in the corresponding covariate. Given the limited number of available studies and the substantial between‐study heterogeneity, all meta‐regression analyses should be considered exploratory and hypothesis‐generating.

Covariate	Coefficient	Standard error	95% lower	95% upper	p value
Model 1
Intercept	−16.391	14.546	−44.901	12.120	0.260
Mean age (yrs)	0.025	0.032	−0.037	0.088	0.424
HR (bpm)	0.190	0.109	−0.024	0.403	0.081
SBP (mmHg)	−0.002	0.071	−0.141	0.136	0.976

Model 2
Intercept	4.353	33.505	−61.316	70.022	0.896
BMI (Kg/m2)	−1.044	1.149	−3.296	1.208	0.363
HR (bpm)	0.171	0.119	−0.063	0.406	0.152
SBP (mmHg)	0.064	0.053	−0.04	0.168	0.227

Abbreviations: BMI, body mass index; HR, heart rate; LBBB, left bundle branch block; LV‐GLS, left ventricular global longitudinal strain; SBP, systolic blood pressure; SMD, standardized mean difference.

Sensitivity analyses using a leave‐one‐out approach confirmed the persistence of impaired LV longitudinal mechanics in LBBB populations despite moderate fluctuations in pooled effect size estimates following sequential study exclusion. Overall, the direction and statistical significance of the pooled association remained largely preserved, supporting the robustness of the observed relationship between LBBB and impaired LV‐GLS.

3.5.5. Meta‐Analysis of Differences in Left Ventricular Global Longitudinal Strain Between RBBB Patients and Healthy Controls

The results of the meta‐analysis evaluating differences in LV‐GLS between patients with RBBB and healthy control subjects are illustrated in the forest plot (Figure 10).

FIGURE 10.

Forest plot showing pooled SMDs in LV‐GLS between patients with RBBB and healthy controls. Subgroup analyses according to STE and CMR‐FT are reported. Negative SMD values indicate impaired LV longitudinal deformation among patients with RBBB. CI, confidence interval; CMR‐FT, cardiac magnetic resonance feature tracking; LV‐GLS, left ventricular global longitudinal strain; RBBB, right bundle branch block; SMD, standardized mean difference; STE, speckle‐tracking echocardiography.

Using a random‐effects model because of the marked between‐study heterogeneity, pooled analysis demonstrated no statistically significant overall difference in LV‐GLS values between RBBB patients and controls, with an overall SMD of 0.064 (95% CI −0.134 to 0.262; p = 0.527). These findings suggest that RBBB may exert a less pronounced impact on LV longitudinal mechanics compared with LBBB populations.

Subgroup analyses according to imaging modality demonstrated substantial differences between STE‐ and CMR‐FT–derived measurements. Among STE studies, pooled analysis demonstrated a trend toward impaired LV‐GLS values in RBBB patients compared with controls (SMD −1.404, 95% CI −2.823 to 0.016; p = 0.053), although statistical significance was not reached. Conversely, the single available CMR‐FT study demonstrated no significant difference in LV‐GLS between RBBB patients and controls (SMD 0.093, 95% CI −0.107 to 0.294; p = 0.361). Between‐subgroup heterogeneity was statistically significant (Q_between = 4.189, p = 0.041), suggesting that imaging modality influenced the magnitude and direction of the observed deformation findings.

Overall between‐study heterogeneity was extremely high, with an I ² value of 96.8% (Q = 63.166, p < 0.001). Heterogeneity was particularly pronounced among STE investigations (I ² = 93.8%), whereas heterogeneity was absent within the CMR‐FT subgroup because only one study was available. The observed variability likely reflects differences in study populations, underlying structural heart disease burden, acquisition protocols, and strain analysis methodologies.

Potential publication bias was evaluated using funnel plot inspection (Figure 11). Visual assessment demonstrated moderate asymmetry, with smaller studies tending to report larger negative effect sizes. However, interpretation remains limited because of the very small number of included investigations.

FIGURE 11.

Funnel plot illustrating study precision versus effect size for investigations comparing LV‐GLS between patients with RBBB and controls. LV‐GLS, left ventricular global longitudinal strain; RBBB, right bundle branch block; SMD, standardized mean difference.

Egger's regression testing did not demonstrate statistically significant evidence of publication bias, although the limited number of included studies substantially reduced the reliability and statistical power of this analysis.

Because only three studies were available for quantitative synthesis, meta‐regression analyses were not performed. Similarly, the interpretation of publication bias analyses should remain cautious.

Sensitivity analyses using a leave‐one‐out approach demonstrated moderate instability of pooled effect estimates. Sequential exclusion of individual studies resulted in substantial fluctuations in pooled SMD values, with loss of statistical significance across several iterations. These findings suggest that the overall pooled estimate was strongly influenced by individual studies and should therefore be interpreted cautiously. Nevertheless, the available evidence overall suggests a less consistent and less pronounced impairment of LV longitudinal mechanics in RBBB populations compared with patients affected by LBBB.

3.5.6. Meta‐Analysis of Differences in Left Ventricular Global Longitudinal Strain Between LBBB and RBBB Patients

The results of the meta‐analysis evaluating differences in LV‐GLS between patients with LBBB and RBBB are illustrated in the forest plot (Figure 12).

FIGURE 12.

Forest plot showing pooled SMDs in LV‐GLS between patients with LBBB and RBBB. Results are presented separately according to imaging modality (STE and CMR‐FT), together with the overall pooled estimate. Negative SMD values indicate greater impairment of LV longitudinal mechanics in patients with LBBB compared with RBBB. CI, confidence interval; CMR‐FT, cardiac magnetic resonance feature tracking; LBBB, left bundle branch block; LV‐GLS, left ventricular global longitudinal strain; RBBB, right bundle branch block; SMD, standardized mean difference; STE, speckle‐tracking echocardiography.

Using a fixed‐effects model because of the absence of statistically significant between‐study heterogeneity, pooled analysis demonstrated significantly more impaired LV‐GLS values in patients with LBBB compared with RBBB populations, with an overall SMD of −0.436 (95% CI −0.595 to −0.276; p < 0.001). These findings suggest a more pronounced detrimental impact of LBBB on LV longitudinal mechanics compared with RBBB.

Subgroup analyses according to imaging modality demonstrated consistent findings across STE and CMR‐FT investigations. The STE study demonstrated significantly lower LV‐GLS values in LBBB patients compared with RBBB patients (SMD −0.758, 95% CI −1.191 to −0.326; p = 0.001). Similarly, the CMR‐FT study demonstrated significantly impaired LV‐GLS values in LBBB populations (SMD −0.385, 95% CI −0.556 to −0.214; p < 0.001). Between‐subgroup heterogeneity was not statistically significant, suggesting relative consistency between echocardiographic and CMR‐derived deformation findings.

Overall between‐study heterogeneity was moderate (I ² = 59.5%), although statistical significance for heterogeneity was not reached. Given the limited number of included studies, these findings should nevertheless be interpreted cautiously.

Because only two studies were available for quantitative synthesis, funnel plot inspection, Egger's regression testing, and meta‐regression analyses were not performed according to the predefined methodological criteria.

Sensitivity analyses using a leave‐one‐out approach demonstrated persistent statistical significance after sequential study exclusion, supporting the robustness of the observed association between LBBB and greater impairment of LV longitudinal mechanics compared with RBBB. Overall, these findings reinforce the concept that left‐sided conduction abnormalities exert a more pronounced adverse effect on ventricular mechanical synchrony and myocardial deformation than isolated right‐sided conduction disturbances.

3.5.7. Methodological Quality of the Included Studies

Methodological quality assessment of the included studies was performed using the NIH Quality Assessment Tool for Observational Cohort and Cross‐Sectional Studies, and the detailed results are reported in Table 8 [19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34]. Overall, the methodological quality of the included investigations was considered generally acceptable to good, with no studies categorized as having critically low methodological quality.

TABLE 8.

Risk‐of‐bias assessment of the included studies [19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34] using the National Institutes of Health (NIH) quality assessment tool for observational cohort and cross‐sectional studies. Studies are presented in chronological order from the oldest to the most recent publication. The overall quality rating was assigned according to the number of fulfilled criteria and the methodological relevance of unmet items for each specific study design. Cross‐sectional studies were assessed using the same instrument; criteria related to temporal sequence, follow‐up duration, or loss to follow‐up were classified as not applicable (NA) when appropriate.

Study	Q1	Q2	Q3	Q4	Q5	Q6	Q7	Q8	Q9	Q10	Q11	Q12	Q13	Q14	Overall
Maréchaux S. (2014) [19]	Y	Y	NR	Y	NR	Y	Y	Y	Y	N	Y	NR	Y	Y	10 (Good)
Dobson L.E. (2017) [20]	Y	Y	NR	Y	Y	Y	Y	Y	Y	Y	Y	NR	Y	Y	12 (Good)
Hwang I.C. (2018) [21]	Y	Y	NR	Y	NR	Y	Y	Y	Y	N	Y	NR	Y	Y	10 (Good)
Wang Y. (2018) [22]	Y	Y	NR	Y	NR	NA	NA	Y	Y	N	Y	NR	NA	Y	7 (Fair)
Nakazawa N. (2020) [23]	Y	Y	NR	Y	NR	NA	NA	Y	Y	N	Y	NR	NA	N	6 (Fair)
Burke G.M. (2021) [24]	Y	Y	NR	CD	NR	Y	Y	Y	Y	Y	Y	Y	CD	N	9 (Fair)
Kim H.M. (2023) [25]	Y	Y	NR	Y	NR	Y	Y	Y	Y	Y	Y	NR	Y	Y	11 (Good)
Layec J. (2023) [26]	Y	Y	NR	Y	NR	Y	Y	Y	Y	N	Y	NR	Y	Y	10 (Good)
Yuan Y. (2023) [27]	Y	Y	NR	Y	NR	Y	Y	Y	Y	N	Y	NR	Y	Y	10 (Good)
Naseer N.K. (2024) [28]	Y	Y	NR	Y	Y	Y	Y	Y	Y	Y	Y	NR	Y	N	11 (Good)
Pastorini G. (2024) [29]	Y	Y	NR	Y	NR	Y	Y	Y	Y	N	Y	NR	Y	Y	10 (Fair)
Chen M. (2024) [30]	Y	Y	NR	Y	NR	NA	NA	Y	Y	N	Y	NR	NA	Y	7 (Fair)
Margulescu A.D. (2024) [31]	Y	Y	NR	Y	NR	Y	Y	Y	Y	Y	Y	NR	Y	N	10 (Fair)
Seçkin Göbüt Ö. (2025) [32]	Y	Y	NR	Y	NR	NA	NA	Y	Y	N	Y	NR	NA	Y	7 (Fair)
Atabekov T. (2025) [33]	Y	Y	NR	Y	NR	Y	Y	Y	Y	Y	Y	NR	Y	Y	11 (Good)
Zhou D. (2025) [34]	Y	Y	NR	Y	NR	NA	NA	Y	Y	N	Y	NR	NA	Y	7 (Fair)

Abbreviations: CD, cannot determine; CRT, cardiac resynchronization therapy; CMR, cardiac magnetic resonance; DCM, dilated cardiomyopathy; LBBB, left bundle branch block; NA, not applicable; NIH, National Institutes of Health; NR, not reported; RBBB, right bundle branch block; TAVR, transcatheter aortic valve replacement; Y, yes. Additional note for Q1–Q14: Q1, research question clearly stated; Q2, study population clearly specified and defined; Q3, participation rate ≥50%; Q4, uniform recruitment and eligibility criteria; Q5, sample‐size justification or power calculation provided; Q6, exposure measured before outcome; Q7, sufficient timeframe to detect an association; Q8, exposure levels or exposure‐response relationship examined; Q9, exposure measures clearly defined and reliable; Q10, repeated exposure assessment over time; Q11, outcome measures clearly defined and reliable; Q12, outcome assessors blinded to exposure status; Q13, loss to follow‐up ≤20%; Q14, adjustment for key confounding variables.

Most studies clearly defined the study objectives, patient populations, inclusion and exclusion criteria, imaging acquisition protocols, and outcome measures. Standardized STE and/or CMR‐FT methodologies were consistently implemented across the majority of investigations, supporting the overall reliability and reproducibility of myocardial deformation assessment. Several studies additionally incorporated multivariable adjustment models, longitudinal reassessment, matched control populations, serial imaging evaluation, or blinded offline strain analysis, thereby strengthening the methodological robustness of the available evidence.

According to predefined NIH quality thresholds, eight studies were classified as good quality and eight as fair quality, whereas no investigations were categorized as poor quality. Studies rated as good quality generally demonstrated more comprehensive confounding adjustment, clearer longitudinal design, repeated imaging reassessment, or more robust statistical methodology. Conversely, studies classified as fair quality were mainly limited by cross‐sectional design, relatively small sample size, incomplete reporting of assessor blinding procedures, or limited adjustment for potential confounding variables.

The most frequently identified methodological limitations across the included literature included the absence of formal sample‐size or power calculations, incomplete reporting of blinded outcome assessment, lack of repeated exposure evaluation over time, and limited longitudinal follow‐up in several cross‐sectional investigations. In addition, some studies were potentially affected by referral bias, single‐center design, or modest sample size, potentially limiting generalizability. Nevertheless, no major systematic concerns emerged regarding imaging methodology, outcome assessment consistency, or data extraction reliability.

Importantly, for several cross‐sectional studies, temporal exposure–outcome sequence and repeated follow‐up assessment were not applicable according to the structure of the NIH assessment tool and were therefore classified as “not applicable” rather than methodological deficiencies.

4. Discussion

4.1. Main Findings

The present systematic review and meta‐analysis provides a comprehensive multimodality evaluation of conventional systolic function and myocardial deformation abnormalities associated with LBBB and RBBB assessed by STE and CMR‐FT. Overall, our findings support the concept that bundle branch conduction abnormalities are not merely electrical disorders but are closely associated with significant alterations in ventricular mechanics and systolic performance.

A principal finding of the present analysis is that patients with LBBB demonstrated significantly reduced conventional LV systolic function compared with healthy controls, with pooled analyses consistently showing lower LVEF values across imaging modalities. These findings are consistent with the established pathophysiological concept that LBBB induces marked electromechanical dyssynchrony, resulting in inefficient myocardial contraction, abnormal septal motion, impaired ventricular energetics, and progressive deterioration of global systolic performance. In contrast, isolated RBBB was not associated with a significant reduction in LVEF, suggesting a less pronounced impact on global LV pump function. However, this finding should be interpreted with considerable caution given the limited number of available studies, the substantial heterogeneity observed across analyses, and the instability of pooled estimates during sensitivity analyses. In light of these considerations, the currently available evidence should be considered insufficient to draw definitive conclusions regarding the impact of isolated RBBB on global LV systolic function.

Furthermore, interpretation of these findings should take into account the substantial clinical heterogeneity of the included populations. The analyzed studies encompassed patients with isolated LBBB and otherwise normal cardiac structure, as well as individuals with heart failure, dilated cardiomyopathy, and post‐TAVR conduction abnormalities. Consequently, the observed reduction in LVEF cannot be attributed exclusively to the conduction abnormality itself. Rather, the pooled estimates likely reflect the combined effects of electrical dyssynchrony, underlying myocardial disease, ventricular remodeling, and heart failure burden. Accordingly, the present findings do not allow complete disentanglement of the direct electromechanical consequences of LBBB from the contribution of concomitant structural cardiac abnormalities.

Myocardial deformation analyses further demonstrated significant impairment of LV longitudinal mechanics in patients with conduction abnormalities. Pooled LV‐GLS analyses revealed significantly reduced strain values in both LBBB and RBBB populations compared with controls, although the magnitude of impairment was substantially greater among patients with LBBB. Direct comparisons between conduction phenotypes consistently showed more pronounced abnormalities in LBBB than in RBBB, supporting the concept that left‐sided conduction delay represents a more advanced electromechanical phenotype characterized by greater ventricular dyssynchrony and myocardial inefficiency. However, the evidence supporting myocardial deformation abnormalities in isolated RBBB remains limited because only a small number of studies were available for quantitative synthesis, heterogeneity was substantial, and sensitivity analyses demonstrated dependence on individual studies. Taken together, the currently available data remain insufficient to establish the presence or absence of clinically meaningful alterations in LV longitudinal mechanics among patients with isolated RBBB.

Subgroup analyses revealed differences between STE‐ and CMR‐FT–derived measurements, with STE studies generally demonstrating larger effect sizes and greater heterogeneity than CMR‐FT investigations. Notably, the magnitude of the observed differences between imaging modalities was substantial across several comparisons, particularly in LBBB populations, where STE‐derived estimates consistently revealed considerably larger abnormalities than those detected by CMR‐FT. These findings suggest that the two techniques may not be entirely interchangeable and may differ in their sensitivity to detect dyssynchrony‐related mechanical abnormalities. Although differences in temporal resolution, tracking algorithms, and post‐processing methodologies likely contribute to this discordance, the possibility that STE and CMR‐FT capture partially distinct aspects of ventricular mechanics cannot be excluded. Considerable between‐study heterogeneity was observed across several pooled analyses, likely reflecting differences in study populations, imaging protocols, software vendors, and underlying cardiac substrates. In addition, the relatively limited number of available studies, particularly for RBBB and CMR‐FT analyses, may have further contributed to the observed variability and should be taken into account when interpreting the pooled estimates. Nevertheless, sensitivity analyses consistently yielded stable pooled estimates, supporting the overall robustness of the observed findings.

Collectively, these findings provide supportive evidence for the role of myocardial deformation imaging in characterizing ventricular mechanical abnormalities associated with bundle branch block, particularly LBBB; however, they should be interpreted as hypothesis‐generating rather than definitive pending confirmation in larger prospective investigations.

4.2. Mechanistic Insights Into Left Ventricular Systolic and Deformation Abnormalities in Patients With LBBB

Several pathophysiological mechanisms may explain the significant impairment in LVEF and LV‐GLS observed among patients with LBBB in the present meta‐analysis. LBBB induces marked electrical and mechanical dyssynchrony characterized by delayed activation of the lateral and posterolateral left ventricular walls together with early septal contraction [35]. This abnormal activation sequence produces inefficient ventricular mechanics, paradoxical septal motion, reduced systolic coordination, and impaired myocardial work efficiency [36, 37]. Over time, these alterations may promote adverse ventricular remodeling, progressive systolic dysfunction, and worsening myocardial energetics [38, 39, 40].

Importantly, LV‐GLS abnormalities appeared more pronounced and more consistently impaired than conventional LVEF reductions across the included studies, supporting the concept that myocardial deformation imaging may detect earlier stages of electromechanical dysfunction before overt impairment of global pump function becomes clinically evident [41, 42]. Longitudinal myocardial fibers, predominantly located within the subendocardial layer, are particularly vulnerable to abnormal wall stress, dyssynchronous contraction, increased oxygen demand, and microvascular dysfunction induced by conduction delay [43]. Consequently, GLS impairment may represent one of the earliest manifestations of mechanical dysfunction in patients with bundle branch block patterns.

Another important consideration is that LBBB‐related dyssynchrony may itself contribute to progressive structural myocardial remodeling independently of the underlying cardiomyopathic substrate. Experimental and clinical investigations have demonstrated that chronic dyssynchronous activation may induce regional differences in myocardial workload, asymmetric hypertrophy, altered calcium handling, mitochondrial dysfunction, and interstitial fibrosis [44, 45, 46]. Such mechanisms may partially explain why LBBB populations frequently demonstrate progressive reductions in both conventional systolic performance and myocardial strain values even in the absence of severe baseline structural heart disease [47, 48].

The substantially greater impairment observed among LBBB compared with RBBB populations likely reflects the more direct involvement of LV activation pathways in LBBB. While isolated RBBB mainly affects RV depolarization timing, LBBB directly disrupts coordinated LV contraction, thereby exerting a much greater impact on global LV mechanics and systolic efficiency [49, 50]. This observation is consistent with the markedly higher prevalence of HF, adverse remodeling, and CRT indication among patients with LBBB in contemporary clinical practice [51, 52, 53].

The observed variability between STE‐ and CMR‐FT–derived strain measurements may additionally reflect differences in temporal resolution and tracking algorithms between imaging modalities. STE generally provides higher temporal resolution and may therefore be more sensitive to subtle dyssynchrony‐related abnormalities in myocardial deformation, whereas CMR‐FT offers superior tissue characterization and volumetric reproducibility [54, 55]. Consequently, these techniques should probably be considered complementary rather than competitive approaches for the assessment of myocardial mechanics in conduction abnormalities.

4.3. Potential Clinical Relevance and Multimodality Imaging Perspectives

The present findings may have several important clinical implications. First, the observed impairment in LV‐GLS despite relatively preserved LVEF in selected populations supports the growing role of myocardial deformation imaging for the early identification of subclinical ventricular dysfunction in patients with conduction abnormalities. Conventional LVEF assessment alone may underestimate the true degree of myocardial mechanical impairment, particularly in patients with isolated conduction delay but without advanced structural heart disease [56].

Second, the present findings reinforce the pathophysiological rationale underpinning CRT. In contemporary clinical practice, QRS duration and LBBB morphology remain the principal criteria for CRT selection [57]. However, advanced deformation imaging may provide additional information regarding the severity of electromechanical dysfunction and myocardial discoordination, potentially improving patient phenotyping and identifying individuals at increased risk of adverse remodeling or HF progression.

Another clinically relevant implication concerns the complementary role of multimodality imaging. STE is widely available, reproducible, and relatively inexpensive, making it particularly attractive for routine clinical assessment and longitudinal follow‐up [58]. In contrast, CMR‐FT offers comprehensive evaluation of ventricular volumes together with myocardial tissue characterization, including the assessment of fibrosis and scar burden [59]. The integration of deformation imaging with tissue characterization techniques may therefore improve identification of the structural and functional substrate underlying conduction abnormalities.

The present results also support a potential role for serial myocardial deformation assessment during follow‐up. Progressive deterioration in LV‐GLS may identify patients at increased risk of worsening systolic dysfunction, adverse remodeling, atrial fibrillation, ventricular arrhythmias, or future HF development before significant reductions in LVEF become apparent [60, 61, 62]. Furthermore, serial strain assessment may represent a useful tool for monitoring reverse remodeling and therapeutic response following CRT implantation.

Overall, the current findings support a more integrated approach to the evaluation of bundle branch block, combining electrocardiographic and advanced imaging information to achieve more refined phenotypic characterization and risk stratification in contemporary clinical practice.

4.4. Sources of Heterogeneity, Strengths of the Present Analysis, and Study Limitations

Several factors likely contributed to the substantial heterogeneity observed across the pooled analyses. The included studies differed considerably with respect to patient characteristics, including age distribution, prevalence of ischemic and non‐ischemic cardiomyopathy, degree of ventricular remodeling, baseline systolic function, and burden of cardiovascular comorbidities. Additional variability arose from differences in study design, inclusion criteria, and clinical settings, ranging from isolated conduction abnormalities in otherwise healthy individuals to patients with HF, dilated cardiomyopathy, post‐TAVR conduction disorders, or candidates for CRT. Consequently, the observed abnormalities likely reflected varying contributions of both primary electrical dyssynchrony and underlying myocardial disease.

An additional source of heterogeneity relates to differences in the diagnostic criteria used to define LBBB across studies. While some investigations adopted more stringent electrocardiographic definitions consistent with Strauss criteria [63], which identify a more homogeneous phenotype characterized by more advanced electromechanical dyssynchrony, other studies used conventional guideline‐based criteria relying primarily on QRS morphology and duration ≥120 ms. Consequently, the included LBBB populations may have represented mechanistically distinct phenotypes with differing degrees of ventricular mechanical impairment, remodeling, and myocardial dysfunction. In the present review, two studies [22, 30] explicitly applied Strauss criteria, whereas the remaining LBBB studies used conventional electrocardiographic definitions. This variability may have contributed to between‐study heterogeneity and may partly explain differences in the magnitude of observed systolic and deformation abnormalities.

Methodological differences in imaging acquisition and analysis also represented important sources of heterogeneity. Variations in image quality, frame rate, temporal resolution, post‐processing algorithms, and vendor‐specific strain analysis software are well‐recognized determinants of variability in myocardial deformation measurements. Furthermore, STE‐derived strain parameters are influenced by endocardial border delineation, motion artifacts, operator expertise during image acquisition and post‐processing, and loading conditions, all of which may affect measurement reproducibility and accuracy [64, 65, 66]. Myocardial deformation indices may additionally be influenced by extrinsic mechanical factors, including body habitus, thoracic geometry, and anterior chest wall conformation, potentially affecting myocardial motion tracking independently of intrinsic myocardial function [67, 68].

Notwithstanding the sources of heterogeneity discussed above, the present study has several important strengths. To the best of our knowledge, this is among the first systematic reviews and meta‐analyses specifically evaluating the impact of both LBBB and RBBB on conventional systolic function and myocardial deformation assessed using both STE and CMR‐FT. The multimodality design enabled an integrated evaluation of complementary imaging techniques, while modality‐specific subgroup analyses provided additional mechanistic and methodological insights. Moreover, sensitivity analyses consistently confirmed the robustness of the pooled estimates despite the presence of substantial heterogeneity.

Nevertheless, several limitations should be acknowledged. The number of available studies remained limited for some analyses, particularly those involving RBBB and CMR‐FT populations, thereby reducing statistical power and limiting the reliability of publication bias and meta‐regression assessments. Most included studies were observational and predominantly single‐center in design, potentially introducing referral and selection bias. Many investigations also enrolled relatively small populations and lacked formal sample‐size calculations or repeated longitudinal assessments.

A notable limitation concerns the inability to adequately account for QRS duration, which represents a major determinant of electromechanical dyssynchrony and ventricular mechanical dysfunction in patients with bundle branch block. Although QRS duration was reported in several studies and was generally substantially longer in LBBB populations than in control groups, these data were not sufficiently available or consistently reported to permit robust adjustment through meta‐regression analyses across all comparisons. Consequently, the present analyses cannot fully distinguish the independent effects of bundle branch block morphology from the graded effects of QRS prolongation itself.

Specific limitations related to CMR‐FT should also be considered. Compared with echocardiographic imaging, CMR‐FT is characterized by lower temporal resolution, potential inaccuracies related to through‐plane myocardial motion, inter‐vendor variability in post‐processing software, and lower reproducibility of radial strain measurements [69, 70, 71]. These limitations may be particularly relevant in patients with bundle branch block, especially those with markedly prolonged QRS duration and severe electromechanical dyssynchrony. As QRS duration increases, accurate identification of end‐systolic and end‐diastolic frames becomes progressively more challenging, potentially reducing the precision of peak strain measurements. In contrast, the substantially higher frame rate of STE provides superior temporal resolution and may allow more accurate characterization of rapid mechanical events throughout the cardiac cycle. Therefore, prolonged QRS duration itself may represent an additional source of variability when comparing STE‐ and CMR‐FT–derived strain measurements. It is conceivable that the lower temporal sampling of CMR‐FT may attenuate extreme deformation values and reduce the apparent variability of strain measurements, particularly in highly dyssynchronous LBBB populations. Consequently, the lower heterogeneity observed among CMR‐FT studies should not necessarily be interpreted exclusively as evidence of greater reproducibility or standardization, but may partly reflect technical constraints related to temporal resolution and frame‐to‐ECG synchronization in patients with significant conduction delay. The higher costs, reduced availability, and limited accessibility of CMR currently restrict the widespread implementation of CMR‐FT in routine clinical practice.

Finally, the random‐effects analyses were performed using the DerSimonian–Laird estimator. Although alternative approaches such as restricted maximum likelihood (REML) may provide more robust variance estimates in some meta‐analyses with a limited number of studies, the potential impact of estimator selection on the present findings cannot be excluded.

5. Conclusions

The present systematic review and meta‐analysis demonstrates that bundle branch conduction abnormalities, particularly LBBB, are closely associated with significant alterations in LV systolic performance and myocardial mechanics assessed by STE and CMR‐FT. Patients with LBBB consistently exhibited impaired LVEF and markedly reduced LV‐GLS values compared with healthy control subjects, supporting the concept that electromechanical dyssynchrony contributes substantially to abnormal ventricular contraction, inefficient myocardial work, and progressive mechanical dysfunction. In contrast, the currently available evidence is insufficient to establish the impact of isolated RBBB on conventional systolic function and myocardial deformation. Although available studies suggest less pronounced abnormalities than those observed in LBBB, the limited number of investigations, substantial heterogeneity, and instability of pooled estimates preclude definitive conclusions regarding the mechanical consequences of isolated RBBB.

The present findings further support the association between myocardial deformation abnormalities and bundle branch conduction disorders beyond conventional electrocardiographic and volumetric assessment. LV‐GLS appeared consistently more impaired than LVEF across several comparisons, suggesting that myocardial deformation imaging may be more sensitive to the mechanical consequences of conduction abnormalities at a population level. However, the present analysis was not designed to determine whether deformation parameters provide incremental diagnostic or prognostic value beyond conventional systolic function measures in individual patients. Moreover, the integration of STE and CMR‐FT may offer complementary insights into ventricular mechanics, remodeling patterns, and myocardial tissue characteristics.

Nevertheless, given the observational nature of the available evidence, the limited number of eligible studies, the substantial clinical and methodological heterogeneity, and the potential influence of residual confounding factors—including age and underlying structural heart disease—the observed associations should be interpreted with appropriate caution. Future large‐scale prospective multicenter studies using standardized multimodality imaging protocols and rigorous adjustment for relevant clinical covariates are warranted to better define the independent contribution of bundle branch block to ventricular mechanical dysfunction.

Funding

The authors have nothing to report.

Consent

The authors have nothing to report.

Conflicts of Interest

The authors declare no conflicts of interest.

Institutional Review Board Statement

In accordance with the guidelines by the Comitato Etico Territoriale Lombardia 5, ethical review and approval were not required; this work synthesizes previously published data.

Supporting information

Supporting information

Supporting information

Data Availability Statement

Data extracted from included studies will be publicly available on Zenodo (https://zenodo.org).