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INTRODUCTION
The electrocardiographic (ECG) interpretation of electrical end conduction delay (ECD) in the right ventricular (RV) branch has originated several hypotheses; among them, that the right bundle branch (RBB) is not single as anatomically demonstrated, and could be divided into different terminal branches or regions when analyzed through a vectorcardiogram1 (VCG). The electrical branches of the ventricles are originated in the atrioventricular node (AV node). The His bundle originates the RBB and the left bundle branch, composed by special cells capable of conducting electricity, called cardiomyocytes, with conduction velocity greater than the myocardial cells. Anatomically, the RBB ends in the RV free wall, which leads to cell-to-cell depolarization after that. This change in electrical conduction initiated by the RBB has always intrigued researchers, as they question the possibility of this depolarization in the RV free wall, as already suggested, occurring by the intraventricular conduction system of the RV free wall or by preferential pathways in the myocardium.
The electrocardiographic diagnosis of ECD in the RBB is well established worldwide1. In this study, we proposed to perform the analysis of the VCG, which is more accurate device in recording the electrocardiographic path, to monitor the behavior of this delay in the RV free wall in order to identify the divisions of electrical conduction by electrical beams or myocardial sections.
METHODS
Design of the study
Study performed during the period from June 1 to September 30, 2017. The ECG of 227 patients from the department of graphic methods of the Centro Universitário FMABC were analyzed. Only ECGs with ECD were included according to the described criteria.
Inclusion criteria
In the study, patients older than 18 years of age were included, who met the criteria for incomplete right bundle branch block (IRBBB) or ECD with 12-lead ECG, according to the 3rd Guidelines of Electro-Vectorcardiography Interpretation of the Sociedade Brasileira de Cardiologia1. The electro-vectorcardiographic inclusion criteria were:
QRS duration between 90 and 100 ms (<120 ms);
Triphasic morphology in V1 or V1-V2 (rsr’, rSr’, rsR’, RsR’), or morphology in M followed by negative T wave;
Biphasic morphology in V1 (rS), with notch in the ascending ramp of S wave (atypical IRBBB);
Presence of S wave of slow or prolonged (slurred) inscription in the left leads: I, aVL, V5 and V6;
rSr’ pattern with final r or R wave of slow inscription in aVR lead;
Presence of criterion of SI, SII, SIII syndrome;
Presence of extreme SÂQRS shift in the superior quadrants (SÂQRS to the left of -30º) associated with SII ≥ SIII;
In patients who had undergone VCG, only those who had 30 or more dashes with slow inscription at the end of the QRS and located to the right in the frontal and horizontal planes (HPs) were included, following the criteria proposed by Pastore et al2;
QRS loop in the HP, of predominantly clockwise rotation, and sometimes eight-shaped;
Maximum voltage vector usually smaller than normal.
VCG test
After the ECG inclusion criteria were met, all 227 patients were invited to undergo a VCG test.
The VCG is a noninvasive exam, which was performed in the cardiology department of Centro Universitário FMABC by a trained cardiologist following the Frank method3. The exam is performed with the patient in the supine position, lasting approximately 5 minutes. The seven electrodes are positioned on the body surface, trunk, leg and neck as shown in figure 1. This exam does not pose any additional risk to patients. Both the ECGs and VCGs were performed using the DMS Cardioscan 12 equipment.
Figure 1 : Frank’s method – electrodes positioning. Location of electrodes to perform vectorcardiogram using the Frank’s method. Seven electrodes are placed on the body surface. H: Posterior region of the neck; F: Left leg; I: Right mid axillary line (4th or 5th right intercostal space); A: Left mid axillary line (4th or 5th left intercostal space); C: Mid clavicular line (4th or 5th left intercostal space); E: Center of sternum (4th or 5th left intercostal space); M: Spinal apophysis (4th or 5th left intercostal space)
The VCG tracings were analyzed (figure 2) to confirm the presence of ECD and its behavior in the recording. For this analysis, the frontal plane (FP) was selected because they have the leads where the electrical axes of the heart are calculated, since in this plane the heart and its electrical bundles can be almost entirely observed.
RESULTS
All 227 patients selected for evaluation of VCG attended the examination. There were 118 men and 109 women, aged between 18 and 82 years (average of 50 years), weight between 65 and 121 kg, and height between 1.58 to 1.89 m. No risk factors, with three asymptomatic cardiovascular risk factors, and baseline patient characteristics are described in table 1.
Table 1 : Cardiovascular and electrocardiographic characteristics of patients. ECG: electrocardiogram; DVRA: diffuse disturbance of ventricular repolarization; LAFB: Left anterior fascicular block; LPFB: Left posterior fascicular block
| n | (%) | |
|---|---|---|
| Women | 109 | 48.1 |
| Men | 118 | 51.9 |
| Cardiovascular risk factors | ||
| 3 factors | 53 | 23.34 |
| 2 factors | 72 | 31.71 |
| 1 factor | 69 | 30.39 |
| No risk factors | 34 | 14.97 |
| Electrocardiogram | ||
| With no other ECG alterations | 137 | 60.35 |
| With DDVR | 40 | 17.62 |
| With LAFB | 41 | 18.06 |
| With LPFB | 4 | 1.76 |
| ST segment alteration | 5 | 2.20 |
Analyzing the VCG tracings in the FP of patients who presented characteristic of ECD without apparent structural heart disease. The recording of ECD in different sectors of the right quadrant was found; According to the location of ECD in the FP, we made a classification into 3 types (figure 3): Type I, when ECD is located in the right superior quadrant in the FP between -120° and -150°; Type II, when ECD is located in the right inferior quadrant in the FP between +110° and +140°; Type III, when ECD is located between +170° and -170° in the FP.
Figure 3 : Types I, II and III of ECD. The figure shows the location of ECD at the right of the final/terminal portion of the QRS loop in the FP. The criterion used was ≥15 dashes (≥30 ms) closer to each other at the end of the QRS loop in at least two dashes
According to the rotation of the QRS loop in the FP, we divided type I into three subtypes: IA, when the QRS loop turns in a counterclockwise rotation and the QRS axis presents extreme leftward shift. This subtype could be difficult to differentiate from left anterior fascicular block; IB, when the QRS loop rotation is clockwise. This subtype may shift the electrical QRS axis to the right, and at times, it suggests differential diagnosis with left posterior fascicular block (LPFB); IC, when the rotation of the QRS loop is eight-shaped, resembling a monoplane propeller (figure 4).
Table 2 contains information previously published by this research group4,5. Here, in this study, we present these data with the addition of differential diagnosis between type IA of ECD and left anterior fascicular block.
Table 2 : Electro-vectorcardiographic characteristics of type IA
| 10 ms initial vector of QRS loop | With downward and rightward direction | With downward and leftward direction |
|---|---|---|
| qrs morphology in I and aVL | qR pattern | Rs |
| SII/SIII ratio | SIII | SII>SIII (low sensitivity) |
| Location of ECD | In the left upper quadrant when present | In the right upper quadrant2 |
| Prominent R wave in aVR (R ≥ 0.3 mV) | Absent | It could be present and is called aVR sign in BrS6 |
| Morphology of QRS circuit of vectorial cardiogram in the horizontal plane | Similar to normal | Similar to type-C right slurring pattern: initial vector at the front and the left, counterclockwise rotation and ≥20% of the loop area located in the right posterior quadrant in the horizontal plane7 |
Electro-vectorcardiographic characteristics of type IA
SÂQRS with extreme shift in the left superior quadrant between -30° and -90°; QRS loop of counterclockwise rotation in the FP; rapid passage from left to right of the QRS loop; predominantly negative QRS complexes in inferior leads: prominent S wave in these leads; SII>SIII: useful for differential diagnosis with left anterior fascicular block; prominent and/or wide R wave of aVR; aVR of qR or QR type, with R wave frequently wide.
Electro-vectorcardiographic characteristics of type IB
SÂQRS difficult to be determined: indeterminate or perpendicular to the FP, suggesting the presence in all FP axes, with isoelectric complexes that make this determination difficult. Pointed, eight-shaped QRS loop in the FP, with the initial portions located in the left inferior quadrant, and the final portions in the right superior quadrant, where the ECD can be located. The aspect of QRS loop is similar to the propellers of a plane.
Electro-vectorcardiographic characteristics of type IC
SÂQRS not shifted or shifted to the right; spikey aspect of the QRS loop in the FP with clockwise rotation; ECD in the right superior quadrant in the FP; frequent SI-SII-SIII; wide R wave in aVR; morphology of IRBBB; rSR’ in V1; sagittal plane clearly shows QRS loop perpendicular to Y line; discrete ECD of 30 ms (15 dashes) located in the right superior quadrant between -100° and -160°, or greater.
When the basic cause is QrS, the presence of prominent final R wave in lead aVR: R wave ≥3 mm or R/q ≥0.75 in lead aVR (aVR sign).
Electro-vectorcardiographic characteristics of type II
Characterized by ECD located in the right inferior quadrant. It corresponds to the right inferior bundle territory (LPFB), which makes the differential diagnosis (table 3).
Table 3 : Differential diagnosis between type II ECD and LPFB
| Type II ECD | LPFB | |
|---|---|---|
| Normal | Frequent prolongation | |
| Association with inferior infarction | No | Frequent |
| Pressure of RII and RIII | ≤10 mm | ≥15 mm |
| RII/RIII pressure ratio | RII >RIII | RIII > RII |
| Notch in R wave descending slope in inferior leads | Absent | Constant notch at the middle-end |
| Intrinsic shift in aVF, V5 and V6 | Normal | Increase: up to 30 ms |
| Intrinsic deflection in AVL | Normal | Decrease: up to 15 ms |
| QRS loop appearance in frontal plane | Clockwise and with characteristic rapid passage from left to right, between 30 to 50 ms | Clockwise, appearance of “fat” loop and maximum vector close to + 120º |
| Clinical factors that should be excluded | Not stated | Vertical heart, left ventricular remodeling and lateral infarction |
ECG: ÂQRS between +70° and +100°; normal QRS duration; S1-R2-R3 pattern with R2 and R3 non-increased pressure (generally ≤10 mm), never reaching 15 mm (essential element for the differential diagnosis with LPFB); R2≥R3 (in LPFB R3>R2); aVR of QS type; possible notch in the descending ramp in inferior leads; deeper s wave in V2 and/or V3; persistent S wave up to V5 and/or V6; V1: rS, RS or rSR’ with S of V1 and V2 possibly enlarged.
VCG FP: initial vectors always on the left, above and below; clockwise rotation; predominant location in inferior quadrants; rapid change from left to right between 30 ms and 50 ms; ECD at the right and below between +120° and +150°. HP: QRS loop of counterclockwise rotation; rapid change from left to right, between 40 and 50 ms; ECD backward and rightward. Initial vectors upward and downward; clockwise rotation; posteroinferior rotation; ECD downward and backward.
DISCUSSION
The electrocardiographic tracings with ECD and concomitant alterations such as LAFB and LPFB, myocardial infarction of inferior wall, electro-vectorcardiographic pattern of Brugada syndrome, or a subpopulation of arrhythmogenic right ventricular dysplasia/cardiomyopathy may, according to the electro-vectorcardiographic recording, have an unspecific diagnosis of ECD. This identifies the right bundle branch as a single branch, which if it occurred as proposed, would depolarize the whole right ventricular free wall simultaneously as a block; however, we identified that in the final portion of the right ventricular free wall there may be depolarization in different portions or sectors, which characterize the right branch or anatomical subdivision of the electrical bundle, or by cell-to-cell trajectory5.
The right bundle branch does not present anatomically distinguishable pathways and is considered a single fascicle. The tetrafascicular system (three dependent fascicles that are part of the left bundle branch: left anterior fascicle, left posterior fascicle and left septal fascicle, and continuation of the right bundle branch) activates the Purkinje network, a subendocardial plexiform layer of dense intramural branches capable of finally activating the small segments corresponding to the myocardium. For this reason, in normal conditions, the myocardium is activated from the endocardium toward the epicardium8.
Nagao et al.9 studied the conduction system in endocardial excitation spreading through the right ventricle (RV). The role of the Purkinje network in an excitation sequence in the RV endocardial surface was studied using an isolated perfused dog preparation. This was electrically stimulated in the proximal right bundle, and the activation time was mapped using contiguous bipolar electrodes, or a microelectrode, or both. The first muscle activation was observed at the junction between the ventricular septum and the free wall at the front of the anterior papillary muscle. After the initial activation, the propagation of ventricular muscular excitation has a radial propagation form and a velocity of 1.67±0.20 m/sec. Muscle activation in this area was almost always preceded by activation in Purkinje fibers by 2 to 6 ms. Thus the Purkinje system is indispensable for widespread excitation in this area. In the lower third of the septum, the excitation sequence was essentially similar to the RV free wall, indicating a contribution of rapid conduction by the Purkinje system. In contrast, in the upper two-thirds of the RV free wall activation of ventricular muscle propagation from apex to base with a significantly delayed conduction and velocity of 0.41 +/- 0.88 m/s, and was not preceded by activation of Purkinje fibers, thus indicating a lack or a drastic decrease of involvement of the Purkinje system in the basal areas of the RV, justifying the physiological ECD of the QRS loop.
The anterior, posterior and septal branches of the right bundle in the RV free wall is a functional distribution. The propagation of excitation of the ventricular endocardial muscle was confirmed by selective transection of one of those special fibers, suggesting the etiological significance of the lesion in the right bundle branch as a cause for several electrocardiographic patterns of IRBBB. In spite of having true right bundle branches in the RV free wall, these proven three preferential pathways justify a trifascicular free wall: it is at least functional.
The functional distribution of the three main right bundle branches through the incisional interruption of the free wall was investigated, and the data obtained revealed that the anterior branch was responsible for the activation of the anterior septum, anterior paraseptal free wall and right ventricular outflow tract. The lateral and posterior branches contributed to the free wall and posterior septum activation. The most severe distortion of the wavefronts was induced by lateral branch interruption. This finding supports the important role of the Purkinje system in the dissemination of RV activation to the free wall muscle.
Conduction delay in the upper septum after anterior or posterior branch incision may reflect the distribution of these branches toward the inferior septum. The maximum delay of ventricular muscular activation induced by incision ranged from 6 to 12 ms. However, when the anterior or posterior branches were interrupted, the maximum delay in activation was, at times, observed in the area proximal to the incision lines. This could be attributed to artificial damage to the septal muscle during the incision procedure. Because of the anatomy of these branches, it was quite difficult to only cut the conducting tissue. Thus, the interruption of the branches may have caused an undesirable lesion in the underlying septal muscle. The current findings are in general agreement with previous in vivo studies, where the effects of RV distal interruption were investigated. Moore et al.10, by cutting false tendons, found a similar delayed activation area in the epicardial surface of the RV. Smith et al.11 verified a partial delay in the epicardium after making a large laceration on the septal surface of the RV; this delayed area was almost consistent with that obtained in our study, splitting the posterior branch. These two groups recorded an IRBBB pattern in ECG simultaneously. Uhley et al.12 produced two types of IRBBB in the ECG by cutting peripheral RBBB bundles. All these findings tend to suggest a possible etiological significance of lesions on each main RBBB branch as a cause for several types of IRBBB with pattern I. However, more extensive clinical studies are necessary to confirm such possibility, since there are differences between species in the anatomical characteristics of the His-Purkinje system13, and between the effects of activation delay within the right ventricular endocardium in the QRS configuration.
The mammalian heart must function as an efficient pump while simultaneously carrying out electrical impulses to conduct the contraction process. In the ventricles, electrical activation begins at the points of insertion of the Purkinje system into the endocardium. As the diffusion component of the subsequent excitation wave propagates from the endocardium in the normal cardiac wall of the free wall without creating directional biases9.
The chronology of electrical events that mechanically activate the myocardium has been described as beginning at the level of the septum, spreading to the apex, then to the bodies of both ventricles, and eventually to the base of the heart (apex-base activation). Francisco Torrent-Guasp14,15 suggested that the myocardium is a single muscle band that forms a double- helical loop. The contraction of the myocardium would follow the trajectory of muscle fibers that originate in the pulmonary artery towards the body of the ventricles and the aorta (base-to-apex contraction). This would explain the movements in the base of the heart and the twisted movement of the ventricles seen in magnetic resonance studies.
Slow conduction in the RVOT may contribute to a greater risk of arrhythmia6. Many of the cases described in literature as LPFB are, the way we see them, type II ECD, and as their electro-vectorcardiographic differences are very subtle, the diagnosis must always be clinical electro-vectorcardiographic.
CONCLUSION
The electro-vectorcardiographic recording in patients with identified ECDs demonstrates that the RV free wall depolarizes in three distinct sectors that occurs either by special condution cells such as right branch fascicles or sectoral depolarization independent of the final portion of the right bundle branch, but also we not only detected the identification of three distinct sectors in the RV free wall, but it also allows us to identify aberrant tracings that eventually suggest serious adjacent structural heart disease, such as inferior and/or anterior infarctions, chronic obstructive pulmonary disease, fascicular blocks of the right bundle branch similar as left septal fascicular block and LPFB. In addition, these dromotropic disorders can be found in heart diseases that potentially lead to sudden cardiac death, such as arrhythmogenic right ventricular cardiomyopathy/dysplasia. The scarce dissemination of these concepts is surprising, taking into account the relevance of their differential diagnoses.
