Mapping and Ablating Ventricular Premature Contractions That Trigger VF
Mapping and Ablating Ventricular Premature Contractions That Trigger VF
The Purkinje system is the most frequent site of initiation of VF. Recent work has demonstrated that the Purkinje network is critical in the triggering and maintenance of VF in animal experiments and patients. Catheter ablation targeting the Purkinje potentials responsible for triggering VF has been shown to be possible and efficacious in a number of conditions such as idiopathic VF (short-coupled variant of torsade de pointes), ischemic VF, and chronic myocarditis. What is still undetermined is whether the mechanism of the ablation effect is due to the suppression of the trigger or substrate modification.
During activation mapping of the triggering VPC, attention should be paid to the preceding sharp Purkinje-like signals. Mapping should be focused on the earliest activation of this potential, and determining the earliest potential is the key to a successful ablation. However, the potential may sometimes be seen to occur with intra-Purkinje block to the myocardium, and not produce a VPC. This means that there is the possibility that not only the elimination of the triggering VPC, but also conduction block in the Purkinje network can suppress the triggering VPC and VF. In fact, dissociated firing from the Purkinje network is sometimes seen after a successful ablation. The following case is an example of the successful suppression of VF by the modification of the Purkinje network.
A 54-year-old man with idiopathic VF (short-coupled variant of torsade de pointes) underwent catheter ablation for frequent episodes of ICD shocks. Nonsustained polymorphic VT with the same QRS morphology as the clinical polymorphic VT was repeatedly inducible by atrial pacing after an intravenous administration of cibenzoline (Fig. 2A). There was no change in the QRST complexes in any of the electrograms after the intravenous administration of cibenzoline. The first VPC (VPC1) had an RBBB configuration with right-axis deviation and the second one (VPC2) had an RBBB pattern with a northwest axis. The coupling interval (CI) of VPC1 to the preceding normally conducted QRS complex was 250 milliseconds. During the polymorphic VT, diastolic and presystolic Purkinje potentials were recorded from an octapolar electrode catheter with 1.25-mm electrode widths and 2-mm interelectrode spacings placed on the left ventricular septum (Fig. 2A and B). Diastolic Purkinje potentials were recorded earlier from the proximal than distal electrodes, and fused presystolic Purkinje potentials were recorded earlier from the distal than proximal electrodes. During sinus rhythm, recording at the same site demonstrated fused Purkinje potentials before the onset of the QRS. Because the earliest Purkinje activation site before VPC1 could not be determined and seemed to be a more proximal site than the site of electrodes 7 and 8, RF energy was delivered to the site of electrodes 3 and 4. A Purkinje potential from this site preceded the onset of VPC1 by 15 milliseconds and VPC2 by 60 milliseconds. The intracardiac electrograms recorded after the ablation showed the abolition of the local Purkinje potentials at the middle portion and a slight delay in the occurrence of the local ventricular electrogram during sinus rhythm (Fig. 2C). The polymorphic VT became noninducible and only an isolated VPC was inducible. The morphology of this isolated VPC differed from the previous triggering VPCs (VPC1 or VPC2). Further, Purkinje firing was observed before this VPC and intra-Purkinje block occurred. Holter monitoring after the ablation revealed no VPCs. He was followed up without any drugs or episodes of syncope or VF recurrences during a period of 14 years. These observations suggest that the VF initiation was caused by activity from the Purkinje tissue. However, the suppression of the VF was achieved with catheter ablation of the Purkinje network, not of the earliest Purkinje activation of the initial triggering beat in this patient. If the early phase of VF is perpetuated by variable reentrant loops within the Purkinje network, the mechanism of VF suppression in this patient can be explained by intra-Purkinje block.
(Enlarge Image)
Figure 2.
Catheter mapping during polymorphic VT in a male patient with a short-coupled variant of torsade de pointes. A: During the polymorphic VT, which was induced by rapid atrial pacing after the administration of intravenous cibenzoline, diastolic Purkinje potentials and presystolic Purkinje potentials were recorded from the left ventricular septum. During sinus rhythm, fused Purkinje potentials were recorded before the onset of the QRS. B: Representation of an octapolar electrode catheter placed on the left ventricular septum. C: Intracardiac electrograms recorded after ablation showing the abolition of the local Purkinje potential (P) at the middle portion and a slight delay in the occurrence of the local ventricular electrogram during sinus rhythm (arrow). The polymorphic VT became noninducible and only an isolated VPC was inducible. The morphology of this VPC differed from the previous triggering VPC and intra-Purkinje block was also observed before this VPC (arrowhead). HBE = His-bundle electrogram; HRA = high right atrium; LAO = left anterior oblique view; LV = left ventricle; P = Purkinje potential; RAO = right anterior oblique view; SA = atrial pacing stimulus. (From Nogami A, Sugiyasu A, Kubota S, Kato K: Mapping and ablation of idiopathic ventricular fibrillation from Purkinje system. Heart Rhythm 2005;2:646–649. With permission from Elsevier.)
In the report by Haïssaguerre et al., electrocardiograms recorded after ablation showed the abolition of the local Purkinje potentials and a slight delay in the occurrence of the local ventricular electrogram. However, they did not determine how much of the complex Purkinje network was involved in each patient and the issue of multiple foci versus differing activation routes from limited foci remains unsolved. In our case, catheter mapping revealed that the constantly changing polymorphic QRS morphology resulted from the changing propagation in the Purkinje arborization and the polymorphic VT became noninducible after the catheter ablation of the Purkinje network. We did not ablate the earliest site of the Purkinje activation, and the isolated VPC with diastolic Purkinje activation was still inducible after the catheter ablation.
Of course, the earliest activation site of the Purkinje activation during the triggering VPC should be searched and ablated; however, a modification of the Purkinje network might be applied when the earliest site cannot be determined or is located close to the His-bundle. In my experience, the right-sided triggers usually arise from the distal right bundle branch and the most proximal site of the origins on the left side was the bifurcation of the left anterior and posterior fascicles. If the earliest site is located proximal to the bifurcation, ablation of just the distal site is recommended for the initial application. It is possible to create substrate modification and eliminate the origin nearby because the Purkinje network can be easily ablated.
Because the Purkinje network in humans is mostly localized to the subendocardium, a transmural lesion creation is not needed. Further, the ventricular myocardium of the culprit Purkinje network in idiopathic VF is usually healthy. This differs from ischemic VF, in which the ventricular myocardium at the culprit Purkinje network usually has a low voltage and is located near a scar border. During the Purkinje network modification, the creation of bundle-branch block or hemi-block is not required. While some change in the frontal axis has been observed in some patients after the ablation during a left septal Purkinje ablation, the QRS width remains almost the same. Catheter manipulation sometimes produces transient bundle-branch block. As a result, peripheral Purkinje potentials no longer precede the local ventricular activation in sinus rhythm, and it makes mapping of the Purkinje network difficult. For this reason the creation of bundle branch block should be avoided.
Substrate Modification of the Purkinje Network
The Purkinje system is the most frequent site of initiation of VF. Recent work has demonstrated that the Purkinje network is critical in the triggering and maintenance of VF in animal experiments and patients. Catheter ablation targeting the Purkinje potentials responsible for triggering VF has been shown to be possible and efficacious in a number of conditions such as idiopathic VF (short-coupled variant of torsade de pointes), ischemic VF, and chronic myocarditis. What is still undetermined is whether the mechanism of the ablation effect is due to the suppression of the trigger or substrate modification.
During activation mapping of the triggering VPC, attention should be paid to the preceding sharp Purkinje-like signals. Mapping should be focused on the earliest activation of this potential, and determining the earliest potential is the key to a successful ablation. However, the potential may sometimes be seen to occur with intra-Purkinje block to the myocardium, and not produce a VPC. This means that there is the possibility that not only the elimination of the triggering VPC, but also conduction block in the Purkinje network can suppress the triggering VPC and VF. In fact, dissociated firing from the Purkinje network is sometimes seen after a successful ablation. The following case is an example of the successful suppression of VF by the modification of the Purkinje network.
A 54-year-old man with idiopathic VF (short-coupled variant of torsade de pointes) underwent catheter ablation for frequent episodes of ICD shocks. Nonsustained polymorphic VT with the same QRS morphology as the clinical polymorphic VT was repeatedly inducible by atrial pacing after an intravenous administration of cibenzoline (Fig. 2A). There was no change in the QRST complexes in any of the electrograms after the intravenous administration of cibenzoline. The first VPC (VPC1) had an RBBB configuration with right-axis deviation and the second one (VPC2) had an RBBB pattern with a northwest axis. The coupling interval (CI) of VPC1 to the preceding normally conducted QRS complex was 250 milliseconds. During the polymorphic VT, diastolic and presystolic Purkinje potentials were recorded from an octapolar electrode catheter with 1.25-mm electrode widths and 2-mm interelectrode spacings placed on the left ventricular septum (Fig. 2A and B). Diastolic Purkinje potentials were recorded earlier from the proximal than distal electrodes, and fused presystolic Purkinje potentials were recorded earlier from the distal than proximal electrodes. During sinus rhythm, recording at the same site demonstrated fused Purkinje potentials before the onset of the QRS. Because the earliest Purkinje activation site before VPC1 could not be determined and seemed to be a more proximal site than the site of electrodes 7 and 8, RF energy was delivered to the site of electrodes 3 and 4. A Purkinje potential from this site preceded the onset of VPC1 by 15 milliseconds and VPC2 by 60 milliseconds. The intracardiac electrograms recorded after the ablation showed the abolition of the local Purkinje potentials at the middle portion and a slight delay in the occurrence of the local ventricular electrogram during sinus rhythm (Fig. 2C). The polymorphic VT became noninducible and only an isolated VPC was inducible. The morphology of this isolated VPC differed from the previous triggering VPCs (VPC1 or VPC2). Further, Purkinje firing was observed before this VPC and intra-Purkinje block occurred. Holter monitoring after the ablation revealed no VPCs. He was followed up without any drugs or episodes of syncope or VF recurrences during a period of 14 years. These observations suggest that the VF initiation was caused by activity from the Purkinje tissue. However, the suppression of the VF was achieved with catheter ablation of the Purkinje network, not of the earliest Purkinje activation of the initial triggering beat in this patient. If the early phase of VF is perpetuated by variable reentrant loops within the Purkinje network, the mechanism of VF suppression in this patient can be explained by intra-Purkinje block.
(Enlarge Image)
Figure 2.
Catheter mapping during polymorphic VT in a male patient with a short-coupled variant of torsade de pointes. A: During the polymorphic VT, which was induced by rapid atrial pacing after the administration of intravenous cibenzoline, diastolic Purkinje potentials and presystolic Purkinje potentials were recorded from the left ventricular septum. During sinus rhythm, fused Purkinje potentials were recorded before the onset of the QRS. B: Representation of an octapolar electrode catheter placed on the left ventricular septum. C: Intracardiac electrograms recorded after ablation showing the abolition of the local Purkinje potential (P) at the middle portion and a slight delay in the occurrence of the local ventricular electrogram during sinus rhythm (arrow). The polymorphic VT became noninducible and only an isolated VPC was inducible. The morphology of this VPC differed from the previous triggering VPC and intra-Purkinje block was also observed before this VPC (arrowhead). HBE = His-bundle electrogram; HRA = high right atrium; LAO = left anterior oblique view; LV = left ventricle; P = Purkinje potential; RAO = right anterior oblique view; SA = atrial pacing stimulus. (From Nogami A, Sugiyasu A, Kubota S, Kato K: Mapping and ablation of idiopathic ventricular fibrillation from Purkinje system. Heart Rhythm 2005;2:646–649. With permission from Elsevier.)
In the report by Haïssaguerre et al., electrocardiograms recorded after ablation showed the abolition of the local Purkinje potentials and a slight delay in the occurrence of the local ventricular electrogram. However, they did not determine how much of the complex Purkinje network was involved in each patient and the issue of multiple foci versus differing activation routes from limited foci remains unsolved. In our case, catheter mapping revealed that the constantly changing polymorphic QRS morphology resulted from the changing propagation in the Purkinje arborization and the polymorphic VT became noninducible after the catheter ablation of the Purkinje network. We did not ablate the earliest site of the Purkinje activation, and the isolated VPC with diastolic Purkinje activation was still inducible after the catheter ablation.
Of course, the earliest activation site of the Purkinje activation during the triggering VPC should be searched and ablated; however, a modification of the Purkinje network might be applied when the earliest site cannot be determined or is located close to the His-bundle. In my experience, the right-sided triggers usually arise from the distal right bundle branch and the most proximal site of the origins on the left side was the bifurcation of the left anterior and posterior fascicles. If the earliest site is located proximal to the bifurcation, ablation of just the distal site is recommended for the initial application. It is possible to create substrate modification and eliminate the origin nearby because the Purkinje network can be easily ablated.
Because the Purkinje network in humans is mostly localized to the subendocardium, a transmural lesion creation is not needed. Further, the ventricular myocardium of the culprit Purkinje network in idiopathic VF is usually healthy. This differs from ischemic VF, in which the ventricular myocardium at the culprit Purkinje network usually has a low voltage and is located near a scar border. During the Purkinje network modification, the creation of bundle-branch block or hemi-block is not required. While some change in the frontal axis has been observed in some patients after the ablation during a left septal Purkinje ablation, the QRS width remains almost the same. Catheter manipulation sometimes produces transient bundle-branch block. As a result, peripheral Purkinje potentials no longer precede the local ventricular activation in sinus rhythm, and it makes mapping of the Purkinje network difficult. For this reason the creation of bundle branch block should be avoided.
Source...