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How to map and ablate papillary muscle ventricular arrhythmias
Accepted Manuscript How to Map and Ablate Papillary Muscle Ventricular Arrhythmias Andres Enriquez, MD, Gregory Supple, MD, Francis Marchlinski, MD, Fermin Garcia, MD PII:
S1547-5271(17)30838-X
DOI:
10.1016/j.hrthm.2017.06.036
Reference:
HRTHM 7223
To appear in:
Heart Rhythm
Received Date: 17 April 2017
Please cite this article as: Enriquez A, Supple G, Marchlinski F, Garcia F, How to Map and Ablate Papillary Muscle Ventricular Arrhythmias, Heart Rhythm (2017), doi: 10.1016/j.hrthm.2017.06.036. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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How to Map and Ablate Papillary Muscle Ventricular Arrhythmias
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Andres Enriquez MD, 1Gregory Supple MD, 1Francis Marchlinski MD, 1Fermin Garcia MD
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Short title: How to map and ablate papillary muscle arrhythmias
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Word count: 2914 words.
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1. Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
Funded in part by The F. Harlan Batrus Electrophysiology Research Fund
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Disclosures: None
Corresponding Author: Dr. Fermin Garcia, MD Section of Cardiac Electrophysiology Hospital of the University of Pennsylvania 9 Founders Pavilion, 3400 Spruce Street, Philadelphia, Pennsylvania Email: [email protected]. Fax: + 1-215-6626006 Tel: + 1-215-6155441 1
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Introduction The papillary muscles (PMs) are a source of ventricular arrhythmias (VAs) both in structurally normal and abnormal hearts. Presentation includes isolated premature
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ventricular contractions (PVCs), non-sustained ventricular tachycardia (VT) and sustained recurrent VT. In addition, PVCs arising from the PMs may play a role as triggers of ventricular fibrillation (VF)1,2. Due to their highly variable and complex anatomy and
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independent motion during the cardiac cycle, catheter ablation is challenging, with lower procedural success and higher recurrence rates compared with other locations3. In this
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review, we present our practical approach to mapping and ablation of PM VAs.
Anatomy
The PMs are an integral part of the mitral valve (MV) and tricuspid valve (TV)
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apparatus (Figure 1). In the left ventricle (LV) they originate from the mid or apical 1/3 of the LV and protrude like fingers into the LV cavity4. The anterolateral PM (APM) originates from the anterolateral LV wall and provides chordae to the anterolateral half of
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the anterior and posterior mitral leaflets. In the majority of cases it has a single head and dual blood supply from the left anterior descending and circumflex coronary arteries. The
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posteromedial PM (PPM) originates from the infero-septal LV wall and provides chordae to the posteromedial half of both leaflets. It typically has 2 heads and is either supplied by the right or circumflex coronary artery based on dominance. In the right ventricle (RV), the moderator band (MB) is a prominent muscular
trabeculation that crosses from the septum to the free wall of the RV and provides support to the anterior PM of the TV5. The right bundle branch of the conducting system enters the 2
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MB at the interventricular septum and continues by way of the MB to the base of the anterior PM, where it branches into the subendocardial plexus of the Purkinje system8. There are usually 2 RV PMs: the anterior PM provides chordae to the anterior and posterior
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TV leaflets, while the posterior PM provides chordae to the posterior and septal leaflets.
Histologically, the PMs are composed of ventricular myocytes and a rich subendocardial network of Purkinje fibers covered by a layer of endothelium. Connection
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between the ventricular muscle and the Purkinje network only occurs only at discrete, localized regions near the PM base6. This explains that in areas without direct Purkinje-
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muscular connection, separate Purkinje and muscle potentials can be recorded.
Mechanism
Idiopathic VAs from the PMs are frequently sensitive to catecholamines,
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noninducible by programmed stimulation and non entrainable, which suggests triggered activity or abnormal automaticity as the electrophysiological mechanism7,8. It is postulated that decreased Purkinje-ventricular coupling at the PM affects the
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electrical loading of the Purkinje cells by the neighboring myocardium, and might facilitate automaticity or triggered activity9. In addition, abrupt changes in the fiber orientation or the
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complexities observed at the Purkinje-muscle junction at the PM base may be associated with conduction delays and microreentry10. Animal studies show that the PMs may serve as anchoring sites for reentrant wavefronts, contributing to the maintenance of VT/VF. In canine models of VF, Pak et al. showed that the highest dominant frequency and majority of reentrant wavefronts during VF were located at the PM. RF ablation targeted at the PPM reduced the VF inducibility from 100% at baseline to 22% after ablation10. 3
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The PMs may also be involved in post-infarction VAs and the mechanism in these cases is likely to be reentrant as in other scar-related arrhythmias. In these patients, VTs are typically inducible by programmed stimulation and can be terminated by overdrive pacing.
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In addition, the PMs often exhibit evidence of scar on DE (delayed enhancement)-MRI11.
Electrocardiographic recognition
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The PM VAs have distinct electrocardiographic characteristics2,8,12,13 and their recognition is important for pre-procedural planning (Figure 2).
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VT/PVCs arising from the APM typically demonstrate a right bundle branch block (RBBB) morphology, right axis (negative in I and aVL, positive in aVR), transition at V3V5 and frequently inferior lead discordance (negative II, positive III). VT/PVCs from the PPM show a RBBB morphology, left superior axis (positive in I and aVL, negative in aVR,
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negative in II and III) and transition at V3-V5.
VAs originated from the PMs should be distinguished from other idiopathic LV arrhythmias such as fascicular or mitral annular VAs, which also exhibit a RBBB pattern.
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Compared with fascicular arrhythmias, the QRS is wider in PM VAs (150±15 vs. 127±11 ms;p=0.001)14. An rsR’ pattern in lead V1 is characteristic of fascicular arrhythmias,
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whereas this pattern is not present in PM VAs. In addition, fascicular arrhythmias typically have a small q wave in either lead I or aVL (qR or qRs), whereas PM VAs have a monophasic R wave or Rs pattern15. We postulate that this indicates early left-to-right septal depolarization during fascicular VAs. The PPM is a slightly more lateral structure and septal depolarization occurs later in the QRS, hence the absence of q waves in the lateral leads. Mitral annular VAs, due to their basal location, often display positive 4
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concordance, a pattern that is not seen in PM or fascicular VAs, in which the exit lies in the midsegment of the LV16. Some patients with PM VAs may exhibit slight beat-to-beat
into the LV.
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variability in the ECG morphology, which may represent a change in the exit from the PM
Finally, VT/PVCs from the MB and RV intracavitary structures demonstrate a
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LBBB morphology, left superior axis and late transition (≥V4)13.
Pre-procedural planning
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Analysis of the available 12-lead ECGs is the basis to suspect a PM origin, while Holter study allows to assess the PVC burden and confirm a unifocal origin or variable morphologies. Pre-procedural echocardiography and cardiac MRI are useful for anatomic characterization and may show the presence of myocardial scar in patients with underlying
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cardiomyopathy. Increased echogenicity on echocardiography or DE on MRI can sometimes be seen in the tip or base of the PM, suggesting a potential arrhythmogenic
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focus.
Procedure setup
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The electrophysiology study is conducted under minimal sedation. Agents with
inherent arrhythmia suppression, like propofol, should be avoided as some PM VAs are very catecholamine-sensitive. We use remifentanil, as it has rapid onset and offset. When possible, antiarrhythmic medications should be discontinued for at least 5 half-lives and intravenous antiarrhythmic medications should be stopped at least 12 hours before the procedure. 5
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For LV PM arrhythmias, both a retro-aortic or trans-septal access to the LV may be used. In our experience, the PPM and the medial aspect of the APM are best approached with a retro-aortic access, while the lateral aspect of the APM is best approached in a trans-
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septal fashion. A trans-septal approach is also preferred in patients with aortic valve prosthesis and those with severe atheromatous peripheral or aortic disease. For retro-aortic access, it is very helpful to use a long SL0 or SL1 sheath (St. Jude Medical, St. Paul, MN)
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with the tip of the sheath placed through the aortic valve into the LV. This facilitates catheter manipulation and stability. If a trans-septal approach is used, an Agilis steerable
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sheath with a large curve (St. Jude Medical, St. Paul, MN) is advanced into the left atrium and placed with the tip near the MV annulus. We use the same sheath for mapping of PM and MB VAs in the RV.
A quadripolar catheter is positioned into the RV apex and a phased-array intra-
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cardiac echocardiography (ICE) catheter (Siemens, Montain View, CA) is advanced into the right atrium (RA). We use a Carto mapping system (Biosense Webster, Diamond Bar, CA) and the CartoSound module allows integration of the anatomic shell based on the
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echo images with the electroanatomic map. Thus, prior to mapping we create a detailed ICE-based anatomic reconstruction of both ventricles with CartoSound. The contours of
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the PMs and MB are carefully delineated and these structures are separately incorporated into the overall LV or RV anatomic map.
Mapping Localization of PM VAs relies mainly on activation mapping of the clinical VT/PVCs, usually complemented with pacemapping. The 2 main requisites for mapping 6
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are the presence of spontaneous or inducible VT/PVCs and the ability to image the PMs in real-time with ICE (Supplementary Figure S1). If no spontaneous ectopy is present, induction is attempted with burst pacing from
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the RV apex or high RA. Drive trains of variable cycle length and variable numbers of paced beats are used to stimulate ventricular ectopy. Sedation is frequently turned off, and isoproterenol (2-20 µg/min) may be infused during burst pacing.
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ICE is essential to ensure adequate catheter-tissue contact and correct orientation of the catheter tip during mapping and ablation. In addition, ICE imaging may identify
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increased echogenicity in the PMs, suggesting a focal area of scar that may correspond to the site of arrhythmia origin. These echogenic areas may correspond to areas of low voltage and late potentials in sinus rhythm. As shown in Figure 3, the PMs are nicely imaged with ICE from the RV. From the homeview, the ICE catheter is deflected anteriorly and
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advanced across the TV, followed by deflection release. Upon entering the RV, the inferior RV free wall comes into view. Clockwise rotation of the catheter generates a long axis view of the LV with the PPM and the MV. Further clockwise rotation brings into view the APM.
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As mentioned, the use of CartoSound allows real-time integration of the ICE views into the mapping system anatomic display
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A detailed activation mapping is performed using the ablation catheter or a
multielectrode mapping catheter (Pentaray, Biosense Webster, Diamond Bar, CA) and attention is directed to the sites of earliest pre-potential bipolar activity. Sites with activation -30 ms pre-QRS suggest close proximity to the arrhythmia focus and ablation here is very likely to result in arrhythmia elimination. In addition, the characteristics of the signal on the ablation catheter have significance, with sharp early signals indicating a more 7
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superficial location and far-field signals suggesting a deeper location within the PM core. In approximately 40% of cases, a sharp Purkinje potential can be recorded at the successful ablation site, which suggests involvement of the Purkinje system in the arrhythmogenic
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mechanism12,17. Also, in our experience, the site of successful ablation sometimes exhibits a late potential in sinus rhythm that becomes pre-systolic during PVC/VT (Figures 4 and 5). This finding often coexists with evidence of PM scar (low voltage and late potentials in
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sinus rhythm), either DE on cardiac MRI or hyperechogenicity on ICE.
Pacemapping is useful, but not sufficient by itself. Sites of successful ablation
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usually exhibit an excellent pacemap (≥11/12), but conversely, ablation at sites with perfect pacemaps may fail to terminate the arrhythmia. This is likely because the exit site at the base of the PM may be located far from the site of origin, which may be higher in the body
Ablation
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of the PM.
Ablation is often challenging due to the anatomical variability of PM anatomy,
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potentially deep intramural site of arrhythmia origin and the stability issues related to the ablation of a mobile target.
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The two main energy modalities for ablating PM VAs are radiofrequency (RF) and
cryoablation. Our strategy in the majority of cases is to start with RF as initial approach using an ablation catheter with contact force (CF) capabilities, which provides not only contact force information, but also shows vector orientation of the catheter tip. RF ablation catheters are more steerable, allow deeper lesions and are necessary for creating an electroanatomic activation map. One of the main drawbacks of RF is the induction of 8
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mechanical and thermally provoked ectopy that further complicates catheter stability and interpretation of the activation map. Targets for ablation include sites with ventricular activation earlier than -30 ms pre-
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QRS and a QS pattern in the local unipolar recording. These sites usually exhibit an excellent pacemap. The presence of a Purkinje potential in the ablation site has also been associated with successful arrhythmia suppression17. RF application is delivered at 30-50
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Watts of power with temperature limited to 42°C, targeting an impedance drop of 10-15 Ω or 10% of the starting impedance value. High power is usefull as it may overcome the
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challenges imposed by poor stability. The only area where careful attention should be exercised is the base of the PM at its intersection with the LV free wall. If the catheter is “wedged” in this position there is a risk of steam pops and LV perforation given a higher impedance and less ability to cool. As such, we recommend to start with lower power (20
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Watts) in this area. Stability can be improved by pacing faster and providing a more stable cycle to cycle variation, specially if the patient is bradycardic (bigeminy), and we particularly try to avoid deep inspirations.
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We typically apply RF for 60-90 seconds, however for sites that are suspected to be deeper in the myocardium, longer lesions (4-5 minutes) may need be delivered. A deep
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intramyocardial origin is suspected when the best site of activation is ≤ 20 ms pre-QRS, the signal appears far-field looking and the QRS morphology changes with initial RF application. Another alternative for deep intramural arrhythmia sources is to surround the base of the PM with lesions aiming for exit block18. CF technology is of great value when ablating the PMs and currently 2 types of catheter with CF capabilities are available: TactiCath (St. Jude Medical, St. Paul, MN) and 9
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Thermocool SmartTouch (Biosense Webster, Diamond Bar, CA), which are integrated into the NavX and Carto mapping systems, respectively. TactiCath uses a fiberoptic sensor mounted in the catheter tip which detects changes in contact force. Measurement of the area
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under the force-time curve gives a novel parameter to guide ablation, the force-time integral, which is measured in grams per second. In SmartTouch the contact force is measured via recordings of microdeformation of a precision spring connecting the tip and
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the shaft of the catheter. The CF information is displayed numerically in grams and also as a graphical representation where the vector force is visualized as an arrow head
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(Supplementary Figure S2). We aim for a force of at least 10 g, although we realize it is often difficult to reach a significant force without sliding, especially at the PM tip. Often, several RF lesions on different parts of the PM are required to completely eliminate the VT/PVC. This is likely because a single arrhythmogenic focus may exhibit
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preferential conduction to multiple exit sites at the base of the PM or connect via false tendons15. Because of this phenomenon, the 12-lead ECG should be monitored at all times and particular attention should be paid to slight changes in the QRS morphology after the
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initial RF applications, which suggests a shift in the exit site and makes necessary to reposition the ablation catheter and map for a different site (Supplementary Figure S3). In
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MB VAs the most common site of successful ablation is the free-wall insertion of this structure, followed by the septal insertion or the body13 (Figure 6). The endpoint of ablation is VT/PVC suppression and non-inducibility with isoproterenol and/or burst ventricular pacing. We recommend a minimum 30-minute waiting period after the successful RF lesion.
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The role of cryoablation When catheter stability is an issue, cryoablation is an alternative, as the cryocatheter adherence to the tissue limits mobility and improves contact (Supplementary Video 1). The
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disadvantages of cryoablation are a comparative less maneuverability, reduced lesion depth and the inability to accurately project the catheter tip onto the electroanatomic map. We use a 6-mm Freezor Xtra catheter (Medtronic, Minneapolis, MN), which is able to fit through
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an Agilis or SL0 sheath. We typically use a freeze-thaw-freeze cycle (3-4 minutes per freeze) to the region of interest, and if there is acute suppression of the arrhythmia, this
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region is targeted with several additional lesions surrounding the area. We do not use an 8mm cryocatheter because: (1) it is more difficult to manipulate; (2) its larger diameter requires switching to a bigger sheath (10 French); (3) its shorter length (90 cm) makes it insufficient to reach some LV structures. In addition, mapping with a larger tip catheter
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may fail to record a near-field pre-potential at the site of interest.
Rivera et al. described a series of 21 patients with PM VAs that were targeted with either cryoablation (n=12) or RF (n=9)19. Acute procedural success was reported in all 12
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patients who underwent cryoablation and in 7/9 patients undergoing RF ablation (100% vs. 78%; P=0.08). In our experience, when RF ablation fails in eliminating PM PVCs/VT,
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switching to cryoablation can achieve successful arrhythmia elimination in >90% of cases20.
Complications
In our experience, procedure-related complications are infrequent. When a retrograde aortic approach is used, damage to the aortic valve is a possibility. This is a 11
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concern especially if cryoablation is used due to the stiffness of the catheter and we recommend to use a long sheath to advance the catheter into the LV. A few case reports have described worsening mitral regurgitation following ablation and mechanisms may
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include PM dysfunction or catheter entrapment in the MV apparatus21,22. VF induction may occur during RF application at the MB or PMs, requiring external defibrillation, and a new
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RBBB may develop post-procedure in 40% of patients with MB VAs.
Summary
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The PMs are a potential source of VAs in patients with and without structural heart disease. The mechanism may be focal or reentrant and they have distinguishing ECG features. Catheter ablation is highly effective, but challenging due to the complexity and variability of PM anatomy and their constant motion during the cardiac cycle. The use of
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ICE is fundamental to allow real-time visualization of these intracavitary structures and ensure proper catheter-tissue contact. Cryoablation is an option to improve catheter stability
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and improve outcomes.
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References 1. Van Herendael H, Zado ES, Haqqani H, et al. Catheter ablation of ventricular fibrillation: importance of left ventricular outflow tract and papillary muscle triggers. Heart
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Rhythm 2014;11:566-73.
2. Santoro F, Di Biase L, Hranitzky P, Sanchez JE, Santangeli P, Perini AP, Burkhardt JD, Natale A. Ventricular fibrillation triggered by PVCs from papillary muscles: clinical
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features and ablation. J Cardiovasc Electrophysiol 2014;25:1158-64.
3. Latchamsetty RY, Yokokawa M, Morady F, et al. Multicenter outcomes for catheter
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ablation of idiopathic premature ventricular complexes. JACCCEP 2015;1:116-123. 4. Dal-Bianco JP, Levine RA. Anatomy of the mitral valve apparatus: role of 2D and 3D echocardiography. Cardiol Clin 2013;31:151-64.
5. Loukas M, Klaassen Z, Tubbs RS, Derderian T, Paling D, Chow D, Patel S, Anderson
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RH. Anatomical observations of the moderator band. Clin Anat 2010;23:443-50. 6. Rawling DA, Joyner RW, Overholt ED. Variations in the functional electrical coupling between the subendocardial Purkinje and ventricular layers of the canine left ventricle. Circ
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7. Abouezzeddine O, Suleiman M, Buescher T, Kapa S, Friedman PA, Jahangir A, Mears
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JA, Ladewig DJ, Munger TM, Hammill SC, Packer DL, Asirvatham SJ. Relevance of endocavitary structures in ablation procedures for ventricular tachycardia. J Cardiovasc Electrophysiol 2010;21:245-54. 8. Doppalapudi H, Yamada T, McElderry HT, Plumb VJ, Epstein AE, Kay GN. Ventricular tachycardia originating from the posterior papillary muscle in the left ventricle: a distinct clinical syndrome. Circ Arrhythm Electrophysiol 2008;1:23-9. 13
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9. Li ZY, Wang YH, Maldonado C, Kupersmith J. Role of junctional zone cells between Purkinje fibres and ventricular muscle in arrhythmogenesis. Cardiovasc Res 1994;28:127784.
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10. Y. Pak HN, Kim YH, Lim HE, Chou CC, Miyauchi Y, Fang YH, Sun K, Hwang C, Chen PS. Role of the posterior papillary muscle and purkinje potentials in the mechanism of ventricular fibrillation in open chest dogs and Swine: effects of catheter ablation. J
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Cardiovasc Electrophysiol 2006;17:777-83.
11. Bogun F, Desjardins B, Crawford T, Good E, Jongnarangsin K, Oral H, Chugh A,
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Pelosi F, Morady F. Post-infarction ventricular arrhythmias originating in papillary muscles. J Am Coll Cardiol 2008;51:1794-802.
12. Yamada T, Doppalapudi H, McElderry HT, et al. Electrocardiographic and electrophysiological characteristics in idiopathic ventricular arrhythmias originating from
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the papillary muscles in the left ventricle: relevance for catheter ablation. Circ Arrhythm Electrophysiol 2010;3:324-31.
13. Sadek MM, Benhayon D, Sureddi R, et al. Idiopathic ventricular arrhythmias
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originating from the moderator band: Electrocardiographic characteristics and treatment by catheter ablation. Heart Rhythm 2015;12:67-75.
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14. Good E, Desjardins B, Jongnarangsin K, Oral H, Chugh A, Ebinger M, Pelosi F, Morady F, Bogun F. Ventricular arrhythmias originating from a papillary muscle in patients without prior infarction: a comparison with fascicular arrhythmias. Heart Rhythm 2008;5:1530-7.
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15. Deyell MW, Man JP, Supple GE, Hutchinson MD, Frankel DS, Marchlinski FE. ECG Differentiation Of Ventricular Arrhythmias Arising From The Left Posterior Fascicle And Postero-medial Papillary Muscle. Heart Rhythm 2012;9(5S):S474.
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16. Al'Aref SJ, Ip JE, Markowitz SM, Liu CF, Thomas G, Frenkel D, Panda NC, Weinsaft JW, Lerman BB, Cheung JW. Differentiation of papillary muscle from fascicular and mitral annular ventricular arrhythmias in patients with and without structural heart disease. Circ
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Arrhythm Electrophysiol 2015;8:616-24.
17. Yokokawa M, Good E, Desjardins B, Crawford T, Jongnarangsin K, Chugh A, Pelosi F
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Jr, Oral H, Morady F, Bogun F. Predictors of successful catheter ablation of ventricular arrhythmias arising from the papillary muscles. Heart Rhythm 2010;7:1654-9. 18. Wo HT, Liao FC, Chang PC, Chou CC, Wen MS, Wang CC, Yeh SJ. Circumferential ablation at the base of the left ventricular papillary muscles: A highly effective approach for
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ventricular arrhythmias originating from the papillary muscles. Int J Cardiol 2016;220:876-
19. Rivera S, Ricapito Mde L, Tomas L, et al. Results of Cryoenergy and Radiofrequency-
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Based Catheter Ablation for Treating Ventricular Arrhythmias Arising From the Papillary Muscles of the Left Ventricle, Guided by Intracardiac Echocardiography and Image
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Integration. Circ Arrhythm Electrophysiol 2016;9:e003874. 20. Gordon J, Zado E, Hutchinson M, Garcia F, Santangeli P, Betensky B, Fahed J, Mendelson T, Shaw G, Supple G. Effectiveness of cryoablation on papillary muscle PVCs and VT after radiofrequency has failed. Heart Rhythm 2016;13:PO06-150.
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21. Mochizuki A, Nagahara D, Takahashi H, Saito R, Fujito T, Miura T. Worsening of mitral valve regurgitation after radiofrequency catheter ablation of ventricular arrhythmia originating from a left ventricular papillary muscle. Heart Rhythm Case Rep 2017;3:215-8.
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22. Desimone CV, Hu T, Ebrille E, Syed FF, Vaidya VR, Cha YM, Valverde AM, Friedman PA, Suri RM, Asirvatham SJ. Catheter ablation related mitral valve injury: the importance of early recognition and rescue mitral valve repair. J Cardiovasc Electrophysiol
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2014;25:971-5.
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Figures Figure 1. Anatomy of the PMs and MB. APM = anterolateral papillary muscle; LV = left ventricle; MB = moderator band; PM = papillary muscle; PPM = posteromedial papillary
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muscle; RV = right ventricle. Reproduced from Dr K. Shivkumar with permission. Copyright UCLA Cardiac Arrhythmia Center, Wallace A. McAlpine Collection.
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Figure 2. Examples of patients with PVCs arising from the APM, PPM and MB showing the typical electrocardiographic characteristics. APM and PPM PVCs have a RBBB pattern
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with transition at V3-V5 and rS pattern in V6. The PPM is distinguished from the APM by a superior axis. APM PVCs are often characterized by a rightward axis with some negativity in lead II, but mainly positivity in lead III. MB PVCs are characterized by a LBBB pattern with transition at V4-V6, positive QRS in lead I, usually somewhat positive
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in lead II and negative in lead III.
Figure 3. Standard ICE image obtained from the RV inflow and CartoSound
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reconstruction of the LV cavity and the PMs. Notice the ICE catheter in the RV (red arrowhead) and the fan emitted from the tip of the ICE catheter that corresponds to the
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respective echocardiographic slice. A. Once in the RV, with gentle clockwise motion the first PM in view is the PMPM. Notice the ablation catheter in the posterior aspect of the PM. The circle in green is the catheter tip when cut by the ICE fan, helping in visualizing the location of the tip in real time. B. Further clockwise motion from the PMPM exposes the ALPM, in this case with 2 heads. PMPM: posterior medial papillary muscle. ALPM: anterolateral papillary muscle. LV: left ventricle. 17
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Figure 4. Mapping guided by ICE of an APM PVC. A. Initial ICE evaluation of the APM shows 2 heads with an echogenic appearance in one of the heads. B. CartoSound reconstruction of the anatomical structures and 2 separate structures created for the base of
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the PM and the echogenic area. This will aid when performing the electroanatomic mapping. C. Catheter guided with ICE via a transeptal approach to the suspected abnormal area, with careful monitoring of contact force and vector orientation at the tip of the PM. D.
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Continuous recordings of a sinus rhythm beat showing the presence of a late potential, followed by one pacemap beat with 12/12 match and a third complex demonstrating the late
at the site of successful ablation.
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potential becoming early during the PVC, with and exact timing to the spike to QRS signal
Figure 5. Ablation of monomorphic VT arising from the PPM. Increased echogenicity in
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one of the heads of the PM is noted on ICE, suggestive of a focal area of scar (blue arrow). Note the late potential observed in sinus rhythm that becomes presystolic during PVC (red
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arrow).
Figure 6. Ablation of PVC-triggered VF in a 28-year-old patient with structurally normal
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heart and resuscitated sudden cardiac death. Earliest ventricular activation during clinical PVCs was mapped to the free wall insertion of the MB (16 ms pre-QRS), with close, but not perfect pacemap. Radiofrequency application resulted in durable PVC suppression. A RBBB was induced and persistent until the end of the case.
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S1547-5271(17)30838-X
DOI:
10.1016/j.hrthm.2017.06.036
Reference:
HRTHM 7223
To appear in:
Heart Rhythm
Received Date: 17 April 2017
Please cite this article as: Enriquez A, Supple G, Marchlinski F, Garcia F, How to Map and Ablate Papillary Muscle Ventricular Arrhythmias, Heart Rhythm (2017), doi: 10.1016/j.hrthm.2017.06.036. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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How to Map and Ablate Papillary Muscle Ventricular Arrhythmias
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Andres Enriquez MD, 1Gregory Supple MD, 1Francis Marchlinski MD, 1Fermin Garcia MD
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Short title: How to map and ablate papillary muscle arrhythmias
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Word count: 2914 words.
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1. Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
Funded in part by The F. Harlan Batrus Electrophysiology Research Fund
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Disclosures: None
Corresponding Author: Dr. Fermin Garcia, MD Section of Cardiac Electrophysiology Hospital of the University of Pennsylvania 9 Founders Pavilion, 3400 Spruce Street, Philadelphia, Pennsylvania Email: [email protected]. Fax: + 1-215-6626006 Tel: + 1-215-6155441 1
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Introduction The papillary muscles (PMs) are a source of ventricular arrhythmias (VAs) both in structurally normal and abnormal hearts. Presentation includes isolated premature
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ventricular contractions (PVCs), non-sustained ventricular tachycardia (VT) and sustained recurrent VT. In addition, PVCs arising from the PMs may play a role as triggers of ventricular fibrillation (VF)1,2. Due to their highly variable and complex anatomy and
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independent motion during the cardiac cycle, catheter ablation is challenging, with lower procedural success and higher recurrence rates compared with other locations3. In this
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review, we present our practical approach to mapping and ablation of PM VAs.
Anatomy
The PMs are an integral part of the mitral valve (MV) and tricuspid valve (TV)
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apparatus (Figure 1). In the left ventricle (LV) they originate from the mid or apical 1/3 of the LV and protrude like fingers into the LV cavity4. The anterolateral PM (APM) originates from the anterolateral LV wall and provides chordae to the anterolateral half of
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the anterior and posterior mitral leaflets. In the majority of cases it has a single head and dual blood supply from the left anterior descending and circumflex coronary arteries. The
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posteromedial PM (PPM) originates from the infero-septal LV wall and provides chordae to the posteromedial half of both leaflets. It typically has 2 heads and is either supplied by the right or circumflex coronary artery based on dominance. In the right ventricle (RV), the moderator band (MB) is a prominent muscular
trabeculation that crosses from the septum to the free wall of the RV and provides support to the anterior PM of the TV5. The right bundle branch of the conducting system enters the 2
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MB at the interventricular septum and continues by way of the MB to the base of the anterior PM, where it branches into the subendocardial plexus of the Purkinje system8. There are usually 2 RV PMs: the anterior PM provides chordae to the anterior and posterior
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TV leaflets, while the posterior PM provides chordae to the posterior and septal leaflets.
Histologically, the PMs are composed of ventricular myocytes and a rich subendocardial network of Purkinje fibers covered by a layer of endothelium. Connection
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between the ventricular muscle and the Purkinje network only occurs only at discrete, localized regions near the PM base6. This explains that in areas without direct Purkinje-
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muscular connection, separate Purkinje and muscle potentials can be recorded.
Mechanism
Idiopathic VAs from the PMs are frequently sensitive to catecholamines,
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noninducible by programmed stimulation and non entrainable, which suggests triggered activity or abnormal automaticity as the electrophysiological mechanism7,8. It is postulated that decreased Purkinje-ventricular coupling at the PM affects the
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electrical loading of the Purkinje cells by the neighboring myocardium, and might facilitate automaticity or triggered activity9. In addition, abrupt changes in the fiber orientation or the
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complexities observed at the Purkinje-muscle junction at the PM base may be associated with conduction delays and microreentry10. Animal studies show that the PMs may serve as anchoring sites for reentrant wavefronts, contributing to the maintenance of VT/VF. In canine models of VF, Pak et al. showed that the highest dominant frequency and majority of reentrant wavefronts during VF were located at the PM. RF ablation targeted at the PPM reduced the VF inducibility from 100% at baseline to 22% after ablation10. 3
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The PMs may also be involved in post-infarction VAs and the mechanism in these cases is likely to be reentrant as in other scar-related arrhythmias. In these patients, VTs are typically inducible by programmed stimulation and can be terminated by overdrive pacing.
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In addition, the PMs often exhibit evidence of scar on DE (delayed enhancement)-MRI11.
Electrocardiographic recognition
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The PM VAs have distinct electrocardiographic characteristics2,8,12,13 and their recognition is important for pre-procedural planning (Figure 2).
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VT/PVCs arising from the APM typically demonstrate a right bundle branch block (RBBB) morphology, right axis (negative in I and aVL, positive in aVR), transition at V3V5 and frequently inferior lead discordance (negative II, positive III). VT/PVCs from the PPM show a RBBB morphology, left superior axis (positive in I and aVL, negative in aVR,
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negative in II and III) and transition at V3-V5.
VAs originated from the PMs should be distinguished from other idiopathic LV arrhythmias such as fascicular or mitral annular VAs, which also exhibit a RBBB pattern.
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Compared with fascicular arrhythmias, the QRS is wider in PM VAs (150±15 vs. 127±11 ms;p=0.001)14. An rsR’ pattern in lead V1 is characteristic of fascicular arrhythmias,
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whereas this pattern is not present in PM VAs. In addition, fascicular arrhythmias typically have a small q wave in either lead I or aVL (qR or qRs), whereas PM VAs have a monophasic R wave or Rs pattern15. We postulate that this indicates early left-to-right septal depolarization during fascicular VAs. The PPM is a slightly more lateral structure and septal depolarization occurs later in the QRS, hence the absence of q waves in the lateral leads. Mitral annular VAs, due to their basal location, often display positive 4
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concordance, a pattern that is not seen in PM or fascicular VAs, in which the exit lies in the midsegment of the LV16. Some patients with PM VAs may exhibit slight beat-to-beat
into the LV.
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variability in the ECG morphology, which may represent a change in the exit from the PM
Finally, VT/PVCs from the MB and RV intracavitary structures demonstrate a
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LBBB morphology, left superior axis and late transition (≥V4)13.
Pre-procedural planning
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Analysis of the available 12-lead ECGs is the basis to suspect a PM origin, while Holter study allows to assess the PVC burden and confirm a unifocal origin or variable morphologies. Pre-procedural echocardiography and cardiac MRI are useful for anatomic characterization and may show the presence of myocardial scar in patients with underlying
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cardiomyopathy. Increased echogenicity on echocardiography or DE on MRI can sometimes be seen in the tip or base of the PM, suggesting a potential arrhythmogenic
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focus.
Procedure setup
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The electrophysiology study is conducted under minimal sedation. Agents with
inherent arrhythmia suppression, like propofol, should be avoided as some PM VAs are very catecholamine-sensitive. We use remifentanil, as it has rapid onset and offset. When possible, antiarrhythmic medications should be discontinued for at least 5 half-lives and intravenous antiarrhythmic medications should be stopped at least 12 hours before the procedure. 5
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For LV PM arrhythmias, both a retro-aortic or trans-septal access to the LV may be used. In our experience, the PPM and the medial aspect of the APM are best approached with a retro-aortic access, while the lateral aspect of the APM is best approached in a trans-
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septal fashion. A trans-septal approach is also preferred in patients with aortic valve prosthesis and those with severe atheromatous peripheral or aortic disease. For retro-aortic access, it is very helpful to use a long SL0 or SL1 sheath (St. Jude Medical, St. Paul, MN)
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with the tip of the sheath placed through the aortic valve into the LV. This facilitates catheter manipulation and stability. If a trans-septal approach is used, an Agilis steerable
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sheath with a large curve (St. Jude Medical, St. Paul, MN) is advanced into the left atrium and placed with the tip near the MV annulus. We use the same sheath for mapping of PM and MB VAs in the RV.
A quadripolar catheter is positioned into the RV apex and a phased-array intra-
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cardiac echocardiography (ICE) catheter (Siemens, Montain View, CA) is advanced into the right atrium (RA). We use a Carto mapping system (Biosense Webster, Diamond Bar, CA) and the CartoSound module allows integration of the anatomic shell based on the
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echo images with the electroanatomic map. Thus, prior to mapping we create a detailed ICE-based anatomic reconstruction of both ventricles with CartoSound. The contours of
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the PMs and MB are carefully delineated and these structures are separately incorporated into the overall LV or RV anatomic map.
Mapping Localization of PM VAs relies mainly on activation mapping of the clinical VT/PVCs, usually complemented with pacemapping. The 2 main requisites for mapping 6
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are the presence of spontaneous or inducible VT/PVCs and the ability to image the PMs in real-time with ICE (Supplementary Figure S1). If no spontaneous ectopy is present, induction is attempted with burst pacing from
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the RV apex or high RA. Drive trains of variable cycle length and variable numbers of paced beats are used to stimulate ventricular ectopy. Sedation is frequently turned off, and isoproterenol (2-20 µg/min) may be infused during burst pacing.
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ICE is essential to ensure adequate catheter-tissue contact and correct orientation of the catheter tip during mapping and ablation. In addition, ICE imaging may identify
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increased echogenicity in the PMs, suggesting a focal area of scar that may correspond to the site of arrhythmia origin. These echogenic areas may correspond to areas of low voltage and late potentials in sinus rhythm. As shown in Figure 3, the PMs are nicely imaged with ICE from the RV. From the homeview, the ICE catheter is deflected anteriorly and
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advanced across the TV, followed by deflection release. Upon entering the RV, the inferior RV free wall comes into view. Clockwise rotation of the catheter generates a long axis view of the LV with the PPM and the MV. Further clockwise rotation brings into view the APM.
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As mentioned, the use of CartoSound allows real-time integration of the ICE views into the mapping system anatomic display
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A detailed activation mapping is performed using the ablation catheter or a
multielectrode mapping catheter (Pentaray, Biosense Webster, Diamond Bar, CA) and attention is directed to the sites of earliest pre-potential bipolar activity. Sites with activation -30 ms pre-QRS suggest close proximity to the arrhythmia focus and ablation here is very likely to result in arrhythmia elimination. In addition, the characteristics of the signal on the ablation catheter have significance, with sharp early signals indicating a more 7
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superficial location and far-field signals suggesting a deeper location within the PM core. In approximately 40% of cases, a sharp Purkinje potential can be recorded at the successful ablation site, which suggests involvement of the Purkinje system in the arrhythmogenic
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mechanism12,17. Also, in our experience, the site of successful ablation sometimes exhibits a late potential in sinus rhythm that becomes pre-systolic during PVC/VT (Figures 4 and 5). This finding often coexists with evidence of PM scar (low voltage and late potentials in
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sinus rhythm), either DE on cardiac MRI or hyperechogenicity on ICE.
Pacemapping is useful, but not sufficient by itself. Sites of successful ablation
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usually exhibit an excellent pacemap (≥11/12), but conversely, ablation at sites with perfect pacemaps may fail to terminate the arrhythmia. This is likely because the exit site at the base of the PM may be located far from the site of origin, which may be higher in the body
Ablation
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of the PM.
Ablation is often challenging due to the anatomical variability of PM anatomy,
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potentially deep intramural site of arrhythmia origin and the stability issues related to the ablation of a mobile target.
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The two main energy modalities for ablating PM VAs are radiofrequency (RF) and
cryoablation. Our strategy in the majority of cases is to start with RF as initial approach using an ablation catheter with contact force (CF) capabilities, which provides not only contact force information, but also shows vector orientation of the catheter tip. RF ablation catheters are more steerable, allow deeper lesions and are necessary for creating an electroanatomic activation map. One of the main drawbacks of RF is the induction of 8
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mechanical and thermally provoked ectopy that further complicates catheter stability and interpretation of the activation map. Targets for ablation include sites with ventricular activation earlier than -30 ms pre-
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QRS and a QS pattern in the local unipolar recording. These sites usually exhibit an excellent pacemap. The presence of a Purkinje potential in the ablation site has also been associated with successful arrhythmia suppression17. RF application is delivered at 30-50
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Watts of power with temperature limited to 42°C, targeting an impedance drop of 10-15 Ω or 10% of the starting impedance value. High power is usefull as it may overcome the
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challenges imposed by poor stability. The only area where careful attention should be exercised is the base of the PM at its intersection with the LV free wall. If the catheter is “wedged” in this position there is a risk of steam pops and LV perforation given a higher impedance and less ability to cool. As such, we recommend to start with lower power (20
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Watts) in this area. Stability can be improved by pacing faster and providing a more stable cycle to cycle variation, specially if the patient is bradycardic (bigeminy), and we particularly try to avoid deep inspirations.
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We typically apply RF for 60-90 seconds, however for sites that are suspected to be deeper in the myocardium, longer lesions (4-5 minutes) may need be delivered. A deep
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intramyocardial origin is suspected when the best site of activation is ≤ 20 ms pre-QRS, the signal appears far-field looking and the QRS morphology changes with initial RF application. Another alternative for deep intramural arrhythmia sources is to surround the base of the PM with lesions aiming for exit block18. CF technology is of great value when ablating the PMs and currently 2 types of catheter with CF capabilities are available: TactiCath (St. Jude Medical, St. Paul, MN) and 9
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Thermocool SmartTouch (Biosense Webster, Diamond Bar, CA), which are integrated into the NavX and Carto mapping systems, respectively. TactiCath uses a fiberoptic sensor mounted in the catheter tip which detects changes in contact force. Measurement of the area
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under the force-time curve gives a novel parameter to guide ablation, the force-time integral, which is measured in grams per second. In SmartTouch the contact force is measured via recordings of microdeformation of a precision spring connecting the tip and
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the shaft of the catheter. The CF information is displayed numerically in grams and also as a graphical representation where the vector force is visualized as an arrow head
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(Supplementary Figure S2). We aim for a force of at least 10 g, although we realize it is often difficult to reach a significant force without sliding, especially at the PM tip. Often, several RF lesions on different parts of the PM are required to completely eliminate the VT/PVC. This is likely because a single arrhythmogenic focus may exhibit
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preferential conduction to multiple exit sites at the base of the PM or connect via false tendons15. Because of this phenomenon, the 12-lead ECG should be monitored at all times and particular attention should be paid to slight changes in the QRS morphology after the
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initial RF applications, which suggests a shift in the exit site and makes necessary to reposition the ablation catheter and map for a different site (Supplementary Figure S3). In
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MB VAs the most common site of successful ablation is the free-wall insertion of this structure, followed by the septal insertion or the body13 (Figure 6). The endpoint of ablation is VT/PVC suppression and non-inducibility with isoproterenol and/or burst ventricular pacing. We recommend a minimum 30-minute waiting period after the successful RF lesion.
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The role of cryoablation When catheter stability is an issue, cryoablation is an alternative, as the cryocatheter adherence to the tissue limits mobility and improves contact (Supplementary Video 1). The
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disadvantages of cryoablation are a comparative less maneuverability, reduced lesion depth and the inability to accurately project the catheter tip onto the electroanatomic map. We use a 6-mm Freezor Xtra catheter (Medtronic, Minneapolis, MN), which is able to fit through
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an Agilis or SL0 sheath. We typically use a freeze-thaw-freeze cycle (3-4 minutes per freeze) to the region of interest, and if there is acute suppression of the arrhythmia, this
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region is targeted with several additional lesions surrounding the area. We do not use an 8mm cryocatheter because: (1) it is more difficult to manipulate; (2) its larger diameter requires switching to a bigger sheath (10 French); (3) its shorter length (90 cm) makes it insufficient to reach some LV structures. In addition, mapping with a larger tip catheter
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may fail to record a near-field pre-potential at the site of interest.
Rivera et al. described a series of 21 patients with PM VAs that were targeted with either cryoablation (n=12) or RF (n=9)19. Acute procedural success was reported in all 12
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patients who underwent cryoablation and in 7/9 patients undergoing RF ablation (100% vs. 78%; P=0.08). In our experience, when RF ablation fails in eliminating PM PVCs/VT,
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switching to cryoablation can achieve successful arrhythmia elimination in >90% of cases20.
Complications
In our experience, procedure-related complications are infrequent. When a retrograde aortic approach is used, damage to the aortic valve is a possibility. This is a 11
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concern especially if cryoablation is used due to the stiffness of the catheter and we recommend to use a long sheath to advance the catheter into the LV. A few case reports have described worsening mitral regurgitation following ablation and mechanisms may
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include PM dysfunction or catheter entrapment in the MV apparatus21,22. VF induction may occur during RF application at the MB or PMs, requiring external defibrillation, and a new
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RBBB may develop post-procedure in 40% of patients with MB VAs.
Summary
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The PMs are a potential source of VAs in patients with and without structural heart disease. The mechanism may be focal or reentrant and they have distinguishing ECG features. Catheter ablation is highly effective, but challenging due to the complexity and variability of PM anatomy and their constant motion during the cardiac cycle. The use of
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ICE is fundamental to allow real-time visualization of these intracavitary structures and ensure proper catheter-tissue contact. Cryoablation is an option to improve catheter stability
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and improve outcomes.
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References 1. Van Herendael H, Zado ES, Haqqani H, et al. Catheter ablation of ventricular fibrillation: importance of left ventricular outflow tract and papillary muscle triggers. Heart
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2. Santoro F, Di Biase L, Hranitzky P, Sanchez JE, Santangeli P, Perini AP, Burkhardt JD, Natale A. Ventricular fibrillation triggered by PVCs from papillary muscles: clinical
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features and ablation. J Cardiovasc Electrophysiol 2014;25:1158-64.
3. Latchamsetty RY, Yokokawa M, Morady F, et al. Multicenter outcomes for catheter
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ablation of idiopathic premature ventricular complexes. JACCCEP 2015;1:116-123. 4. Dal-Bianco JP, Levine RA. Anatomy of the mitral valve apparatus: role of 2D and 3D echocardiography. Cardiol Clin 2013;31:151-64.
5. Loukas M, Klaassen Z, Tubbs RS, Derderian T, Paling D, Chow D, Patel S, Anderson
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RH. Anatomical observations of the moderator band. Clin Anat 2010;23:443-50. 6. Rawling DA, Joyner RW, Overholt ED. Variations in the functional electrical coupling between the subendocardial Purkinje and ventricular layers of the canine left ventricle. Circ
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JA, Ladewig DJ, Munger TM, Hammill SC, Packer DL, Asirvatham SJ. Relevance of endocavitary structures in ablation procedures for ventricular tachycardia. J Cardiovasc Electrophysiol 2010;21:245-54. 8. Doppalapudi H, Yamada T, McElderry HT, Plumb VJ, Epstein AE, Kay GN. Ventricular tachycardia originating from the posterior papillary muscle in the left ventricle: a distinct clinical syndrome. Circ Arrhythm Electrophysiol 2008;1:23-9. 13
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9. Li ZY, Wang YH, Maldonado C, Kupersmith J. Role of junctional zone cells between Purkinje fibres and ventricular muscle in arrhythmogenesis. Cardiovasc Res 1994;28:127784.
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10. Y. Pak HN, Kim YH, Lim HE, Chou CC, Miyauchi Y, Fang YH, Sun K, Hwang C, Chen PS. Role of the posterior papillary muscle and purkinje potentials in the mechanism of ventricular fibrillation in open chest dogs and Swine: effects of catheter ablation. J
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Pelosi F, Morady F. Post-infarction ventricular arrhythmias originating in papillary muscles. J Am Coll Cardiol 2008;51:1794-802.
12. Yamada T, Doppalapudi H, McElderry HT, et al. Electrocardiographic and electrophysiological characteristics in idiopathic ventricular arrhythmias originating from
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the papillary muscles in the left ventricle: relevance for catheter ablation. Circ Arrhythm Electrophysiol 2010;3:324-31.
13. Sadek MM, Benhayon D, Sureddi R, et al. Idiopathic ventricular arrhythmias
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originating from the moderator band: Electrocardiographic characteristics and treatment by catheter ablation. Heart Rhythm 2015;12:67-75.
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14. Good E, Desjardins B, Jongnarangsin K, Oral H, Chugh A, Ebinger M, Pelosi F, Morady F, Bogun F. Ventricular arrhythmias originating from a papillary muscle in patients without prior infarction: a comparison with fascicular arrhythmias. Heart Rhythm 2008;5:1530-7.
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15. Deyell MW, Man JP, Supple GE, Hutchinson MD, Frankel DS, Marchlinski FE. ECG Differentiation Of Ventricular Arrhythmias Arising From The Left Posterior Fascicle And Postero-medial Papillary Muscle. Heart Rhythm 2012;9(5S):S474.
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16. Al'Aref SJ, Ip JE, Markowitz SM, Liu CF, Thomas G, Frenkel D, Panda NC, Weinsaft JW, Lerman BB, Cheung JW. Differentiation of papillary muscle from fascicular and mitral annular ventricular arrhythmias in patients with and without structural heart disease. Circ
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17. Yokokawa M, Good E, Desjardins B, Crawford T, Jongnarangsin K, Chugh A, Pelosi F
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Jr, Oral H, Morady F, Bogun F. Predictors of successful catheter ablation of ventricular arrhythmias arising from the papillary muscles. Heart Rhythm 2010;7:1654-9. 18. Wo HT, Liao FC, Chang PC, Chou CC, Wen MS, Wang CC, Yeh SJ. Circumferential ablation at the base of the left ventricular papillary muscles: A highly effective approach for
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ventricular arrhythmias originating from the papillary muscles. Int J Cardiol 2016;220:876-
19. Rivera S, Ricapito Mde L, Tomas L, et al. Results of Cryoenergy and Radiofrequency-
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Based Catheter Ablation for Treating Ventricular Arrhythmias Arising From the Papillary Muscles of the Left Ventricle, Guided by Intracardiac Echocardiography and Image
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Integration. Circ Arrhythm Electrophysiol 2016;9:e003874. 20. Gordon J, Zado E, Hutchinson M, Garcia F, Santangeli P, Betensky B, Fahed J, Mendelson T, Shaw G, Supple G. Effectiveness of cryoablation on papillary muscle PVCs and VT after radiofrequency has failed. Heart Rhythm 2016;13:PO06-150.
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21. Mochizuki A, Nagahara D, Takahashi H, Saito R, Fujito T, Miura T. Worsening of mitral valve regurgitation after radiofrequency catheter ablation of ventricular arrhythmia originating from a left ventricular papillary muscle. Heart Rhythm Case Rep 2017;3:215-8.
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22. Desimone CV, Hu T, Ebrille E, Syed FF, Vaidya VR, Cha YM, Valverde AM, Friedman PA, Suri RM, Asirvatham SJ. Catheter ablation related mitral valve injury: the importance of early recognition and rescue mitral valve repair. J Cardiovasc Electrophysiol
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Figures Figure 1. Anatomy of the PMs and MB. APM = anterolateral papillary muscle; LV = left ventricle; MB = moderator band; PM = papillary muscle; PPM = posteromedial papillary
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muscle; RV = right ventricle. Reproduced from Dr K. Shivkumar with permission. Copyright UCLA Cardiac Arrhythmia Center, Wallace A. McAlpine Collection.
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Figure 2. Examples of patients with PVCs arising from the APM, PPM and MB showing the typical electrocardiographic characteristics. APM and PPM PVCs have a RBBB pattern
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with transition at V3-V5 and rS pattern in V6. The PPM is distinguished from the APM by a superior axis. APM PVCs are often characterized by a rightward axis with some negativity in lead II, but mainly positivity in lead III. MB PVCs are characterized by a LBBB pattern with transition at V4-V6, positive QRS in lead I, usually somewhat positive
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in lead II and negative in lead III.
Figure 3. Standard ICE image obtained from the RV inflow and CartoSound
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reconstruction of the LV cavity and the PMs. Notice the ICE catheter in the RV (red arrowhead) and the fan emitted from the tip of the ICE catheter that corresponds to the
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respective echocardiographic slice. A. Once in the RV, with gentle clockwise motion the first PM in view is the PMPM. Notice the ablation catheter in the posterior aspect of the PM. The circle in green is the catheter tip when cut by the ICE fan, helping in visualizing the location of the tip in real time. B. Further clockwise motion from the PMPM exposes the ALPM, in this case with 2 heads. PMPM: posterior medial papillary muscle. ALPM: anterolateral papillary muscle. LV: left ventricle. 17
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Figure 4. Mapping guided by ICE of an APM PVC. A. Initial ICE evaluation of the APM shows 2 heads with an echogenic appearance in one of the heads. B. CartoSound reconstruction of the anatomical structures and 2 separate structures created for the base of
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the PM and the echogenic area. This will aid when performing the electroanatomic mapping. C. Catheter guided with ICE via a transeptal approach to the suspected abnormal area, with careful monitoring of contact force and vector orientation at the tip of the PM. D.
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Continuous recordings of a sinus rhythm beat showing the presence of a late potential, followed by one pacemap beat with 12/12 match and a third complex demonstrating the late
at the site of successful ablation.
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potential becoming early during the PVC, with and exact timing to the spike to QRS signal
Figure 5. Ablation of monomorphic VT arising from the PPM. Increased echogenicity in
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one of the heads of the PM is noted on ICE, suggestive of a focal area of scar (blue arrow). Note the late potential observed in sinus rhythm that becomes presystolic during PVC (red
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arrow).
Figure 6. Ablation of PVC-triggered VF in a 28-year-old patient with structurally normal
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heart and resuscitated sudden cardiac death. Earliest ventricular activation during clinical PVCs was mapped to the free wall insertion of the MB (16 ms pre-QRS), with close, but not perfect pacemap. Radiofrequency application resulted in durable PVC suppression. A RBBB was induced and persistent until the end of the case.
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