- Email: [email protected]
Catheter ablation of ventricular tachycardia: Skill versus technology
Catheter ablation of ventricular tachycardia: Skill versus technology John M. Miller, MD, John A. Scherschel, MD From Indiana University School of Medicine, Krannert Institute of Cardiology, Indianapolis, Indiana. Despite the increasing number of sophisticated, computerized tools available to the practicing electrophysiologist for facilitating catheter ablation of ventricular tachycardia, the procedure is often quite challenging. Use of these tools needs to be kept in perspective, subservient to the judgment of the physician. This review
explores a series of principles that should be applied in these procedures. KEYWORDS Ventricular tachycardia; Ablation; Mapping (Heart Rhythm 2009;6:S86 –S90) © 2009 Heart Rhythm Society. All rights reserved.
Introduction
substrates. These patients often have comorbidities to which the electrophysiologist must pay attention prior to and during the procedure (residual ischemia, heart failure, diabetes, lung disease) and may alter the approach to mapping and ablation (severe peripheral vascular disease, presence of left ventricular thrombus, inadequately anticoagulated atrial fibrillation). In contrast, in patients without structural heart disease, comorbidities and procedural constraints are less common. Some patients are referred for VT ablation after a failed attempt at another institution; understanding what occurred at that procedure and why it may have failed can be important in planning the next one. Failure to appreciate these characteristics can result in significant difficulties during an already stressful procedure.
Catheter ablation of ventricular tachycardia (VT) remains a challenging procedure. Patient presentations, comorbid conditions, general illness of many VT patients, and technical difficulties encountered during these procedures explain the reluctance of some electrophysiologists to attempt VT ablation. With careful planning and execution, however, a safe and successful procedure can be delivered for most patients with VT. Sophisticated mapping systems and other complex technologies have been developed to assist the operator with mapping and ablation; however, it is the skill of the physician in using and interpreting information from these systems as well as standard equipment that make the difference between a successful and failed procedure, rather than the presence of abundant technology. Accordingly, we review 10 principles (“rules”) that should be observed in these procedures in order to obtain the desired outcomes. Only the last six of these deal with the actual procedure; the first four concern necessary preparation.
Rule 1—Understand Your Patient’s Substrate for VT Patients with VT often have significant structural heart disease that is responsible for facilitating their arrhythmia. Scar-based macroreentrant VT is observed in patients with prior myocardial infarction, dilated cardiomyopathy as well as arrhythmogenic right ventricular cardiomyopathy/dysplasia, sarcoidosis, Chagas disease, patients who have undergone ventricular repair of congenital heart disease, and other
Dr. Miller is a consultant for Medtronic, Inc., and Stereotaxis, Inc.; receives speaking honoraria from Medtronic, Inc., St. Jude Medical, and Boston Scientific Corp. (each modest compensation); and receives substantial funding for fellowship training from Medtronic, Inc., Boston Scientific Corp., and Biosense-Webster, Inc. Dr. Scherschel has no industry relationships to disclose. Address reprint requests and correspondence: Dr. John M. Miller, Krannert Institute of Cardiology, 1800 North Capitol Avenue, Indianapolis, Indiana 46202. E-mail address: [email protected].
Rule 2—Establish Your Goals for Ablation Although the goal in most standard ablation procedures is to cure the patient, this may not be appropriate for all patients with VT. Certainly, in those who have no structural heart disease, successful VT ablation will eliminate bothersome symptoms that prompted consideration of ablation. However, this goal should be pursued only to the extent that it does not impinge on patient safety. If a 19-year-old woman’s mildly symptomatic VT origin is found to be very near the His bundle and ablation incurs a significant risk for heart block, certainty that this outcome is worth the risk for this patient is critical. Extensive ablation in a normal heart, in relentless pursuit of an elusive VT, probably is not a worthwhile strategy. Most patients with VT who have significant structural heart disease already have an implantable cardioverter-defibrillator (ICD), and their indication for ablation is frequent shocks/recurrent symptomatic VT episodes terminated by antitachycardia pacing. Because it often is impossible to know which of several induced VT morphologies triggered ICD activity (only information available is rate and stored ICD electrogram in VT), one should ordinarily target all inducible VTs. However, the primary goal of ablation in these patients should be palliation: elimination of
1547-5271/$ -see front matter © 2009 Heart Rhythm Society. All rights reserved.
doi:10.1016/j.hrthm.2009.02.014
Miller and Scherschel
VT Ablation: Skill vs Technology
the problematic VT(s) during a 2- to 3-hour procedure rather than spending an additional 3 to 4 hr pursuing other, especially rapid, VTs that can be initiated but have not been observed clinically. The additional time spent often increases risk of complications. In the rare patient with structural heart disease who does not already have an ICD and either refuses one or is not an ICD candidate, a more aggressive approach may be warranted.
Rule 3—Determine Where to Focus Mapping Attention Knowledge of likely arrhythmogenic areas can greatly speed the mapping process and enhance its efficacy. Tools for this purpose include identifying regions of scar (ECG, echocardiogram, computed tomography or magnetic resonance images1), gathering the 12-lead ECGs of VT and applying existing algorithms2 to guide mapping efforts (Figure 1), and collecting ICD electrograms of episodes to compare cycle lengths (CLs) of spontaneous with induced VTs. Of critical importance is understanding the likely tachycardia mechanism, broadly categorized as macroreentry (as in most scar-based VT) or focal (triggered activity, automaticity, microreentry). The timing and properties of the correct ablation site electrogram depend on which of these is present. If one incorrectly assumes a macroreentrant mechanism (when it actually is focal) and begins searching for a mid-diastolic potential that does not exist, the procedure will be long, frustrating, and ultimately unsuccessful. An additional source of frustration is failure to diagnose bundle branch reentrant VT. One may suspect this unusual type of VT (clinical setting, ECG morphology, lack of presystolic activation despite thorough endocardial map-
S87 ping), but it will escape diagnosis unless appropriate techniques are used (His recordings, premature stimulation, entrainment). Noninducibility of the clinical (or sometimes, any) VT is an occasional problem; more common is hemodynamic intolerance of clinically relevant VTs. These problems can be addressed by using medications or mechanical devices to assist in hemodynamic support (inotropic medications, intraaortic balloon pump, ventricular assist devices) or using substrate-based mapping and ablation techniques.
Rule 4 —Make Sure Equipment and Personnel Are Ready Few frustrations exceed that of being in a stressful procedure, having spent 30 minutes finding the perfect site to ablate, only to discover that an essential cable to the radiofrequency generator is missing. Missing or malfunctioning equipment is not uncommon in these procedures, and one should make sure all necessary equipment is present and in working order. Equally important is having a staff of experienced, capable nurses and technologists who can monitor vital signs, operate and troubleshoot mapping and ablation equipment, and anticipate needed medications (sedation, inotropic agents, isoproterenol).
Rule 5—Use a Three-Dimensional Mapping System A computerized, three-dimensional mapping system can greatly facilitate VT ablation.3 With such systems, one can electronically “tag” sites of interest that are worth revisiting (or where ablation energy should not be delivered, such as the His bundle); perform substrate (voltage/scar/channel) mapping; maintain a catalog of sites already ablated to
Figure 1 Scheme of regions of ventricular tachycardia exit sites in postinfarction patients. INF ⫽ inferior axis; L ⫽ left; LBBB ⫽ left bundle branch block pattern; R ⫽ right; RBBB ⫽ right bundle branch block pattern; RWP ⫽ precordial R-wave progression pattern (diagrammed in table at bottom); SUP ⫽ superior axis.
S88 facilitate linear lesions; and potentially decrease fluoroscopic exposure for patient and staff. Although these systems have very useful and ever expanding features, they are no substitute for careful analysis by an experienced electrophysiologist who understands both the capabilities and the shortcomings of these mapping systems. Seemingly minor errors in assigning activation times during VT or accepting an atrial electrogram’s voltage instead of ventricular and being misled as to scar extent can cause great confusion. Erroneous data also can result in unnecessary ablation of irrelevant areas (low apparent voltage due to poor contact) or ignoring important areas that should be ablated (electrode artifact simulating a large electrogram in an area of low-amplitude signals). Noncontact mapping arrays, although able to simultaneously acquire activation data from multiple sites, suffer from poor signal quality at the poles of the array and at sites more than 2 cm from its surface. These are significant limitations, especially in dilated ventricles with apical VT origins. Substantial manipulation of gain and filtering of acquired signals is often needed to yield a reasonable representation of ventricular activation. Thus, familiarity with the limitations of a mapping system and knowing how far to trust the information it displays are as important as knowing its benefits.
Rule 6 —Use Pacemapping and Entrainment Correctly Pacing during either sinus rhythm or VT (entrainment) is an important tool in the electrophysiologist’s arsenal but must be used correctly to avoid confusion. Pacing during sinus rhythm to replicate a 12-lead ECG configuration of a known VT morphology (pacemapping) can corroborate the information derived from activation mapping or serve as an indicator of exit sites of VT from scarred areas when mapping is precluded due to hemodynamic intolerance or noninducibility of VT. Pitfalls include imperfect specificity (pacing at sites over a relatively large area can yield similar/ identical pacemaps) and sensitivity (pacing within a circuit may not yield a match if slow propagation through the VT isthmus competes with more rapid conduction in a different direction). Pacemapping is most useful when a “perfect” match is obtained (superimposable with VT) rather than a “9/12 leads” match. With entrainment (overdrive pacing during tachycardia), although comparison of postpacing interval with VT CL and stimulus–QRS with activation time in VT are critical in determining whether the paced site is in the circuit (and where in the circuit), it is vital to clarify that entrainment actually has occurred as well as what tissue has been captured. Common mistakes are pacing for too short a duration or at a CL too close to VT to actually entrain. Pacing too rapidly can terminate VT, change to a different VT, or produce fibrillation. Inadequate output and noncapture, when pacing at a rate similar to VT, can easily simulate a perfect QRS match and tempt one to make postpacing measurements that are irrelevant and misleading (because capture never occurred). Although pacing with adequate current to capture clearly is vital to either technique, pacing
Heart Rhythm, Vol 6, No 8S, August Supplement 2009 at as low an output as consistently captures is important to avoid far-field capture and loss of specificity.
Rule 7—Don’t Miss Serendipitous Findings Although the operator is intent on activation, pacemapping, and entrainment, unexpected events during VT mapping can provide useful information and should not be ignored. They include the following: 1. Spontaneous variations in VT CL that can reveal the relationship of a mid-diastolic potential to the previous or subsequent QRS complex. If the potential-to-QRS interval is constant despite changes in VT CL, the potential likely is integral to the circuit. However, if the variability of CL is related to changes in the potentialto-QRS interval, the potential likely is passively activated and not essential for ongoing VT. 2. Termination of VT with a nonpropagated stimulus.4 This phenomenon, when reproducible, indicates that the electrode delivering the stimulus is at an area that is essential for VT perpetuation. Although extrastimuli are not often delivered during VT, entrainment is commonly used, and occasionally one of the first few stimuli of a pacing train terminates VT without propagation, followed by capture with a QRS configuration different from that of VT (Figure 2). It is easy to miss this transition and dismiss it as pacing from a site remote from the VT circuit because the final QRS configuration often is disparate from VT. When entrainment attempts at a “good” site result in a sudden change in QRS configuration, one should consider the possibility that a nonpropagated stimulus terminated VT and therefore is critical to the VT circuit. 3. Intermittent potentials during VT.5 In areas of scarred myocardium, some diastolic potentials are produced by tissue bundles that do not conduct every cycle. Most often, the potential occurs every other beat (a 2:1 relationship); although their timing elicits interest as possible ablation sites, these potentials are obviously not related to ongoing VT. Evaluating several VT cycles will show if diastolic potentials are consistently present or not (computerized mapping systems typically evaluate only 1 cycle). 4. “Bump” mapping. Mild catheter trauma occasionally terminates VT that sometimes cannot be reinitiated. When this occurs, it indicates that the vulnerable region for the VT is small as well as superficial. Although these features are attractive from an ablation perspective, quite often the catheter tip has brushed past the critical site of termination and is now in a different location; ablation at this new location may not be of any benefit.
Rule 8 —If the VT Isn’t Eliminated Where You Are Ablating, Look Somewhere Else Sometimes, despite a careful exploration of the region from which the VT’s diastolic corridor was predicted to occur from ECG or scar location, no suitable ablation sites are found. In this situation, additional mapping with finer detail and adequate display gain to ensure that very small signals
Miller and Scherschel
VT Ablation: Skill vs Technology
S89
Figure 2 Termination of ventricular tachycardia (VT) by a nonpropagated stimulus during attempted entrainment. Shown are surface ECG leads and intracardiac recordings from the right atrium (RA), ablation electrodes [distal (Abldist) and proximal (Ablprox)], and right ventricular apex (RVA) during VT. Stimulation (S) from the ablation catheter is initiated at a site with a mid-diastolic potential (arrow). The first stimulus appears not to capture, yet VT terminates (nonpropagated stimulus). Subsequent stimuli are followed by QRS complexes different from VT, indicating a different direction of propagation from the pacing site.
are not missed should be used. If this also fails to reveal any sites at which ablation should be attempted (or has been, without effect), other sites should be considered. In idiopathic outflow tract VT, sites in the great arteries (pulmonary artery, aortic sinuses of Valsalva) as well as deeper septal or epicardial sites are worth exploring. In some substrates, such as cardiomyopathy (dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy/dysplasia), there is a higher likelihood of needing epicardial mapping and ablation. Additional clues suggesting epicardial substrate include poor matches with pacemapping, long postpacing intervals following entrainment, and electroanatomic mapping showing a large area (diameter 2–3 cm) with similar and minimally presystolic activation times. It is better to consider and explore alternative mapping regions when the initial region explored yields unsatisfactory results than to deliver multiple applications of energy to suboptimal sites, especially in patients without structural heart disease.
Rule 9 —Contact, Contact, Contact Using all the techniques described can help get the ablation electrode to the correct site for successful ablation, but unless adequate energy can be delivered, VT will persist. A prominent reason for lack of effect with ablation is poor catheter–tissue contact. Several factors contribute to this: concern about perforation, difficult angle of contact with tissue, lack of stabilizing features on the endocardium (trabeculations) in scarred regions, and interposed organized thrombus. Techniques to help stabilize catheter position include making a large loop with the catheter shaft to brace it against one ventricular wall, pacing at the VT rate during ablation such that sudden cessation of tachycardia does not result in a shift of catheter position, and use of long vascular sheaths. A stable catheter position on fluoroscopy or mapping system and a stable electrogram are not reliable indicators of good catheter contact. If the fluoroscopic catheter position or electrogram contour is clearly changing, catheter
contact probably is poor and ablation at that site is likely to fail (despite having other features predictive of success).
Rule 10 —More Power Isn’t Necessarily Better In most patients with VT without structural heart disease, only a small area of myocardium is responsible for the arrhythmia; thus, only a small amount of damage will eliminate it. It is tempting to think that if a small application energy is good, a lot of energy delivery must be better. Despite the known presence of scar tissue in regions suitable for ablation in patients with structural heart disease and the perception that more energy is necessary to have an effect similar to that achieved in the absence of such disease, elimination of the target arrhythmia in many of these cases also requires relatively little ablation. Among postmyocardial infarction patients, greater than 50% of cases of successfully ablated VTs terminate within 5 seconds of onset of power delivery. This implies a very superficial vulnerable zone in these patients. Although this may not apply in all cases, the idea that all patients with scar-based VT require high power settings to penetrate deeply into scar in order ablate successfully is erroneous. This is clearly not the case in the majority of patients without structural heart disease in whom high power delivery can destroy very large amounts of tissue and result in complications such as embolism or perforation. The tradeoff of having the ability to make large enough lesions using high power so that the target will be destroyed (along with additional innocent tissue) instead of more precise targeting is not a bargain for the patient.
Summary In most patients with VT without structural heart disease, ablation of the arrhythmia is straightforward and can be accomplished with excellent efficacy and safety. However, in some of these patients as well as in many patients with structural heart disease, VT ablation is a much more challenging procedure. The number and sophistication of tools to aid the electrophysiologist continue to expand but are no substitute for
S90
Heart Rhythm, Vol 6, No 8S, August Supplement 2009
careful and thoughtful analysis of the information they provide. The ability to make very large lesions should be exercised with caution. Keeping several fundamental principles in mind during these procedures can help maintain and improve outcomes of these increasingly common procedures.
References 1.
Ashikaga H, Sasano T, Dong J, et al. Magnetic resonance-based anatomical analysis of scar-related ventricular tachycardia: implications for catheter ablation. Circ Res 2007;101:939 – 47.
2.
3.
4.
5.
Miller JM, Marchlinski FE, Buxton AE, et al. Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease. Circulation 1988;77: 759 –766. Darbar D, Olgin JE, Miller JM, et al. Localization of the origin of arrhythmias for ablation: from electrocardiography to advanced endocardial mapping systems. J Cardiovasc Electrophysiol 2001;12:1309 –1325. Bogun F, Krishnan SC, Marine JE, et al. Catheter ablation guided by termination of postinfarction ventricular tachycardia by pacing with nonglobal capture. Heart Rhythm 2004;1:422– 426. Miller JM, Vassallo JA, Hargrove WC, et al. Intermittent failure of local conduction during ventricular tachycardia. Circulation 1985;72:1286 –1292.
explores a series of principles that should be applied in these procedures. KEYWORDS Ventricular tachycardia; Ablation; Mapping (Heart Rhythm 2009;6:S86 –S90) © 2009 Heart Rhythm Society. All rights reserved.
Introduction
substrates. These patients often have comorbidities to which the electrophysiologist must pay attention prior to and during the procedure (residual ischemia, heart failure, diabetes, lung disease) and may alter the approach to mapping and ablation (severe peripheral vascular disease, presence of left ventricular thrombus, inadequately anticoagulated atrial fibrillation). In contrast, in patients without structural heart disease, comorbidities and procedural constraints are less common. Some patients are referred for VT ablation after a failed attempt at another institution; understanding what occurred at that procedure and why it may have failed can be important in planning the next one. Failure to appreciate these characteristics can result in significant difficulties during an already stressful procedure.
Catheter ablation of ventricular tachycardia (VT) remains a challenging procedure. Patient presentations, comorbid conditions, general illness of many VT patients, and technical difficulties encountered during these procedures explain the reluctance of some electrophysiologists to attempt VT ablation. With careful planning and execution, however, a safe and successful procedure can be delivered for most patients with VT. Sophisticated mapping systems and other complex technologies have been developed to assist the operator with mapping and ablation; however, it is the skill of the physician in using and interpreting information from these systems as well as standard equipment that make the difference between a successful and failed procedure, rather than the presence of abundant technology. Accordingly, we review 10 principles (“rules”) that should be observed in these procedures in order to obtain the desired outcomes. Only the last six of these deal with the actual procedure; the first four concern necessary preparation.
Rule 1—Understand Your Patient’s Substrate for VT Patients with VT often have significant structural heart disease that is responsible for facilitating their arrhythmia. Scar-based macroreentrant VT is observed in patients with prior myocardial infarction, dilated cardiomyopathy as well as arrhythmogenic right ventricular cardiomyopathy/dysplasia, sarcoidosis, Chagas disease, patients who have undergone ventricular repair of congenital heart disease, and other
Dr. Miller is a consultant for Medtronic, Inc., and Stereotaxis, Inc.; receives speaking honoraria from Medtronic, Inc., St. Jude Medical, and Boston Scientific Corp. (each modest compensation); and receives substantial funding for fellowship training from Medtronic, Inc., Boston Scientific Corp., and Biosense-Webster, Inc. Dr. Scherschel has no industry relationships to disclose. Address reprint requests and correspondence: Dr. John M. Miller, Krannert Institute of Cardiology, 1800 North Capitol Avenue, Indianapolis, Indiana 46202. E-mail address: [email protected].
Rule 2—Establish Your Goals for Ablation Although the goal in most standard ablation procedures is to cure the patient, this may not be appropriate for all patients with VT. Certainly, in those who have no structural heart disease, successful VT ablation will eliminate bothersome symptoms that prompted consideration of ablation. However, this goal should be pursued only to the extent that it does not impinge on patient safety. If a 19-year-old woman’s mildly symptomatic VT origin is found to be very near the His bundle and ablation incurs a significant risk for heart block, certainty that this outcome is worth the risk for this patient is critical. Extensive ablation in a normal heart, in relentless pursuit of an elusive VT, probably is not a worthwhile strategy. Most patients with VT who have significant structural heart disease already have an implantable cardioverter-defibrillator (ICD), and their indication for ablation is frequent shocks/recurrent symptomatic VT episodes terminated by antitachycardia pacing. Because it often is impossible to know which of several induced VT morphologies triggered ICD activity (only information available is rate and stored ICD electrogram in VT), one should ordinarily target all inducible VTs. However, the primary goal of ablation in these patients should be palliation: elimination of
1547-5271/$ -see front matter © 2009 Heart Rhythm Society. All rights reserved.
doi:10.1016/j.hrthm.2009.02.014
Miller and Scherschel
VT Ablation: Skill vs Technology
the problematic VT(s) during a 2- to 3-hour procedure rather than spending an additional 3 to 4 hr pursuing other, especially rapid, VTs that can be initiated but have not been observed clinically. The additional time spent often increases risk of complications. In the rare patient with structural heart disease who does not already have an ICD and either refuses one or is not an ICD candidate, a more aggressive approach may be warranted.
Rule 3—Determine Where to Focus Mapping Attention Knowledge of likely arrhythmogenic areas can greatly speed the mapping process and enhance its efficacy. Tools for this purpose include identifying regions of scar (ECG, echocardiogram, computed tomography or magnetic resonance images1), gathering the 12-lead ECGs of VT and applying existing algorithms2 to guide mapping efforts (Figure 1), and collecting ICD electrograms of episodes to compare cycle lengths (CLs) of spontaneous with induced VTs. Of critical importance is understanding the likely tachycardia mechanism, broadly categorized as macroreentry (as in most scar-based VT) or focal (triggered activity, automaticity, microreentry). The timing and properties of the correct ablation site electrogram depend on which of these is present. If one incorrectly assumes a macroreentrant mechanism (when it actually is focal) and begins searching for a mid-diastolic potential that does not exist, the procedure will be long, frustrating, and ultimately unsuccessful. An additional source of frustration is failure to diagnose bundle branch reentrant VT. One may suspect this unusual type of VT (clinical setting, ECG morphology, lack of presystolic activation despite thorough endocardial map-
S87 ping), but it will escape diagnosis unless appropriate techniques are used (His recordings, premature stimulation, entrainment). Noninducibility of the clinical (or sometimes, any) VT is an occasional problem; more common is hemodynamic intolerance of clinically relevant VTs. These problems can be addressed by using medications or mechanical devices to assist in hemodynamic support (inotropic medications, intraaortic balloon pump, ventricular assist devices) or using substrate-based mapping and ablation techniques.
Rule 4 —Make Sure Equipment and Personnel Are Ready Few frustrations exceed that of being in a stressful procedure, having spent 30 minutes finding the perfect site to ablate, only to discover that an essential cable to the radiofrequency generator is missing. Missing or malfunctioning equipment is not uncommon in these procedures, and one should make sure all necessary equipment is present and in working order. Equally important is having a staff of experienced, capable nurses and technologists who can monitor vital signs, operate and troubleshoot mapping and ablation equipment, and anticipate needed medications (sedation, inotropic agents, isoproterenol).
Rule 5—Use a Three-Dimensional Mapping System A computerized, three-dimensional mapping system can greatly facilitate VT ablation.3 With such systems, one can electronically “tag” sites of interest that are worth revisiting (or where ablation energy should not be delivered, such as the His bundle); perform substrate (voltage/scar/channel) mapping; maintain a catalog of sites already ablated to
Figure 1 Scheme of regions of ventricular tachycardia exit sites in postinfarction patients. INF ⫽ inferior axis; L ⫽ left; LBBB ⫽ left bundle branch block pattern; R ⫽ right; RBBB ⫽ right bundle branch block pattern; RWP ⫽ precordial R-wave progression pattern (diagrammed in table at bottom); SUP ⫽ superior axis.
S88 facilitate linear lesions; and potentially decrease fluoroscopic exposure for patient and staff. Although these systems have very useful and ever expanding features, they are no substitute for careful analysis by an experienced electrophysiologist who understands both the capabilities and the shortcomings of these mapping systems. Seemingly minor errors in assigning activation times during VT or accepting an atrial electrogram’s voltage instead of ventricular and being misled as to scar extent can cause great confusion. Erroneous data also can result in unnecessary ablation of irrelevant areas (low apparent voltage due to poor contact) or ignoring important areas that should be ablated (electrode artifact simulating a large electrogram in an area of low-amplitude signals). Noncontact mapping arrays, although able to simultaneously acquire activation data from multiple sites, suffer from poor signal quality at the poles of the array and at sites more than 2 cm from its surface. These are significant limitations, especially in dilated ventricles with apical VT origins. Substantial manipulation of gain and filtering of acquired signals is often needed to yield a reasonable representation of ventricular activation. Thus, familiarity with the limitations of a mapping system and knowing how far to trust the information it displays are as important as knowing its benefits.
Rule 6 —Use Pacemapping and Entrainment Correctly Pacing during either sinus rhythm or VT (entrainment) is an important tool in the electrophysiologist’s arsenal but must be used correctly to avoid confusion. Pacing during sinus rhythm to replicate a 12-lead ECG configuration of a known VT morphology (pacemapping) can corroborate the information derived from activation mapping or serve as an indicator of exit sites of VT from scarred areas when mapping is precluded due to hemodynamic intolerance or noninducibility of VT. Pitfalls include imperfect specificity (pacing at sites over a relatively large area can yield similar/ identical pacemaps) and sensitivity (pacing within a circuit may not yield a match if slow propagation through the VT isthmus competes with more rapid conduction in a different direction). Pacemapping is most useful when a “perfect” match is obtained (superimposable with VT) rather than a “9/12 leads” match. With entrainment (overdrive pacing during tachycardia), although comparison of postpacing interval with VT CL and stimulus–QRS with activation time in VT are critical in determining whether the paced site is in the circuit (and where in the circuit), it is vital to clarify that entrainment actually has occurred as well as what tissue has been captured. Common mistakes are pacing for too short a duration or at a CL too close to VT to actually entrain. Pacing too rapidly can terminate VT, change to a different VT, or produce fibrillation. Inadequate output and noncapture, when pacing at a rate similar to VT, can easily simulate a perfect QRS match and tempt one to make postpacing measurements that are irrelevant and misleading (because capture never occurred). Although pacing with adequate current to capture clearly is vital to either technique, pacing
Heart Rhythm, Vol 6, No 8S, August Supplement 2009 at as low an output as consistently captures is important to avoid far-field capture and loss of specificity.
Rule 7—Don’t Miss Serendipitous Findings Although the operator is intent on activation, pacemapping, and entrainment, unexpected events during VT mapping can provide useful information and should not be ignored. They include the following: 1. Spontaneous variations in VT CL that can reveal the relationship of a mid-diastolic potential to the previous or subsequent QRS complex. If the potential-to-QRS interval is constant despite changes in VT CL, the potential likely is integral to the circuit. However, if the variability of CL is related to changes in the potentialto-QRS interval, the potential likely is passively activated and not essential for ongoing VT. 2. Termination of VT with a nonpropagated stimulus.4 This phenomenon, when reproducible, indicates that the electrode delivering the stimulus is at an area that is essential for VT perpetuation. Although extrastimuli are not often delivered during VT, entrainment is commonly used, and occasionally one of the first few stimuli of a pacing train terminates VT without propagation, followed by capture with a QRS configuration different from that of VT (Figure 2). It is easy to miss this transition and dismiss it as pacing from a site remote from the VT circuit because the final QRS configuration often is disparate from VT. When entrainment attempts at a “good” site result in a sudden change in QRS configuration, one should consider the possibility that a nonpropagated stimulus terminated VT and therefore is critical to the VT circuit. 3. Intermittent potentials during VT.5 In areas of scarred myocardium, some diastolic potentials are produced by tissue bundles that do not conduct every cycle. Most often, the potential occurs every other beat (a 2:1 relationship); although their timing elicits interest as possible ablation sites, these potentials are obviously not related to ongoing VT. Evaluating several VT cycles will show if diastolic potentials are consistently present or not (computerized mapping systems typically evaluate only 1 cycle). 4. “Bump” mapping. Mild catheter trauma occasionally terminates VT that sometimes cannot be reinitiated. When this occurs, it indicates that the vulnerable region for the VT is small as well as superficial. Although these features are attractive from an ablation perspective, quite often the catheter tip has brushed past the critical site of termination and is now in a different location; ablation at this new location may not be of any benefit.
Rule 8 —If the VT Isn’t Eliminated Where You Are Ablating, Look Somewhere Else Sometimes, despite a careful exploration of the region from which the VT’s diastolic corridor was predicted to occur from ECG or scar location, no suitable ablation sites are found. In this situation, additional mapping with finer detail and adequate display gain to ensure that very small signals
Miller and Scherschel
VT Ablation: Skill vs Technology
S89
Figure 2 Termination of ventricular tachycardia (VT) by a nonpropagated stimulus during attempted entrainment. Shown are surface ECG leads and intracardiac recordings from the right atrium (RA), ablation electrodes [distal (Abldist) and proximal (Ablprox)], and right ventricular apex (RVA) during VT. Stimulation (S) from the ablation catheter is initiated at a site with a mid-diastolic potential (arrow). The first stimulus appears not to capture, yet VT terminates (nonpropagated stimulus). Subsequent stimuli are followed by QRS complexes different from VT, indicating a different direction of propagation from the pacing site.
are not missed should be used. If this also fails to reveal any sites at which ablation should be attempted (or has been, without effect), other sites should be considered. In idiopathic outflow tract VT, sites in the great arteries (pulmonary artery, aortic sinuses of Valsalva) as well as deeper septal or epicardial sites are worth exploring. In some substrates, such as cardiomyopathy (dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy/dysplasia), there is a higher likelihood of needing epicardial mapping and ablation. Additional clues suggesting epicardial substrate include poor matches with pacemapping, long postpacing intervals following entrainment, and electroanatomic mapping showing a large area (diameter 2–3 cm) with similar and minimally presystolic activation times. It is better to consider and explore alternative mapping regions when the initial region explored yields unsatisfactory results than to deliver multiple applications of energy to suboptimal sites, especially in patients without structural heart disease.
Rule 9 —Contact, Contact, Contact Using all the techniques described can help get the ablation electrode to the correct site for successful ablation, but unless adequate energy can be delivered, VT will persist. A prominent reason for lack of effect with ablation is poor catheter–tissue contact. Several factors contribute to this: concern about perforation, difficult angle of contact with tissue, lack of stabilizing features on the endocardium (trabeculations) in scarred regions, and interposed organized thrombus. Techniques to help stabilize catheter position include making a large loop with the catheter shaft to brace it against one ventricular wall, pacing at the VT rate during ablation such that sudden cessation of tachycardia does not result in a shift of catheter position, and use of long vascular sheaths. A stable catheter position on fluoroscopy or mapping system and a stable electrogram are not reliable indicators of good catheter contact. If the fluoroscopic catheter position or electrogram contour is clearly changing, catheter
contact probably is poor and ablation at that site is likely to fail (despite having other features predictive of success).
Rule 10 —More Power Isn’t Necessarily Better In most patients with VT without structural heart disease, only a small area of myocardium is responsible for the arrhythmia; thus, only a small amount of damage will eliminate it. It is tempting to think that if a small application energy is good, a lot of energy delivery must be better. Despite the known presence of scar tissue in regions suitable for ablation in patients with structural heart disease and the perception that more energy is necessary to have an effect similar to that achieved in the absence of such disease, elimination of the target arrhythmia in many of these cases also requires relatively little ablation. Among postmyocardial infarction patients, greater than 50% of cases of successfully ablated VTs terminate within 5 seconds of onset of power delivery. This implies a very superficial vulnerable zone in these patients. Although this may not apply in all cases, the idea that all patients with scar-based VT require high power settings to penetrate deeply into scar in order ablate successfully is erroneous. This is clearly not the case in the majority of patients without structural heart disease in whom high power delivery can destroy very large amounts of tissue and result in complications such as embolism or perforation. The tradeoff of having the ability to make large enough lesions using high power so that the target will be destroyed (along with additional innocent tissue) instead of more precise targeting is not a bargain for the patient.
Summary In most patients with VT without structural heart disease, ablation of the arrhythmia is straightforward and can be accomplished with excellent efficacy and safety. However, in some of these patients as well as in many patients with structural heart disease, VT ablation is a much more challenging procedure. The number and sophistication of tools to aid the electrophysiologist continue to expand but are no substitute for
S90
Heart Rhythm, Vol 6, No 8S, August Supplement 2009
careful and thoughtful analysis of the information they provide. The ability to make very large lesions should be exercised with caution. Keeping several fundamental principles in mind during these procedures can help maintain and improve outcomes of these increasingly common procedures.
References 1.
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