Figure 3.1.1

Discussion

In the electrophysiology (EP) lab, activation mapping from the anterior intraventricular vein (AIV) was slightly earlier than the endocardium just anterior to the aorta (−20 vs. −13 ms from QRS onset). Pacemapping from the AIV had a qS morphology in lead I, consistent with epicardial stimulation; pacemapping from the LV endocardium had a dominant R wave in lead I. Neither site matched the premature ventricular contraction (PVC) morphology (rS) in lead I, as the PVC seemed to be “in between” the pacemaps. In fact, endocardial ablation resulted in late disappearance of the PVCs, followed by a reduction in frequency but not elimination. Afterwards, ablation from the AIV resulted in elimination of the PVCs suggesting a site of origin “in between” the two sites.

Figure 3.2.1

Nonconducted atrial premature contraction (APC; red arrows). Note the pause that is less than compensatory.

Comments

The APC has to get into the sinus node; it resets the node and then the sinus node fires and activates the atrium. The time it takes for the next P wave to appear allows for a junctional escape (yellow arrows)—note the shorter PR interval after the pause.

Patient History

A 63-year-old female was referred to our institution for dyspnea (NYHA II) without any other symptom. Transthoracic echocardiography revealed a moderately reduced left ventricular ejection fraction (40%).

Figure 3.3.1 – Figure 3.3.4 are presented with Lewis diagrams (abbreviations—A: atrium, AVN: atrioventricular node, HPS: His-Purkinje system, and V: ventricle).

Figure 3.3.1

Figure 3.3.2

Figure 3.3.3

Figure 3.3.4

Heart rate is 75 bpm with narrow QRS complexes. There is no P wave just before the QRS. A sinus P wave (positive in leads I, II, III, aVF and negative in leads V₁ and aVR, solid arrow) is present just after each QRS and is fused with the ST segment and the beginning of the T wave.

Two hypotheses can be offered:

1. The P wave is conducted to the ventricle with a PR interval of 600 ms through a slow pathway. In this hypothesis, the fast pathway is blocked antegrade because of a concealed retrograde conduction coming from the previous beat.

2. Isorhythmic dissociation may be present; that is, a junctional rhythm that is a little bit faster than the sinus rate. In that case, there is no relationship between the sinus P wave and QRS.

Sinus rhythm is stable at 75 bpm. The ventricular rhythm is irregular, and there are more QRS complexes than P waves.

1. The first P wave is conducted to the ventricle with a normal PR interval (160 ms), the second with a PR interval of 340 ms, and the third one with PR interval of 180 ms. The variation of the PR interval can be explain by dual AV nodal physiology properties or concealed junctional ectopies.

2. Same sequences described in Figure 3.3.1. The coexistence of P wave conducted to the ventricle with normal, prolonged or very prolonged PR interval support the hypothesis of dual AV nodal physiology. Two narrow QRS complexes (with the same morphology as the normal sinus QRS) are apparently not preceded by P waves (solid arrow). These QRS complexes can be explained by dual AV nodal physiology properties (double ventricular response due to a single atrial depolarization through both AV nodal pathways) or junctional ectopy conducted to the ventricle but not to the atrium. All of these ECG patterns cannot be explained by junctional ectopies, especially when the P wave is conducted to the ventricle with a very prolonged PR interval.

All ECG patterns are explained by the presence of dual AV nodal pathways capable of conduction through the fast pathway, the slow pathway or both at the same time. There is always a concealed retrograde conduction that explains the variation of the PR interval and the self-perpetuation of the mechanism.

1. The first P wave is conducted to the ventricle through the slow pathway with a very prolonged PR interval. Then, the second P wave blocks in the AV node. The third P wave is conducted only through the fast pathway, resulting in a normal PR interval.

2. Double ventricular response to a single P wave occurs through both fast and slow pathways. The second QRS complex that is conducted through the slow pathway is conducted to the ventricle with a complete right bundle branch block (RBBB) and left anterior fascicular aberrancy. This is followed by an atrial ectopy (dotted arrow) that conducts to the ventricle through the fast pathway.

3. Double ventricular response occurs as described in step 2. The following sinus P wave (solid arrow) is fused with the previous T wave and is conducted through the fast pathway with an RBBB and through the slow pathway without ventricular aberrancy.

4. The following P wave is conducted to the ventricle through the slow pathway as described in Figure 3.3.1. Indeed, the fast pathway is blocked anterogradely by the concealed retrograde conduction through the fast pathway, which is coming from the previous beat.

This is the ECG immediately after a slow pathway ablation, which shows sinus P-wave conduction through only the fast pathway (with a normal PR).

All ECG patterns are explained by the presence of dual AV nodal pathways. P-waves can be conducted to the ventricle either through the fast pathway, the slow pathway (which is very slow), or both pathways at the same time. The patient’s symptoms can be explained by a pseudo pacemaker syndrome that was due to the loss of AV synchrony. A slow pathway ablation was performed with an endpoint of complete slow pathway elimination. Patient was asymptomatic after ablation and her left ventricular ejection fraction was normalized 2 months after the ablation, supported the hypothesis of rhythmic cardiomyopathy.

Patient History

A 55-year-old male without medical history presented with recurrent episodes of palpitation. Twelve-lead ECGs during palpitations are presented below.

Question

What is the mechanism (1) of the palpitation, (2) of the blocked P wave, and (3) of the wide QRS? Does the patient need an antiarrhythmic drug and/or a pacemaker implantation?

ECGs are presented with Lewis diagrams (abbreviations: A: atrium, AVN: atrio-ventricular node, HPS: His-Purkinje system, and V: ventricle).

Figure 3.4.1

1. Premature wide QRS complexes that are not preceded by atrial activity. The morphology of the wide QRS is compatible with left bundle branch block (LBBB) aberrancy. This QRS complex is either a premature ventricular contraction (PVC) or ectopy from the His with only anterograde conduction and LBBB aberrancy. This is then followed by a sinus beat that conducts to the ventricle with PR prolongation (PR = 320 ms). The PR prolongation is explained by the concealed conduction of the ectopy (His or PVC) in the AV node but not in the atrium.

2. Premature wide QRS complex that is again not preceded by atrial activity. The morphology is compatible with right bundle branch block (RBBB) aberrancy. It is unlikely that these two wide QRS complexes are two different PVC morphologies mimicking typical LBBB and RBBB. The main hypothesis is His ectopy with only anterograde conduction with RBBB (or LBBB in 1) aberrancy. This is then followed by a sinus beat that conducts to the ventricle with PR prolongation (PR = 280 ms). At this stage, it is impossible to know if the ectopy is junctional or para-Hisian. Electrophysiological study confirmed the diagnosis of parahisian ectopy.

3. PR prolongation followed by a nonconducted P wave that would ordinarily indicate a second-degree AV block, Mobitz type I. But in this patient with suspected His ectopy, the P wave more than likely fails to conduct because of a concealed His ectopy (no resultant QRS or retrograde P wave). PR prolongation is explained by the same mechanism: concealed His ectopy with concealed conduction in the AV node resulting in sinus P-wave conduction to the ventricle with PR prolongation.

4. His ectopy with only anterograde conduction with RBBB and left anterior fascicular aberrancy. This is followed by a sinus beat that conducts to the ventricle with PR prolongation (P-R=280 ms) due to concealed retrograde conduction of the His ectopy in the AV node.

Figure 3.4.2

The basic rhythm is sinus with a PR of 160 ms.

1. His ectopy that is conducted retrogradely to the atrium (negative P wave in inferior leads) but not conducted to the ventricle because the His-Purkinje system is refractory. There is a compensatory pause after His ectopy which indicates that the sinus node has been depolarized by the retrograde conduction of the His ectopy. This beat is followed by a second His ectopy with only anterograde conduction which occurs just before the sinus P wave. The sinus P wave is blocked in the AV node because of a concealed conduction in the AV node coming from a second His ectopy.

2. His ectopy with both anterograde (with RBBB aberrancy) and retrograde conduction (negative P-wave in inferior leads). This is followed by a second His ectopy as described in Figure 3.4.1.

Figure 3.4.3

1. Sudden and unexpected PR prolongation is explained by concealed His ectopy. His ectopy is not conducted in the ventricles or the atria but it is conducted in the AV node only. When the sinus P-wave occurred, the AV node was still in a relative refractory period and therefore the conduction time in the AV node is prolonged. The following P-wave is conducted with a normal PR interval.

2. His ectopy with only anterograde conduction and an incomplete RBBB aberrancy followed by a sinus beat conducted to the ventricle with PR prolongation (PR = 320 ms).

Figure 3.4.4

1. His ectopy with both anterograde (with RBBB and left posterior fascicular aberrancy) and retrograde conduction (negative P wave in inferior leads). Note that the retrograde conduction is slower in the first His ectopy when compared to the second one. The first His ectopy a) occurs slightly earlier then the previous sinus beat, b) the AV node is still in a relative refractory period, and c) the conduction time in the AV node is prolonged.

An EP study confirmed the diagnosis of ectopy located below the His. His ectopy can be concealed, conducted to the atrium and/or to the ventricle. Wide QRS complexes are explained by different aberrancy locations.

This patient was managed with antiarrhythmic drugs and was asymptomatic while under treatment.

Patient History

A 37-year-old female with mitral valve prolapse experienced palpitations. An echocardiogram showed mild left ventricular dysfunction with an ejection fraction of 40%–45%. A Holter monitor recorded frequent premature ventricular contractions (PVCs) 23 100 beats (26% of total). Her electrocardiogram is shown in Figure 3.5.1.

Figure 3.5.1 12-lead electrocardiogram showing PVCs.

Question

Where is the site of origin of the PVC?

Discussion

The most common form of idiopathic monomorphic ventricular arrhythmia arises from the ventricular outflow tracts. These types of arrhythmias can manifest as frequent unifocal PVCs, repetitive monomorphic ventricular tachycardia (VT), or sustained exercise-induced VT. Most of these focal arrhythmias (80%) arise from the right ventricular outflow tract (RVOT) rather than the left ventricular outflow tract (LVOT). Therefore, the majority of these arrhythmias will have a left bundle branch block configuration with an inferiorly directed axis.

The RVOT is a conical-shaped structure that merges with the pulmonary trunk. The description of RVOT locations differs based on fluoroscopic orientation versus the attitudinal position in the chest. The attitudinally posterior aspect is often referred to as the “septal” wall and an attitudinally anterior aspect is often referred to as the “free-wall”. The attitudinally leftward aspect of the RVOT is sometimes described as “anterior” (based on fluoroscopic orientation) whereas the attitudinally rightward aspect is considered “posterior.” Most RVOT arrhythmias originate from “septal” aspect, whereas approximately 10% originate from the “free-wall.”

Since the unipolar ECG lead V₁ is positioned on the right side of the sternum, activation from the RVOT is primarily directed away from the lead, resulting in an rS or QS wave. Therefore, a free-wall RVOT focus, which is positioned along the most attitudinally anterior aspect of the heart is associated with a QS wave in lead V₁. As the arrhythmia focus originates more posteriorly in the chest, along the posterior or “septal” RVOT, there are greater initial anterior forces observed in leads V₁–V₃ and, resulting in a small r waves in V₁. Therefore, a “septal” RVOT focus will have an earlier precordial R wave transition (≥ V₃) compared to a free wall focus (≥ V₄). It also follows that a “free wall” focus is often associated with larger S waves because of unopposed posterior forces (S wave amplitude ≥ 3.0 in lead V₂). Another distinguishing feature of a “septal” versus “free wall” site is that the former has a relatively narrow QRS complex (≤ 140 ms) because it is in closer proximity to the conduction system. On the other hand, a “free wall” location has a relatively wider QRS complex (>140 ms) and can be associated with notched QRS complexes, particularly in the inferior leads.

The frontal plane axis is used to help localize whether the arrhythmia focus is “posterior” (attitudinally rightward) or “anterior” (attitudinally leftward). The former will have more positive polarity in lead I and aVL (qR, RS), because the forces are directed toward those leads, whereas a leftward focus will generate forces away from these leads, generating QS, Qr, or rS waves.

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