Version May 2024
INTRODUCTION — Normal electrical activation of the right and left ventricles during the cardiac cycle follows a precisely defined pattern. After an impulse emerges from the atrioventricular (AV) node, it traverses the His bundle, and propagates down the bundle branches and the fascicles of the bundle branches to the terminal Purkinje fibers and ultimately the ventricular myocardium.
Conduction abnormalities result in asynchronous electrical activation causing asynchronous mechanical activation of the ventricles. This problem can be induced by one of two mechanisms: delayed activation of an area of the ventricles or early activation (preexcitation) of an area of the ventricles.
This topic will present an overview of asynchronous activation and preexcitation. The clinical manifestations of abnormal activation or preexcitation are discussed in detail separately. (See "Right bundle branch block" and "Left bundle branch block" and "Left anterior fascicular block" and "Left posterior fascicular block" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".)
Ventricular dyssynchrony caused by right ventricular pacing is discussed separately. (See "Overview of pacemakers in heart failure", section on 'Clinical effects of pacing'.)
Correction of ventricular dyssynchrony with cardiac physiological pacing, encompassing cardiac resynchronization therapy and conduction system pacing, is also discussed separately. (See "Modes of cardiac pacing: Nomenclature and selection", section on 'Cardiac physiologic pacing' and "Cardiac resynchronization therapy in heart failure: Indications and choice of system" and "Cardiac resynchronization therapy in atrial fibrillation".)
DELAYED ACTIVATION — Delayed activation causes asynchronous activation and may be a result of anatomic abnormalities or of physiologic properties of the cardiac tissues. Activation delay may occur between the ventricles or portions of the ventricles (interventricular delay), within the terminal Purkinje fibers and/or ventricular myocardium (intraventricular delay) or between layers of the heart (intramural delay) [1].
Clinically, conduction delay causing ventricular electrical dyssynchrony is manifest as an abnormal QRS complex on the electrocardiogram (ECG). Specific ECG patterns that are clinically distinguished include right bundle branch block (RBBB), left bundle branch block (LBBB), a prolonged QRS complex without specific features of LBBB or RBBB (usually called "intraventricular conduction delay" or IVCD), left anterior hemiblock, and left posterior hemiblock. While all of these conduction patterns are sometimes referred to collectively as forms of intraventricular conduction delay, the precise location of the conduction disturbance cannot be reliably determined from the surface ECG. In the case of RBBB and LBBB, it is probably more accurate to refer to these entities as forms of "interventricular conduction delay."
Interventricular conduction delay — Delayed or blocked conduction in the bundles or their fascicles results in asynchronous activation and repolarization of the right and left ventricles. This, in turn, gives rise to characteristic ECG patterns. The classic examples of interventricular conduction delay are RBBB and LBBB. Fascicular block is not strictly an interventricular conduction delay, but results from a conduction disturbance in the left anterior or posterior fascicle. It is important to recognize that a bundle branch pattern on an ECG can be due to conduction delay rather than complete block, because delay in the other bundle branch can cause equal delay to the ventricles resulting in apparent resolution of the bundle branch block pattern. (See "Right bundle branch block" and "Left bundle branch block".)
Intraventricular and intramural conduction delay — Intraventricular conduction delay is a delay within the myocardium itself. This occurs commonly in cardiomyopathies, resulting in regional differences in the time to peak systolic contraction. Intramural or transmural delay is a delay in activation between the endocardium and myocardium, also commonly noted in cardiomyopathies. Both intraventricular and intramural conduction delays occur together with interventricular left bundle branch block.
The term parietal block has been used to describe conduction delays in the terminal Purkinje conduction system. This phenomenon may result in a QRS duration in ECG leads V1 to V3 that significantly exceeds the QRS duration in leads V4 to V6 (right ventricular parietal block) or vice versa (left ventricular parietal block). Right ventricular parietal block is seen in some patients with arrhythmogenic right ventricular cardiomyopathy.
Genesis of ECG pattern — Two factors, magnitude and duration, determine the ECG changes seen with a given type of block.
Magnitude — The magnitude (or amplitude) of the extracellular signal generated by the wavefront of unopposed dipoles can be affected by a number of factors. Examples include:
●A gain of force as with ventricular enlargement
●A loss of force as with myocardial infarction
●A change in cancellation due to asynchrony that can increase or decrease unopposed dipoles
With regard to cancellation, the term "activation" is used to describe those unopposed boundaries that result in an electrocardiographically recorded potential. Many other wavefronts exist, however, and "cancel" each other. Normal synchronous ventricular depolarization results in a predictable sequence of opposed and unopposed wavefronts that result in the normal ECG [2,3]. Asynchronous activation generally reduces the amount of signal cancellation, resulting in a larger extracellularly recorded electrogram. With left bundle block, for example, left ventricular activation is delayed, occurring later than activation of the right bundle. As a result, the left ventricular signal is not partially canceled by that from the right ventricle, leading to an increase in amplitude of the QRS complex. This is the reason that standard voltage criteria for ventricular enlargement are invalid in bundle branch blocks.
Duration — Asynchronous activation can also affect the duration of the recorded potential. The time of initiation of activation is unchanged in this setting, but termination is delayed due to slower conduction to the blocked ventricle. The net effect is increased duration of the P wave or QRS complex, depending upon the site of disease.
PREEXCITATION — Ventricular preexcitation can occur when there is a premature ventricular complex/contraction (PVC; also referred to a premature ventricular beats or premature ventricular depolarizations) or when ventricular pacing occurs before the expected timing of ventricular activation through the atrioventricular (AV) node. Ventricular pacing causes asynchronous activation due to preexcitation of either ventricle. Right ventricular pacing preexcites the right ventricle and causes a pattern that has some of the ECG features of left bundle branch block (LBBB); left ventricular pacing preexcites the left ventricle and has some of the ECG features of a right bundle branch block. Preexciting the ventricles with pacing is used in patients with congestive heart failure and ventricular mechanical dyssynchrony caused by an LBBB to resynchronize the ventricles and improve mechanical synchrony. (See "Cardiac resynchronization therapy and conduction system pacing in heart failure: System implantation and programming".)
Preexciting the right ventricle with right ventricular pacing can be used to intentionally induce mechanical dyssynchrony. This has been used to reduce the outflow tract gradient in patients with hypertrophic cardiomyopathy and an outflow tract obstruction. (See "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction", section on 'Therapies of limited benefit'.)
However, the term "ventricular preexcitation" is usually used to refer to preexcitation of the ventricle caused by AV conduction over an accessory pathway. The preexcitation syndromes are conditions in which atrial activation of the ventricles occurs earlier than would be expected if atrioventricular conduction occurred normally through the AV node.
General anatomic considerations — A number of conducting pathways have been described (table 1). These include:
●Accessory atrioventricular connections, often called Kent bundles in the older literature, which directly connect the atria and ventricles [4-6]. These connections are typically located at one of the atrioventricular valves. (See "Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome".)
●James fibers, which connect the atria with the low AV node (atrionodal accessory pathway) or the bundle of His (atriofascicular accessory pathway) [7]. (See "Lown-Ganong-Levine syndrome and enhanced atrioventricular nodal conduction", section on 'Lown-Ganong-Levine pattern'.)
●So-called Mahaim fibers of several types that arise from the atrium and insert into a bundle branch (atriofascicular), arise from the AV node and insert into a bundle branch (nodofascicular), arise from the AV node and insert into ventricular tissue (nodoventricular accessory pathways). An accessory pathway can also arise from the His-bundle or one of the bundle branches and insert into ventricular tissue (fasciculoventricular accessory pathway) [8-11].
Terminology based upon anatomic connections is gradually replacing the venerable eponyms and some attempt has been made at standardization [8]. The European Study Group for Preexcitation suggests that the term "connection" should be used to describe pathways that insert into ventricular myocardium while "tracts" should be applied to pathways that insert into specialized conduction tissue [5]. However, the terms are often used interchangeably and tract is increasingly replacing connection (table 1) [12].
Atrioventricular accessory pathways (connections) — Ninety-five percent of atrioventricular accessory pathways conduct rapidly and have the characteristics of INa (sodium) dependent phase 0 action potentials that occur in normal "fast response" myocardium. (See "Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs".)
Five percent show decremental conduction, the mechanism of which is uncertain. Possible explanations include geometric factors, partial inactivation of the sodium channel, or perhaps dependence on a calcium channel. The fast response pathways often conduct rapidly, have short refractory periods, and can conduct frequently. This poses a particular problem during rapid supraventricular tachycardias such as atrial flutter, which may conduct 1:1, and atrial fibrillation, which may produce ventricular flutter and fibrillation.
In preexcitation syndromes in which the accessory pathway inserts eccentrically, the resultant ventricular depolarization represents a fusion between ventricular activation initiated by the fast response, rapidly conducting bypass pathway and that initiated by the slow response, slowly conducting atrioventricular node. This is the pattern characteristic of patients with the Wolff-Parkinson-White syndrome. The principles of this fusion are illustrated in the figure (figure 1A-C).
●The PR interval is shortened due to the preexcitation
●The eccentric ventricular activation results in a slurred upstroke of the QRS or delta wave
●The QRS duration is increased due to the asynchronous activation between the preexcited and normally excited portions of the ventricular myocardium
How the ECG can be used to identify the location of the accessory pathway is discussed elsewhere. (See "Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome".)
James fibers (intranodal or atrionodal bypass tract)
Lown-Ganong-Levine syndrome — The Lown-Ganong-Levine syndrome is characterized by palpitations in patients with an ECG that shows a short PR interval and a normal QRS duration [13]. For many years, this disorder was thought to be due to tracts that connected the atrium with the low AV node or the His bundle (via James fibers) [7]. (See "Lown-Ganong-Levine syndrome and enhanced atrioventricular nodal conduction".)
The current concept, however, is that the short PR interval with a normal QRS pattern results, in most cases, from enhanced or accelerated AV nodal conduction and less often from an accessory pathway [12,14-16]. A short PR interval appears to be more frequent in patients with concealed accessory pathways, but has also been associated with dual pathway physiology and AV nodal reentrant tachycardia [15]. However, only patients with symptomatic tachyarrhythmias are studied electrophysiologically. As a result, it is uncertain whether all individuals with a short PR interval and normal QRS complex have enhanced AV nodal conduction or accessory pathways near the AV node.
Reentrant SVT — A case of incessant supraventricular tachycardia (SVT), which continued despite AV block, has been reported [17]. An atrial tachycardia, AV nodal reentrant tachycardia, and an orthodromic tachycardia using a concealed accessory AV pathway were excluded as causes. The earliest retrograde atrial activation was at the posterolateral tricuspid annulus, and the tachycardia was eliminated by ablation at this site. These observations strongly suggest a concealed atrionodal pathway as the cause.
Role of Mahaim fibers — Mahaim pathways arise from the atria, AV node, fascicle, or one of the bundle branches and insert into fascicle or ventricular tissue. The precise characteristics of Mahaim fibers have been debated [10]. It was presumed that certain of these pathways, in which the AV node was normally traversed, could explain the situation in which the PR interval was normal but the QRS was widened (presumably due to eccentric activation of the ventricles) [18]. Some patients also had a prolonged PR interval with eccentric ventricular activation. This could be explained by slowed AV nodal conduction and anomalous connections at the level of or below the AV node.
However, surgical and catheter ablation studies suggest that electrophysiologic characteristics attributed to nodoventricular Mahaim fibers are due to atriofascicular accessory connections with decremental conduction [19-24]. One report, for example, suggests the presence of an atrioventricular connection in the tricuspid ring [21]. This connection has slow and rate-dependent conduction, blocks with adenosine, has intrinsic automaticity, and links to a rapidly conducting insulated pathway that generates a "His-like" potential. Despite these observations, some experts still believe that nodofascicular tracts exist and are functional [12]. An orthodromic AVRT with atrioventricular dissociation has been presented as evidence for a nodoventricular type of Mahaim fiber [25].
Fasciculoventricular pathways can be demonstrated in 1 to 2 percent of adults who show ventricular preexcitation and are referred for electrophysiologic investigation [11,26]. These pathways can be thought of as a loss of insulation around the His-Purkinje system resulting in a direct connection to the local ventricular myocardium causing ventricular preexcitation. These pathways do not participate in reentrant rhythms and must be recognized during an EP study, mostly so that ablation is not attempted unnecessarily.
Enhanced AV nodal conduction with a short AH interval is common, but normal AH interval lengthening may occur during incremental atrial pacing [11,26]. The administration of adenosine may help to reveal the relationship between the fasciculoventricular pathway and its connection to the AV node and the infranodal conduction system. With AV nodal connections, a high degree of AV block or even complete AV block may occur with preexcited conducted beats.
Familial Mahaim syndrome has been reported and suggests possible genetic transmission in some patients [27].
Classification of arrhythmias associated with accessory pathways — The accessory pathways have two effects, which facilitate the development of certain supraventricular tachyarrhythmias: they can provide a pathway for reentry; and they can produce preexcitation, which results in a wide complex tachycardia.
The atrioventricular reentrant tachycardias (AVRT) can utilize both the AV node and an accessory pathway in the reentrant circuit. (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".)
●Orthodromic AVRT, the most common form, uses a circuit consisting of antegrade conduction through the AV node and retrograde conduction through the accessory pathway. In the absence of preexisting or functional bundle branch block, this produces a narrow QRS tachycardia in which the P wave follows the QRS complex (figure 2).
●The less common, or antidromic, form of AVRT conducts antegrade through the accessory pathway and retrograde through the AV node, producing a wide QRS complex with a delta wave and a P wave that follows the QRS complex. This would be a reentrant form of a "preexcited tachycardia" that uses the AV node (see below) (figure 3).
●The permanent form of junctional reciprocating tachycardia (PJRT) is a clinical syndrome of a nearly incessant supraventricular tachycardia. It is typically seen in young patients who can present with a tachycardia-mediated cardiomyopathy. The term PJRT is often used interchangeably with a nearly incessant AVRT using a slowly conducting concealed accessory pathway [28]. However, some patients with an atrial tachycardia or atypical AV nodal reentry can also present with a nearly incessant SVT. (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway", section on 'Permanent junctional reciprocating tachycardia'.)
As discussed above, the so-called James and Mahaim fibers may also be involved in reentrant arrhythmias.
Preexcited tachycardias — Preexcited tachycardias, such as the WPW syndrome, are wide complex tachycardias that conduct antegrade over the accessory pathway. They are induced by supraventricular tachycardias, including atrial fibrillation, atrial flutter, and the family of atrial tachycardias including the antidromic form of AVRT. (See "Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".)
SUMMARY
●Delayed activation – Delayed activation causes asynchronous electrical and mechanical activation and may be a result of anatomic abnormalities or of physiologic properties of the cardiac tissues. Clinically, conduction delay causing asynchronous ventricular activation is usually manifest as an abnormal QRS complex on the ECG. Specific ECG patterns that are clinically distinguished include right bundle branch block (RBBB), left bundle branch block (LBBB), a prolonged QRS complex without specific features of LBBB or RBBB (usually called "intraventricular conduction delay" or IVCD), left anterior hemiblock, and left posterior hemiblock. (See 'Delayed activation' above.)
●Genesis of ECG pattern – Two factors, magnitude and duration, determine the ECG changes seen with a given type of block. Normal synchronous ventricular depolarization results in a predictable sequence of opposed and unopposed wavefronts that results in the normal ECG. Asynchronous activation generally reduces the amount of signal cancellation, resulting in a larger extracellularly recorded electrogram. The time of initiation of activation is unchanged in the setting of asynchronous activation, but termination is delayed due to slower conduction to the blocked ventricle. The net effect is an increased duration of the QRS complex. (See 'Genesis of ECG pattern' above.)
●Preexcitation – Ventricular preexcitation can occur when there is a PVC or when ventricular pacing occurs before the expected timing of ventricular activation through the atrioventricular (AV) node. However, the term "ventricular preexcitation" is usually used to refer to preexcitation of the ventricle caused by AV conduction over an accessory pathway. The preexcitation syndromes are conditions in which atrial activation of the ventricles occurs earlier than would be expected if atrioventricular conduction occurred normally through the AV node. (See 'Preexcitation' above.)
●Anatomic considerations – A number of conducting pathways have been described, including those connecting the atria with the ventricles, the atria with the AV node, the atria with the His-Purkinje system, and the AV node with the ventricles (table 1). (See 'General anatomic considerations' above.)
●Effects of accessory pathways – The accessory pathways have two effects which facilitate the development of certain supraventricular tachyarrhythmias: they can provide a pathway for reentry, either orthodromically or antidromically; and they can produce preexcitation, which, during tachycardia and anterograde conduction over the pathway, either as part of the circuit or as a bystander, results in a wide QRS complex tachycardia. (See 'Classification of arrhythmias associated with accessory pathways' above.)
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