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Incomplete right bundle branch block (iRBBB) is a frequent electrocardiographic (ECG) finding, often considered benign. However, recent evidence suggests it may be associated with underlying structural or electrical abnormalities, particularly in selected populations.
Methods
We conducted a narrative review of population-based cohorts, mechanistic studies, and clinical trials focused on the prevalence, pathophysiological mechanisms, differential diagnosis, and prognostic implications of iRBBB.
Results
iRBBB is common in athletes and individuals with pulmonary or structural heart diseases. Although frequently asymptomatic, it may reflect right ventricular strain, pulmonary hypertension, or a predisposition to arrhythmias such as atrial fibrillation. Specific ECG features, comorbidities, and clinical context help to differentiate benign from pathologic iRBBB.
Conclusions
iRBBB should not be routinely regarded as a harmless variant. In high-risk individuals, it may carry clinical and prognostic significance, warranting further evaluation. Standardized criteria and additional prospective studies are needed to better understand its implications.
Incomplete right bundle branch block (iRBBB) is a frequent electrocardiographic (ECG) finding, often dismissed as being benign.
Its potential association with underlying structural or electrical heart disease remains unclear. This review aimed to assess its clinical relevance and diagnostic value.
What was learned from the study?
Most cases of iRBBB are benign, particularly in younger and athletic individuals. However, in certain morphologies or clinical settings, iRBBB may indicate pulmonary hypertension (PH), pulmonary embolism (PE), or arrhythmogenic right ventricular cardiomyopathy (ARVC).
This review supports the use of structured ECG interpretation and clinical context to distinguish benign from pathological iRBBB and guide appropriate diagnostic work-up.
Digital Features
This article is published with digital features, including an infographic, to facilitate understanding of the article. To view digital features for this article, go to https://doi.org/10.6084/m9.figshare.29664707.
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Introduction
The cardiac conduction system is crucial for synchronized myocardial contraction, which ensures efficient pumping function of the heart [1]. Incomplete right bundle branch block (iRBBB) is an electrocardiogram (ECG) finding characterized by a slightly widened QRS complex (100–120 ms) with typical rSR´ morphology in lead V1 and wide S waves in leads I and V6 [1]. This reflects slow conduction of electrical excitation through the right Tawara bundle branch. iRBBB alone does not have a significant impact on hemodynamics, but it may be a marker of other pathological conditions.
The right branch of the Tawara arm ensures propagation of the electrical impulse to the right ventricle (RV) and septum. In the case of iRBBB, this process is slowed, leading to the characteristic changes on the ECG [1] (Fig. 1). This condition can have a number of underlying causes, ranging from structural changes in the myocardium to electrolyte imbalances. Marked hyperkalemia can lead to conduction disturbances that can mimic complete right bundle branch but usually not iRBBB. Most cases are asymptomatic, but in certain clinical contexts, iRBBB can signal severe pathology or be a harbinger of progressive damage to the cardiac conduction system [2].
Fig. 1
Schematic of the cardiac conduction system. iRBBB incomplete right bundle branch block. Created by the authors based on anatomical studies of the right bundle branch. The approximate site of incomplete conduction block is indicated following published anatomical and electroanatomical data
From a pathophysiological perspective, the onset of iRBBB may be associated with delayed conduction of electrical impulses through the right bundle branch of Tawara, which prolongs RV activation. However, the cause of this delay is not uniform. The mechanism in patients with Brugada syndrome or arrhythmogenic right ventricular cardiomyopathy (ARVC) is different from than in healthy subjects with a benign variant, in whom conduction is slightly prolonged due to partial mechanical interruption of the fibers, their congenital absence, or the presence of “short circuits”.
At the molecular level, this pathophysiological mechanism may involve damage to sodium channels (e.g., SCN5A), leading to impaired action potential (AP) propagation [3]. Oxidative stress and inflammatory mediators may further reduce the expression of these channels. Chronic inflammation or mechanical overload of the RV increases the intramyocardial pressure, which causes myocardial remodeling in terms of RV dilation and hypertrophy, impairing electrical connectivity and slowing electrical impulses in the right bundle branch [2].
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This article aims to provide a clinically focused and integrative perspective on iRBBB, highlighting diagnostic and prognostic features that remain underrecognized. Unlike previous publications, we emphasize its differential diagnosis in high-risk populations and offer practical insights for clinical evaluation and risk stratification.
Specifically, we aim to clarify the electrocardiographic criteria for iRBBB, explore its pathophysiological mechanisms, review associated conditions, and discuss its potential prognostic significance.
Methods
We conducted a comprehensive literature search using PubMed, Scopus, and Web of Science databases for articles published between January 1990 and December 2024. The following search terms were used: “incomplete right bundle branch block”, “iRBBB”, “ECG conduction abnormalities”, and “arrhythmia risk”. No language restrictions were applied.
Studies were included if they addressed the pathophysiological mechanisms, diagnostic criteria, differential diagnosis, or prognostic implications of iRBBB. Reviews, guideline documents, population-based cohorts, and mechanistic studies were prioritized. Studies were excluded if they did not specifically address iRBBB, were opinion pieces lacking original data, or were single case reports.
Although no formal risk of bias tool was applied, we considered study design quality, population size, and consistency with guideline recommendations when selecting articles. The primary objective of this review was to synthesize available evidence on the clinical and prognostic relevance of iRBBB and highlight knowledge gaps requiring further investigation.
This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.
Epidemiology
iRBBB is a relatively common finding on an ECG, with prevalence ranging between 2% and 8% in different populations [2, 4]. An increased prevalence is seen in men, athletes (9–30%) [4‐7], and patients with chronic respiratory disease. The crista supraventricularis pattern is a benign variant of depolarization that may mimic iRBBB (Fig. 2); it is more common in specific subgroups, such as children with increased sports activity, in which the prevalence of the crista supraventricularis pattern is 13.3% [8, 9].
Fig. 2
Schematic electrocardiogram pattern in V1 lead illustrating the crista supraventricularis pattern. This normal variant can mimic incomplete right bundle branch block. The QRS duration remains within normal range (≤ 120 ms). Created by the authors
Epidemiological studies suggest that iRBBB may also be associated with physiological adaptation to higher volume RV load in athletes, whereas in certain cases it may be a marker of cardiovascular risk. In particular, iRBBB is a frequent finding in patients with atrial septal defects (ASD) due to chronic volume overload of the right heart (Fig. 3). In patients with chronic respiratory disease, such as chronic obstructive pulmonary disease (COPD) or interstitial lung processes, the prevalence of iRBBB is higher, consistent with the influence of the presence of pulmonary hypertension (PH) on the RV. In Eisenmenger syndrome, iRBBB is a frequent finding and correlates with the severity of PH and heart failure (HF) [10]. Overall, studies suggest that approximately 70–80% of iRBBB cases are benign incidental findings, whereas 20–30% are associated with structural heart disease, PH, or congenital heart defects. The exact prevalence depends on the population studied.
Fig. 3
ECG of a patient with ASD showing iRBBB and right axis deviation. ECG electrocardiograph, ASD atrial septal defect, iRBBB incomplete right bundle branch block. Original ECG recording obtained by the authors from patients at University Hospital Ostrava. Used with appropriate consent and anonymized in accordance with institutional ethical standards
The development of iRBBB can be understood through the lens of both primary (physiological or benign) and secondary (pathological) mechanisms that affect the conduction of electrical impulses in the right bundle branch.
Primary Mechanisms
In many individuals, iRBBB appears without a structural cardiac substrate and is considered a benign, idiopathic phenomenon. These cases often involve conduction delay in the right bundle in the absence of myocardial disease. A common benign ECG variant is the crista supraventricularis pattern, a pattern resulting from delayed activation of this specific RV muscular ridge. Although it mimics iRBBB on surface ECG, it lacks pathological significance [4, 8, 9]. This pattern is illustrated in Fig. 2, showing the anatomical location on the crista supraventricularis and its potential effect on RV conduction.
Another common setting for iRBBB is in athletes, particularly endurance-trained individuals. This has been attributed to increased vagal tone, leading to bradycardia and subtle intraventricular conduction delay. Additionally, exercise-induced remodeling of the RV may contribute to this pattern, particularly in long-term endurance athletes, with increased prevalence reported in this population [6, 11].
The prevalence of iRBBB also increases with age, as fibrosis and conduction system degeneration develop with advancing age. These degenerative changes may occur in the absence of overt heart disease, particularly in elderly individuals [5, 12].
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Secondary Mechanisms
More frequently, iRBBB is associated with various pathological conditions of the heart or pulmonary circulation. These include diseases that result in pressure or volume overload of the RV or direct damage to the conduction system.
A classic example is pulmonary embolism (PE), where acute elevation in pulmonary artery pressure leads to RV dilatation and stretching of the conduction pathways. In PE, iRBBB may represent a transient manifestation during the acute phase [5, 13].
In contrast, chronic PH or advanced COPD can lead to sustained RV hypertrophy and fibrosis of the conduction system, producing persistent iRBBB. Similarly, congenital heart diseases, particularly ASD, result in chronic RV volume overload and a high incidence of iRBBB on ECG [5].
Importantly, there is a documented association between iRBBB and obesity, arterial hypertension (AH), and obstructive sleep apnea. These comorbidities contribute to PH, diastolic dysfunction, and RV strain, all of which may facilitate conduction delay in the right bundle. AH and obesity also induce interstitial myocardial fibrosis and conduction system remodeling, enhancing the risk of conduction defects even in the absence of overt structural disease [14‐17].
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Moreover, patients with left ventricle dysfunction may exhibit right-sided conduction delay as a result of interventricular conduction delay, increased filling pressures, or ventricular interdependence. Diastolic dysfunction, even with preserved ejection fraction, may secondarily affect the timing of RV activation and result in iRBBB morphology [5].
In ischemic heart disease, particularly when involving the right coronary artery, ischemia or infarction may directly damage the right bundle branch. RV infarction is a known cause of transient or permanent iRBBB [16, 18].
Cardiomyopathies, especially ARVC, frequently display conduction delays due to fibrofatty infiltration. The presence of iRBBB, often with T wave inversions in right precordial leads, may be an early manifestation of the disease [10].
Inflammatory (e.g., myocarditis) and infiltrative diseases (e.g., sarcoidosis, amyloidosis) can disrupt conduction via inflammatory cell infiltration or fibrosis involving the right bundle [10, 17].
Electrolyte imbalances, especially hyperkalemia, alter depolarization and repolarization gradients. Severe hyperkalemia can mimic or induce iRBBB morphology [5].
Iatrogenic causes include procedures involving the RV outflow tract or right bundle trajectory. Transcatheter aortic valve implantation (TAVI) is particularly associated with new-onset conduction disturbances, including iRBBB, due to proximity to the conduction axis. This new conduction disturbance may precede complete AV block and has prognostic implications [19].
Emerging evidence suggests a role of neurohumoral activation and endothelial dysfunction in the genesis of iRBBB. Experimental models indicate involvement of NO synthase expression, sympathetic activation, and myocardial stretch signaling, particularly in the setting of volume overload and early-stage HF [14, 15].
An overview of primary and secondary causes of iRBBB is provided in Table 1 and the provided Infographic.
Table 1
Primary and secondary causes of iRBBB
Classification
Cause/condition
Pathophysiological mechanism
Primary
Congenital iRBBB
Benign conduction delay in right bundle
Primary
RV conduction system anomaly
Structural conduction system variation
Primary
Crista supraventricularis pattern
Conduction delay due to muscular ridge
Secondary
RV hypertrophy
Myocardial remodeling and conduction slowing
Secondary
PH
RV pressure overload and remodeling
Secondary
Acute PE
RV dilation, ischemia of RV outflow tract
Secondary
Myocardial ischemia (especially RV infarction)
Transient conduction delay
Secondary
Electrolyte abnormalities (e.g., hyperkalemia)
Altered depolarization pattern
Secondary
ARVC
Fibrofatty replacement of RV myocardium and conduction
Secondary
Brugada syndrome
Channelopathy affecting right bundle conduction
Secondary
ASD
Right volume overload and dilation
iRBBB incomplete right bundle branch block, RV right ventricular, PH pulmonary hypertension, PE pulmonary embolism, ARVC arrhythmogenic right ventricular cardiomyopathy
Pathophysiology
The etiopathogenesis of iRBBB involves changes in electrical conduction through the conduction system, which may be due to slowing of the monophasic AP, leading to delayed propagation of the depolarizing front in the distal part of the right Tawara bundle (Fig. 1). This process may be due to structural changes, such as electromechanical myocardial remodeling, degenerative changes, or disturbances at the ion channel level. The electrical conductivity of cardiac tissue depends on the integrity of myocytes and their interconnection by gap junctions (e.g., connexin-43) [16, 18]. Other factors that can further impair conductivity include inflammatory mediators and oxidative stress, which lead to a decrease in connexin-43, slowing the propagation of excitation at the cellular level [18].
Mechanical overload of the RV leads to its dilatation and hypertrophy, which may lead to effective prolongation of myocardial activation due to a combination of the above changes. Intramyocardial strain alone does not affect conduction, but changes associated with RV dilatation may affect the synchrony of depolarization, which may manifest as iRBBB. For this reason, it is advisable to follow normal values for the velocity of excitation propagation, which are usually between 3 and 4 m/s, compared with 0.5 m/s in working myocardium [15].
The characteristic feature of iRBBB is slowed or partial interruption of electrical signal conduction through the right branch of the arm of Tawara, which causes delayed depolarization of RV [2]. This phenomenon cannot be fully explained at the level of ionic changes in cardiac cells and their effect on the AP waveform, because the cardiac muscle transduction system is a syncytium in which the function depends on gap junction cell connectivity [18].
At the cellular level, the timing of depolarization and repolarization is altered. The mechanism begins with phase 0 of the AP, when sodium ions (Na⁺) influx through voltage-gated channels [2]. The result is a slowing of RV depolarization relative to the LV.
This asynchrony manifests as different timing in ventricle depolarization [2]. Repolarization is influenced by potassium channels (K⁺) that control phase 3 of the AP. Slowing this ion exchange prolongs RV repolarization, contributing to the asynchronous course of the entire cycle between the RV and LV. The overall result involves prolongation of the pulse propagation time and not actual prolongation of the AP or membrane potential.
On the ECG, iRBBB manifests as a slightly widened QRS complex (>100 ms but <120 ms) and the typical morphology of the QRS complex, “rsr’” (Fig. 4a) or “rsR’” (Fig. 4b), in thoracic leads V1–V3 [2, 4]. These changes reflect delayed depolarization and repolarization between the RV and LV.
Fig. 4
ECG in a patient with isolated iRBBB and no structural heart disease with a rSR, b RSr. ECG electrocardiograph, iRBBB incomplete right bundle branch block. Original ECG recording obtained by the authors from patients at University Hospital Ostrava. Used with appropriate consent and anonymized in accordance with institutional ethical standards
Thus, iRBBB results from slowed sodium ion conduction and delayed repolarization of potassium channels, causing asynchronous ventricular activation. At the macroscopic level, this delay manifests as delayed depolarization of the RV on the ECG.
Diagnostics
ECG criteria
Diagnosis of iRBBB is based on specific ECG criteria that include a slightly prolonged QRS complex with a width of 100–120 ms (Fig. 4a, b) [1, 2], reflecting slowing but not complete interruption of impulse conduction through the right bundle branch of Tawara (Fig. 1). While the classical definition of iRBBB includes QRS duration between 100 and 120 ms, we acknowledge that some studies extend the upper limit to 120 ms, which overlaps with partial conduction delay or early-stage RBBB. Therefore, cases with QRS 110–120 ms require careful differential diagnosis, particularly in the presence of structural heart disease or RV overload. The characteristic feature is the morphology of the rSR’ QRS complex in lead V1, with the R’ wave reflecting delayed RV activation (Fig. 4b). A broad and terminally delayed S wave is present in the lateral leads (Fig. 4a, b), indicating desynchronization between LV and RV depolarization. Typically, the cardiac axis is within the physiological range, which distinguishes iRBBB from other conduction system disorders, such as RBBB or fascicular blocks. This ECG finding is usually asymptomatic and does not usually have major hemodynamic consequences, but in the presence of structural or functional heart disease, it may indicate serious changes, such as RV dilatation or hypertrophy.
All of the following criteria must be met for a diagnosis of iRBBB:
1.
QRS complex width in the range of 100–120 ms (i.e., below the value for RBBB, which is ≥120 ms);
2.
QRS complex morphology of “rsr’” (Fig. 4a) or “rsR’” (Fig. 4b) in leads V1-V2, with the R’ wave often higher than the original r wave;
3.
Prolonged terminal section of the S wave in the lateral leads (I, V5, V6), where the S wave exceeds the normal duration for standard LV depolarization (Fig. 4a, b);
4.
Absence of signs of complete RBBB (Fig. 5a) or other conduction disturbances (e.g., LBBB (Fig. 5b).
Fig. 5
ECG with a complete RBBB in a hypertensive patient with LVH, b LBBB in a patient with ischemic cardiomyopathy. ECG electrocardiograph, RBBB right bundle branch block, LVH left ventricular hyperthrophy, LBBB left bundle branch block. Original ECG recording obtained by the authors from patients at University Hospital Ostrava. Used with appropriate consent and anonymized in accordance with institutional ethical standards
Echocardiographic examination may reveal structural changes related to the cause of iRBBB but is not diagnostic for the finding itself.
Secondary Causes of iRBBB
Although iRBBB is a common finding, emphasis must be placed on the differential diagnosis to exclude other pathologies that can present similar changes on an ECG. Thorough recognition of these pathologies is essential to reach an accurate diagnosis and choose an appropriate therapeutic approach.
iRBBB may also occur transiently in the context of acute PE [20], acute myocardial ischemia [21], or electrolyte imbalances, particularly hyperkalemia [22]. In some cases, it may also appear as an early manifestation of more serious pathologies such as ARVC [23] or Brugada syndrome [24]. Importantly, these associations are not frequent, and in the majority of cases, iRBBB remains a benign finding.
Brugada syndrome [24] and ARVC [23] are considered among the most clinically significant conditions that may initially present with iRBBB morphology (Fig. 6a–c). However, these are rare and often accompanied by additional ECG or imaging abnormalities.
Fig. 6
ECG with a Brugada syndrome—type 1, b Brugada syndrome—type 2, c ARVC with epsilon wave, d PE with S1Q3T3 and iRBBB. ECG electrocardiograph, ARVC arrhythmogenic right ventricular cardiomyopathy, PE pulmonary embolism, iRBBB incomplete right bundle branch block. Original ECG recording obtained by the authors from patients at University Hospital Ostrava. Used with appropriate consent and anonymized in accordance with institutional ethical standards
When an iRBBB pattern is observed on ECG, it is important to consider differential diagnoses that may present with a similar QRS morphology, including complete RBBB, Brugada syndrome, ARVC, acute PE, electrolyte disturbances, myocardial ischemia, and certain genetic or structural syndromes, as described below [25].
RBBB
RBBB (Fig. 5a) differs from iRBBB by a longer QRS complex width (>120 ms) and typical QRS complex morphology, which includes a prolonged rSR’ complex in leads V1–V2 and wide S waves in leads I and V6, which are deeper than in iRBBB. The ST segment is usually normal but may be slightly depressed in some cases, whereas the ST segment is usually normal in iRBBB, with smooth inversion of the T wave in leads V1-V2. In the case of iRBBB, it is usually an asymptomatic finding that does not have hemodynamic consequences, unlike RBBB, which may be associated with advanced structural changes and have severe clinical consequences [5, 26].
Brugada syndrome
Brugada syndrome is a genetic arrhythmogenic disorder associated with a risk of malignant arrhythmias leading to SCD. Clinical differences between iRBBB and Brugada syndrome include the presence of a positive family history of SCD and ECG abnormalities that are typical of this syndrome [27, 28]. On the ECG, Brugada syndrome and iRBBB may exhibit similarities, especially in precordial leads V1 and V2, leading to their confusion. However, there are fundamental and diagnostically significant differences between these two conditions, which can be identified mainly in the morphology of the QRS complex, ST segment changes, and T wave inversion, as well as the dynamics of these changes.
The most prominent feature of Brugada syndrome is ST elevation in leads V1–V2, which shows a characteristic “coved-type” pattern (Fig. 6a). This pattern involves a concave ST segment elevation that transitions into a deep and asymmetric negative T wave. In some patients, a “saddleback-type” pattern (Fig. 6b) is observed, which is characterized by a slightly elevated ST segment, but without a pronounced dome-shaped rise, followed by a negative T wave. This pattern is typical of Brugada syndrome types 2 and 3, where ST elevation is not as pronounced as in type 1 but is still pathological. In contrast to iRBBB, in which the ST segment is normal, Brugada syndrome presents as marked ST elevation accompanied by specific T wave changes that are deep and asymmetric (Fig. 6a, b). T wave inversion in Brugada syndrome may extend to lead V3, which is unusual in iRBBB. Another important feature is the dynamics of the changes; in Brugada syndrome, the ECG can change over time depending on provoking factors, such as fever, electrolyte imbalance, or the use of certain medications, which is uncommon in iRBBB [4, 28, 29, 30].
ARVC
ARVC is a genetic disorder characterized by the presence of specific ECG changes such as epsilon waves, T-wave inversions in right precordial leads, and a prolonged S-wave upstroke in V1–V3 are considered diagnostic clues (Fig. 6c).
The distinction between ARVC and idiopathic iRBBB is important because ARVC may require specific treatment, including implantation of a cardioverter-defibrillator to prevent SCD and epicardial catheter ablation.
In ARVC, low notches are present at the end of the QRS complex in leads from the right precordium (so-called epsilon waves), as well as prolonged RV activation and repolarization irregularities, such as T-wave inversion in leads V1–V3 or further away. Another differentiating feature of ARVC is the frequency of ventricular extrasystole of RV origin, which is common and may exhibit LBBB morphology [29]. Differentiation can be challenging, especially in the early stages of the disease; therefore, other diagnostic modalities, such as echocardiography, cardiac magnetic resonance (CMR), or genetic testing, should always be considered. The earlier the disease presents, the worse the prognosis typically is. Structural changes progress more rapidly in the presence of physical stress, often in young competitive athletes.
Acute pulmonary embolism
An acute PE can cause acute overloading of the RV, leading to its dilation and slowing of the power line. The ECG may show iRBBB, but also other changes, such as S1Q3T3 and negative T waves in the right-sided leads [30] (Fig. 6d). In clinical practice, it is important to correlate this finding with other symptoms, such as dyspnea, hypoxia, or chest pain, and to perform diagnostic tests, such as CT angiography of the pulmonary artery, to detect this disease [31].
Electrolyte abnormalities
Electrolyte abnormalities can mimic or exacerbate conduction abnormalities. Hyperkalemia typically causes peaked T waves, a progressive flattening and eventual disappearance of the P wave, and widening of the QRS complex, potentially leading to a sine-wave pattern in severe cases. In contrast, hypokalemia is characterized by ST depression, flattened T waves, prominent U waves, and in more severe forms, QT prolongation predisposing to ventricular arrhythmias [22, 32].
Myocardial ischemia
Myocardial ischemia can cause dynamic changes on the ECG that can mimic iRBBB. These changes are often reversible, and it is important to perform angiographic examination of the coronary arteries to confirm this diagnosis. Acute ischemia in the region of the RV may have similar ECG findings but is usually accompanied by other changes (ST elevation or depression) and symptoms, such as chest pain and positive cardioselective biomarkers [33, 34].
Clinical implications
Most patients with iRBBB are asymptomatic [2] and, thus, this finding is often incidental. However, in certain clinical situations, iRBBB may signal more severe cardiac pathology. Its presence in patients with cardiovascular disease may indicate impaired RV function and be a predictor of progression to complete RBBB [2], which is one of the major clinical risks of iRBBB. This progression occurs in approximately 10% of patients within 5 years [2, 35] and is more common in patients with PH, structural heart defects, or chronic RV damage, such as after an infarction in the RV. A higher incidence of HF and chronic diseases, including CKD, is seen in patients in whom iRBBB transitions to complete RBBB [36].
In addition, iRBBB may signal the risk of arrhythmias, such as atrial fibrillation, in some patients, especially patients with right atrial congestion [37, 38]. Slowing of electrical conduction may impair the synchrony of RV contractions, which increases the predisposition to developing arrhythmias.
Diagnostic Evaluation of iRBBB
Although iRBBB is defined solely by ECG criteria, clinical context plays an essential role in distinguishing benign from pathologic forms. The initial diagnostic approach should include a focused history and physical examination, especially in individuals presenting with symptoms such as exertional dyspnea, palpitations, syncope, or a family history of SCD or inherited cardiomyopathies.
In asymptomatic individuals with incidentally discovered iRBBB and no cardiovascular risk factors, further testing is usually not required. However, in symptomatic patients or those with risk markers (e.g., abnormal ECG morphology, axis deviation, frequent ectopy), targeted evaluation is warranted.
Non-invasive tools such as transthoracic echocardiography and Holter monitoring are commonly used as first-line tests to evaluate for structural abnormalities or arrhythmic events. CMR imaging may be helpful in detecting RV pathology (e.g., ARVC), especially in the presence of suggestive ECG findings or a positive family history.
In selected cases, particularly those with unexplained syncope or suspected pre-excitation syndromes, an electrophysiological study may be considered. Blood tests, including biomarkers (e.g., high-sensitivity troponin, NT-proBNP), can be used to assess myocardial injury or HF, though these are typically normal in benign iRBBB.
In summary, diagnostic evaluation beyond ECG is generally not necessary in asymptomatic individuals with isolated iRBBB, but may be valuable in distinguishing clinically significant disease in high-risk or symptomatic patients.
Management
If iRBBB is present without structural heart disease, specific treatment is usually not necessary. In these situations, regular follow-up is recommended, especially electrocardiography and echocardiography to monitor RV function. If iRBBB is associated with pathological conditions, such as PH or RV infarction, it is crucial to focus on treating the underlying disease, which may help alleviate or stabilize the electrical conduction.
In the context of PH, the aim of therapy is to focus on reducing the burden on the RV and improving its function, which may also lead to improved electrical conduction and avoid progression to RBBB. The use of pulmonary vasodilators, such as sildenafil, may improve RV function and attenuate changes associated with iRBBB. In patients with RV infarction, treatment aims to manage acute symptoms and prevent further cardiovascular complications.
If iRBBB signals progress to full RBBB or impaired RV function, it may be necessary to proceed to invasive monitoring and consider implantation of a permanent pacemaker, especially if symptoms of HF or arrhythmias are present [4, 26].
Clinical cases and associations with other diseases
iRBBB may be associated with a variety of other diseases that affect heart or pulmonary function. In some cases, iRBBB may be present as an incidental finding in otherwise healthy individuals, but in others, it may indicate advanced changes, such as in patients with congenital heart disease, pulmonary disease, or who have had a myocardial infarction.
iRBBB is a common finding in patients with congenital heart defects, such as ASD and VSD, as well as in patients with PH and Eisenmenger syndrome. This condition is caused by volume overload of the RV. In such cases, iRBBB may be an indicator of HF progression and the need for intensive monitoring.
After myocardial infarction, especially if the RV is affected, iRBBB can signal severe changes in the function of the RV. In this context, early recognition of iRBBB and close monitoring of RV function by echocardiography are emphasized, as RV dilation may be a cause or consequence of impaired electrical conduction.
In patients with chronic respiratory diseases, the presence of iRBBB may be a sign of progressive right-sided HF. In these situations, chronic RV overload occurs, impairing RV function and leading to remodeling, which increases the risk of iRBBB. In patients with PE, in whom RV overload can occur suddenly, iRBBB is a frequent finding on the ECG [30]. This condition is associated with acute deterioration of cardiac function and may be associated with a worse prognosis if not recognized early.
iRBBB in athletes
iRBBB is commonly observed in athletes, particularly those engaged in high-level endurance training. In this population, iRBBB is often considered a benign adaptive response to increased vagal tone and RV remodeling. The prevalence of this ECG pattern is significantly higher in endurance athletes compared to strength-trained individuals, reflecting differential hemodynamic loading of the right heart. This physiological remodeling pattern has been particularly well documented by Baggish et al., who demonstrated that long-term intensive training can lead to RV dilation and delayed conduction without underlying pathology [39].
This finding is usually benign and results from the physiological adaptation of the RV to increased load. The crista supraventricularis pattern is often found in athletes and presents with similar ECG changes as iRBBB but is not associated with pathological changes in the heart [4, 8, 9]. It is important to correctly distinguish between these two findings, as the crista supraventricularis pattern is considered a normal variant and does not require further investigation, whereas the presence of iRBBB may indicate cardiovascular risk in some cases.
Predicting iRBBB
iRBBB is an ECG finding that may have varying clinical significance depending on the presence of other pathological factors. In the general population, iRBBB is usually considered a benign condition that does not require specific treatment. However, in patients with comorbidities, such as PH, heart defects, or prior RV infarction, it may signal progressive deterioration of RV function and a potential risk of progression to complete RBBB, which may lead to further complications, such as HF or the development of other arrhythmias [40, 41].
The Framingham Heart Study showed that the presence of iRBBB increases the risk of developing PH by 15% in individuals with other risk factors, such as obesity or AH. This finding is important because PH is a frequent cause of progression to complete RBBB and, therefore, an indicator of worsening RV function [40].
The Atherosclerosis Risk in Communities (ARIC) study did not show that iRBBB affects overall mortality in otherwise healthy individuals, supporting the view that, in this context, the finding is benign [42]. On the other hand, the EPIC-Norfolk study identified an association between iRBBB and subclinical diastolic dysfunction, particularly in obese individuals, suggesting that this ECG finding may be a marker of cardiovascular risk in patients with metabolic syndrome [41].
Interesting results from a study following patients with Eisenmenger syndrome showed that iRBBB is more common in patients with severe PH and significantly increases the risk of HF and arrhythmias if not treated appropriately. The prevalence of iRBBB was higher in patients with congenital heart disease, particularly ASD and VSD, and associated with a worse prognosis [10].
Some studies suggest that slowing impulse conduction in the right Tawara bundle branch may lead to asynchronous depolarization of the RV and LV, increasing the risk of developing atrial fibrillation [37, 38]. This phenomenon may be particularly important in patients with RV dilation or PH, in whom iRBBB is more common. Thus, this finding may indicate not only electrical conduction abnormalities but also impaired RV contractility, which increases the predisposition to arrhythmias.
As iRBBB is often asymptomatic, it makes early diagnosis and recognition of the risk of progression to RBBB challenging. In addition, there are population differences in the prevalence of iRBBB, making it difficult to establish standardized diagnostic criteria, especially in athletes or children. In these specific populations, iRBBB may be a normal variant, making it difficult to interpret.
Limitations
There are several important limitations to consider when interpreting the available data. The first factor is the heterogeneity of patients in different studies. Because iRBBB may be benign or signal more severe pathology, it is difficult to clearly define the risk of progression to complete RBBB or other cardiovascular disease. Therefore, when to start a comprehensive evaluation of a patient with idiopathic iRBBB is unclear. Another limitation is the lack of standardized diagnostic criteria for iRBBB, especially in specific populations, such as athletes or children. Differences in results between studies may also be due to different examination methodologies (e.g., different ECG leads or different values for normal QRS width). Finally, long-term prospective studies that assess the progression of iRBBB to RBBB and its clinical consequences in the general population are lacking.
We acknowledge that this is a narrative review and that our goal was not to introduce new data but to consolidate current knowledge into a clinically applicable reference, which can serve as a resource for clinicians and researchers alike.
As a narrative review, there is inherent subjectivity in the selection and interpretation of studies. We attempted to mitigate bias by including a broad range of studies across different populations and settings. However, the review’s scope is limited by the availability and quality of the underlying literature.
Conclusions
iRBBB is a common but heterogeneous ECG finding, and its clinical significance depends on the context in which it is diagnosed. In healthy individuals, iRBBB is usually benign and does not require specific treatment. However, in patients with cardiovascular or respiratory disease, it may signal severe structural changes, risk progression to complete RBBB, or higher predisposition to arrhythmias and HF.
Differential diagnosis is crucial for correctly recognizing this ECG finding, especially in patients with congenital or acquired heart defects, pulmonary disease, or prior RV myocardial infarction. Thorough assessment of the clinical context and other symptoms is essential to establish an appropriate diagnosis and subsequent therapeutic approach. In the event of progression from iRBBB to complete RBBB or worsening of RV function, intensive clinical care and regular monitoring of the patient are required.
The importance of iRBBB should not be underestimated, especially in patients at risk of developing cardiovascular disease, in whom this finding may signal not only progression to HF, but a possible predisposition to further cardiovascular complications. Even in the presence of benign findings, regular ECG and RV function monitoring is recommended for early detection of any changes in the cardiovascular system.
Acknowledgements
Medical Writing/Editorial Assistance
English language editing was provided by San Francisco Edit (Invoice No. 250045, dated February 13, 2025). This service was funded by the Ministry of Health of the Czech Republic (MH CZ – DRO-FNOs/2025).
Declarations
Conflict of Interest
Jozef Dodulík, Jiří Plášek, Jiří Vrtal, and Jan Václavík have nothing to disclose.
Ethical Approval
This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.
Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.
Villarreal-Molina T, García-Ordóñez GP, Reyes-Quintero ÁE, et al. Clinical spectrum of SCN5A channelopathy in children with primary electrical disease and structurally normal hearts. Genes. 2021;13(1):16–16. https://doi.org/10.3390/genes13010016.CrossRefPubMedPubMedCentral
De Asmundis C, Conte G, Levinstein M, et al. Prevalence and electrocardiographic characteristics of early repolarization pattern in young teen athletes. Acta Cardiol. 2014;69(1):3–6. https://doi.org/10.1080/ac.69.1.3011338.CrossRefPubMed
Diaz-Gonzalez L, Bruña V, Velásquez-Rodriguez J, et al. Young athletes’ ECG: incomplete right bundle branch block vs crista supraventricularis pattern. Scand J Med Sci Sports. 2020;30(10):1992–8. https://doi.org/10.1111/sms.13763.CrossRefPubMed
9.
Martinez-Sellés M, Diaz-Gonzalez L, Lucia A. Right ventricular remodeling in athletes and crista supraventricularis pattern. Clin Cardio. 2020;43(7):657–657. https://doi.org/10.1002/clc.23383.CrossRef
Badertscher P, Knecht S, Zeljković I, et al. Management of conduction disorders after transcatheter aortic valve implantation: results of the EHRA survey. Europace. 2022;24(7):1179–85. https://doi.org/10.1093/europace/euac027.CrossRefPubMed
13.
Seyyedi SR, Sharif-Kashani B, Sadr M, et al. The relationship between electrocardiographic changes and prognostic factors in severely symptomatic pulmonary hypertension. Tanaffos. 2019;18(1):34–40. https://pubmed.ncbi.nlm.nih.gov/31423138/
Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation. 2005;111(5):659–70. https://doi.org/10.1161/01.CIR.0000152479.54298.51. (Epub 2005 Jan 17. Erratum in: Circulation. 2005 Jul 26;112(4):e74. PMID: 15655131).CrossRefPubMed
25.
Brugada J, Katritsis DG, Arbelo E, ESC Scientific Document Group, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J. 2020;41(5):655–720. https://doi.org/10.1093/eurheartj/ehz467. (Erratum in: Eur Heart J. 2020 Nov 21;41(44):4258. 10.1093/eurheartj/ehz827. PMID: 31504425).CrossRefPubMed
26.
Hancock EW, Deal BJ, Mirvis DM, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part V: electrocardiogram changes associated with cardiac chamber hypertrophy: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol. 2009;53(11):992–1002. https://doi.org/10.1016/j.jacc.2008.12.015.CrossRefPubMed
27.
Ohkubo K, Watanabe I, Okumura Y, et al. A new criteria differentiating type 2 and 3 Brugada patterns from ordinary incomplete right bundle branch block. Int Heart J. 2011;52(3):159–63. https://doi.org/10.1536/ihj.52.159.CrossRefPubMed
28.
Zeppenfeld K, Tfelt-Hansen J, de Riva M, et al. 2022 ESC guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2022;43(40):3997–4126. https://doi.org/10.1093/eurheartj/ehac262.CrossRefPubMed
Wellens HJJ, Gorgels AM, Doevendans PAFM. The ECG in acute myocardial infarction and unstable angina.
34.
Ibanez B, James S, Agewall S, ESC Scientific Document Group, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2018;39(2):119–77. https://doi.org/10.1093/eurheartj/ehx393.CrossRefPubMed
Frontera A, Carpenter A, Ahmed N, et al. Demographic and clinical characteristics to predict paroxysmal atrial fibrillation: insights from an implantable loop recorder population. Pacing Clin Electrophysiol. 2015;38(10):1217–22. https://doi.org/10.1111/pace.12692.CrossRefPubMed
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