The Fourth Dimension
2010; Lippincott Williams & Wilkins; Volume: 3; Issue: 4 Linguagem: Inglês
10.1161/circep.110.958280
ISSN1941-3149
AutoresMalini Madhavan, Samuel J. Asirvatham,
Tópico(s)Cardiac electrophysiology and arrhythmias
ResumoHomeCirculation: Arrhythmia and ElectrophysiologyVol. 3, No. 4The Fourth Dimension Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBThe Fourth DimensionEndocavitary Ventricular Tachycardia Malini Madhavan, MBBS and Samuel J. Asirvatham, MD Malini MadhavanMalini Madhavan From the Department of Internal Medicine (M.M.), Division of Cardiovascular Diseases (S.J.A.) and Department of Pediatrics and Adolescent Medicine (S.J.A.), Mayo Clinic, Rochester, Minn. and Samuel J. AsirvathamSamuel J. Asirvatham From the Department of Internal Medicine (M.M.), Division of Cardiovascular Diseases (S.J.A.) and Department of Pediatrics and Adolescent Medicine (S.J.A.), Mayo Clinic, Rochester, Minn. Originally published1 Aug 2010https://doi.org/10.1161/CIRCEP.110.958280Circulation: Arrhythmia and Electrophysiology. 2010;3:302–304Radiofrequency ablation is now a cornerstone in the management of ventricular tachycardia (VT). VT ablation plays a palliative role in decreasing shocks and improving the quality of life in patients with structural heart disease and is often curative in treating VT in patients with normal hearts.1,2 When compared with other types of ablation, however, VT procedures have lower success rates, have a propensity for complications, and are technically challenging. A recognized cause for difficulty is the need to address the 3-dimensional pathological substrate (endocardial, midmyocardial, epicardial). At present, combined endocardial and epicardial approaches3 have largely addressed this problem and, along with a larger electrode and irrigation-based ablation, may allow success for the midmyocardial substrate as well.See article p 324Recently, a novel syndrome of VT arising from the papillary muscles (PMs) has been described.4–6 This arrhythmia, along with VT arising from other endocavitary structures (moderator band, false tendon),7 has brought to light a fourth dimension that the interventional electrophysiologist has to appreciate and navigate during ablation.In this issue of Circulation: Arrhythmia and Electrophysiology, Yamada et al8 report electrophysiological findings in 19 patients who underwent successful ablation of PM VT. We learn from their study the problems related to pace mapping the potential for multiple morphologies arising from a single substrate and the unique mapping and ablation-related difficulty with this entity. When analyzing their findings, we are compelled to address important issues related to the specific mechanism of this novel syndrome, as well as assessing our present general limitations of how we map and ablate VT.Pace MappingThe premise that pacing at the site of a focal arrhythmia origin will reproduce the QRS morphology of the tachycardia is a commonly used strategy with ablation.9,10 Yamada et al8 found that in 17 of 19 patients with PM VT, ablation was unsuccessful at sites with an excellent, carefully executed pace map.What are the potential reasons for this phenomenon? (1) common exit. In other arrhythmias such as fascicular VT, atrial fascicular pathways, supravalvar tachycardia, and pulmonary vein supravalvar and pulmonary vein tachycardias, pace mapping is ineffective. This is because the arrhythmogenic substrate may be far removed from a common exit, and pace mapping simply finds a present exit site while ablation is required farther upstream.11 In the case of PM VT, the origin of the arrhythmia anywhere along the length of the muscle likely exits at its base to the rest of the ventricle. Thus, ablation at these exit sites may not eliminate the arrhythmogenic substrate. (2) capture of adjacent tissue. Because of the geometry of the PM, it can be difficult to place the pacing catheter solely on the PM and completely avoid collateral capture of the adjacent myocardium. Thus, poor pace maps may be obtained, even though catheter contact is at the focus site. (3) In some instances (infra-Hisian conduction system, great arterial sites), different pace maps will be obtained when varying the output for pacing (fascicle only vs fascicle and myocardial capture). Yamada et al8 paced 1 mA above the diastolic threshold. Possibly pacing at high and low output, comparing the results obtained, and correlating this information with activation maps might help distinguish the origin from the exit in PM VT.Multiple MorphologiesIs it essential to identify and target the focus rather than the exit site of VT? If only 1 exit exists for a particular focus, then ablation at the exit should be successful. Yamada et al,8 however, found that in 47% of their patients, multiple QRS morphologies were noted, presumably with similar rates and coupling intervals.8 When multiple exits exist, either the primary substrate should be ablated or the anatomic structure housing the substrate needs to be electrically isolated (pulmonary vein isolation for atrial fibrillation).Prepotentials and the Mechanism of ArrhythmiaThe authors concluded that a focal mechanism for PM VT was likely, given the lack of fractionated potentials, transient entrainment, and because the first beat of tachycardia had a morphology similar to that of subsequent beats. Is PM VT always focal? In their study, Yamada et al8 reported on patients without structural heart disease. Because ischemic heart disease and myocardial infarction may involve the PM,12 scar and slow zones and thus reentry may be housed in a PM as well.7 Sharp near-field prepotentials are reported by Yamada et al8 in 42% of the PM VTs that they studied.8 Prepotentials separated by an isoelectric interval from ventricular activation suggest either a zone of slow conduction between the arrhythmogenic site and the exit or the presence of insulated conduction tissue (fascicle) present at the targeted site, with a subsequent exit to the ventricular myocardium.Novel Disease or Newly Recognized?Recent reports of PM VT suggest that almost 10% of VTs involve endocavitary structures. With several thousand VT ablations having been performed during the last 2 decades, why has endocavitary structure ventricular tachycardia not been previously recognized? It is unlikely that this is a new entity but rather may result from the difficulty of fluoroscopically recognizing PM or moderator band contact. The advent of intracardiac ultrasound and a better appreciation of the anatomy/electrophysiology correlation in recent years have allowed recognition of this entity. Prior successful ablations have been performed on the PM, albeit inadvertently. Whereas this scenario is likely, what were these serendipitously ablated endocavitary structure ventricular tachycardias considered to be? The 12-lead ECG for posterior PM VT is generally similar to what is seen with left posterior fascicular VT,13 and left anterior fascicular VT may be confused with an anterior PM arrhythmia.14,15 In addition, there are striking similarities between fascicular VT and PM VT, including the presence of multiple morphologies/exits, the unreliability of pace mapping, and the finding of sharp prepotentials (Purkinje potentials). It is possible, therefore, that some previously diagnosed fascicular VTs might have, in fact, represented PM VTs.The PMs are myocardial ingrowths into the left ventricular cavity and, like the neighboring tissue, are made up of myocardium and conduction tissue. Could PM VT then be a variant of fascicular VT, with the arrhythmogenic fascicular tissue happening to be located within the endocavitary structure? The branches of the right bundle branch are known to traverse the moderator band, another site of endocavitary structure ventricular tachycardia.Difficulty With Mapping PM VTIn addition to the problems with pace mapping, the study by Yamada et al8 highlights the complex issues related to identifying the PM VT substrate: (1) activation mapping. The authors noted that, in their study, there was no correlation between the pace map score and the earliest local ventricular activation time relative to QRS onset. Possible reasons would include a failure to recognize a "prepotential" and the difficulty with obtaining sufficient catheter stability to obtain multiple activation points along the length of the PM. (2) substrate mapping. In patients with abnormal ventricles, scar and fragmented signal mapping on either the PM or neighboring myocardium can be difficult, as the mapping catheter may be wedged between the PM and the ventricle. Similarly, pacing at a site of actual scar on the PM may result in capture of the adjacent myocardium, which, along with the recorded electrogram, may lead the operator to miss the presence of this potential substrate. (3) electroanatomic mapping. Isochronal or 3-dimensional activation maps may be misleading, with multiple, early sites of simultaneous activation along the base of the PM being observed when specific mapping of the PM itself has not been undertaken. (4) noncontact mapping. Noncontact mapping has been found to be valuable for other common idiopathic VTs.16 This technique, however, uses an inverse solution whereby the geometry of the ventricular walls has been rendered by contact mapping. The muscular ingrowths into the cavity will give rise to signals that cannot be resolved by the system as to which arise from the free wall as opposed to from a structure within the cavity likely contacting the multielectrode array. The aforementioned complexities highlight the need for real-time visualization of endocavitary structures and catheter contact.17Difficulty With AblationIn 1 instance, the authors excluded an epicardial substrate and surmised that the reason for the need for large lesions was substrate deep within the thick PM. Another possibility is that the true focus was along the length of the PM, possibly near the tip, and that extensive lesions were required to ablate all potential exits. Electric isolation of the PM may occur with sufficient ablation at the base.6 With complete isolation, loss of electrograms along the PM would be expected; however, exit block may occur without a corresponding entrance block.Mitral Valve and PM VTA concern with extensive ablation is potential infarction of the PM and the resulting mitral valve dysfunction. Even without obvious mechanical damage, ablation-induced dyssynchrony could affect mitral valve function. If the focus is near the tip of the PM, ablation is probably safer close to the base, modifying the exit.Mitral valve prolapse has been associated with premature ventricular contractions and ventricular arrhythmias.18 In the present reported series, although structural heart disease was excluded, could ventricular arrhythmias known to occur with mitral valve disease be PM related, possibly from mechanical effects? Further characterization of the rare but reported ventricular arrhythmias seen with mitral valve prolapse to assess whether specific features of a potential PM VT can be recognized would help clarify this. Finally, the PM usually connects anatomically only to the rest of the ventricular myocardium at its base. However, in some hearts, false tendons or fascicular structures may traverse the ventricular cavity between the septum and free wall and include the intervening PM (the Figure).19,20Download figureDownload PowerPointFigure. Autopsied heart dissection opening into the left ventricle (LV). Asterisk points to the PM. Note the anatomic basis for the multiple exits that may be present for a focus within the PM. In addition to the base anchored into the ventricular myocardium, other endocavitary structures (arrow points to a bifurcated false tendon) and trabeculae connect to the PM that may result in near-simultaneous activation at various sites in the left ventricle and may be responsible for subtle changes in QRS morphology, depending on which exit is used.Although the subject of the article by Yamada et al8 was monomorphic ventricular arrhythmia, the PM has been implicated as a possibly related substrate for ventricular fibrillation.21 Just as the fascicles may represent the trigger sites for ventricular fibrillation, could the PM house such triggers as well22,23?SummaryYamada et al8 present some important insights into the nature, recognition, and causes of difficulty with mapping and ablation of PM VT.8 Further study is needed to understand the role of the endocavitary structures for VT in patients with structural heart disease, mitral valve disease, and idiopathic ventricular fibrillation.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Correspondence to Samuel J. 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Del Carpio Munoz F, Buescher T and Asirvatham S (2011) Teaching Points With 3-Dimensional Mapping of Cardiac Arrhythmia, Circulation: Arrhythmia and Electrophysiology, 4:6, (e72-e75), Online publication date: 1-Dec-2011.Del Carpio Munoz F, Buescher T and Asirvatham S (2011) Teaching Points With 3-Dimensional Mapping of Cardiac Arrhythmias, Circulation: Arrhythmia and Electrophysiology, 4:2, (e11-e14), Online publication date: 1-Apr-2011. August 2010Vol 3, Issue 4 Advertisement Article InformationMetrics © 2010 American Heart Association, Inc.https://doi.org/10.1161/CIRCEP.110.958280PMID: 20716720 Originally publishedAugust 1, 2010 Keywordsmitral valveEditorialspapillary muscleablationventricular tachycardiaPDF download Advertisement SubjectsArrhythmiasCatheter Ablation and Implantable Cardioverter-Defibrillator
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