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.

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 (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 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 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.

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 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 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].