- Email: [email protected]
Focal and macroreentrant atrial tachycardia: From bench to bedside and back to the bench again
VIEWPOINT
Focal and macroreentrant atrial tachycardia: From bench to bedside and back to the bench again Bruce D. Lindsay, MD From the Department of Clinical Electrophysiology, Washington University School of Medicine, St. Louis, Missouri. A recent position document recommended that atrial arrhythmias be categorized as focal or macroreentrant on the basis of mechanisms and anatomic features.1 This classification reflects progress in understanding the pathophysiology of these arrhythmias and provides a practical basis for discussing their diagnostic features and treatment. Focal atrial tachycardias are characterized by a point source with concentric spread of activation from the origin. They appear to be caused by abnormal automaticity, microreentry, and triggered activity.2,3 The criteria to differentiate these mechanisms depend on the response to isoproterenol, programmed atrial stimulation, whether the onset is sudden or increases gradually, and the response to adenosine, propranolol, or other pharmacologic interventions.2–5 Triggered activity has been associated with delayed after-depolarizations recorded from monophasic action potential catheters. The diagnosis of microreentry depends on evidence of manifest and concealed entrainment. Other focal mechanisms require further study. Inappropriate sinus tachycardia and postural orthostatic tachycardia syndrome are probably caused by autonomic dysfunction. Recent evidence suggests that inappropriate sinus tachycardia is related to an immunologic disorder involving cardiac beta-receptor antibodies.6 This is an important distinction because they are often refractory to common pharmacologic interventions. Moreover, long-term outcomes are highly variable after sinus node ablation in patients with inappropriate sinus tachycardia, and the procedure is ineffective for those with postural orthostatic tachycardia.7 Multifocal atrial tachycardia is another difficult problem because it often occurs in patients with severe cardiopulmonary disease who are not candidates for electrophysiology study. Our clinical insights about the mechanisms and origins of multifocal tachycardia are limited. KEYWORDS Ablation; Atrial arrhythmias; Focal atrial tachycardia; Atrial flutter (Heart Rhythm 2007;4:1361–1363) Address reprint requests and correspondence: Bruce D. Lindsay, M.D., Professor of Medicine, Director, Clinical Electrophysiology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8086, St. Louis, MO 63110. E-mail address: [email protected].
The anatomic origin of focal atrial tachycardias is not an accurate predictor of the mechanism.3 Focal atrial tachycardias arise along the crista terminalis, in the right and left atrial appendages, within the coronary sinus, in the tissue bounded by Koch’s triangle, in the septum, in pulmonary veins, in the floor or roof of the left atrium, along the annulus of the tricuspid and mitral valves, and at the noncoronary aortic cusp.2,3,8 –10 One reason focal atrial tachycardias are attracting more attention is that they are a common cause of palpitations in patients who have undergone pulmonary vein antral isolation. In such cases, the origin may be located well outside the pulmonary vein antrum, and the severity of symptoms can necessitate a second ablation procedure. Studies have shown that the standard electrocardiogram (ECG) can predict the origin of focal atrial tachycardias.11,12 While the observations from these studies are useful, interpretation of the standard ECG is limited by several factors. Focal atrial tachycardias tend to be paroxysmal, which can make it difficult to obtain a representative recording. Even when recordings are available, the P wave may be buried within the T wave, which affects the accuracy of analysis. Under the best circumstances, there are limitations on the diagnostic accuracy of the standard ECG, and the criteria that have been developed may not be as accurate in the presence of significant underlying atrial enlargement or conduction delay. From a practical point of view, it is difficult to predict which medications will be most effective when the decision is based on ambulatory monitor recordings. Treatment with propranolol, calcium channel blockers, or other antiarrhythmic medications may be tried empirically. When medications are ineffective or poorly tolerated, many patients are referred for electrophysiology studies to determine whether the origin can be identified and ablated. The mechanism may determine how focal arrhythmias are induced, but successful ablation depends on the ability to identify the origin and reach the target. One factor limiting ablation of focal atrial tachycardias is that it may be difficult to induce the arrhythmia, which is a constraint for mapping and results in an unreliable endpoint by which the success of the procedure must be judged. Electroanatomic mapping helps the physician to navigate the catheter with greater appreci-
1547-5271/$ -see front matter © 2007 Heart Rhythm Society. All rights reserved.
doi:10.1016/j.hrthm.2007.05.024
1362 ation of the three-dimensional anatomy, but short runs of the arrhythmia or isolated beats make this approach extremely tedious. Noncontact mapping has the advantage of using a single beat to identify the origin, which is extremely useful in patients with arrhythmias that are nonsustained or difficult to induce.10 Atrial macroreentry can involve single reentrant loops or more complex figure-of-8 reentry. It is of particular historical interest that our understanding of these mechanisms dates back to the work of Lewis and coworkers,13 who were able to induce and study atrial reentry in canines. Rosenblueth and Garcia Ramos14 recognized the need for conduction block and demonstrated that the cycle length of reentry was affected by the length of a surgical incision around which their model of reentry circulated. Waldo et al’s15 seminal work in humans used entrainment to show that atrial flutter is a form of reentry with an excitable gap. Subsequent studies employed entrainment mapping to define the reentrant loop associated with common isthmus-dependent right atrial flutter, and Cosio et al16 demonstrated that this circuit could be interrupted by ablation of tissue within the isthmus. The mapping techniques and principles of entrainment that were established in these early studies have been extended to assess and treat other forms of atrial macroreentry. Other clinical studies have confirmed reentry around surgical scars in the left or right atrium in patients who have undergone operations for coronary artery disease, valvular heart disease, or reconstructive surgery required by congenital abnormalities.17–20 These circuits are referred to as lesion atrial reentry. The observations made during these studies show reentry around a region of conduction block, and it is often possible to demonstrate a zone of slow conduction within the reentrant circuit. Successful ablation depends on the use of activation and entrainment mapping to define the circuit, which is interrupted by ablation of tissue from a line of block to a conduction boundary. While this is often defined by an anatomic boundary, sometimes ablation is performed to connect adjacent scars separated by an isthmus of tissue that serves as a critical element of the circuit.20 The ability to ablate circuits associated with macroreentry has unveiled an interesting relationship between these arrhythmias and atrial fibrillation.20 –25 While in some cases atrial fibrillation is induced by macroreentry, the converse occurs frequently. Long-term follow-up of patients who have undergone ablation of typical isthmus-dependent right atrial flutter shows a propensity for them to develop atrial fibrillation. Those with a history of atrial fibrillation or structural heart disease are at greatest risk. In many cases, this becomes apparent in the laboratory or during short-term follow-up. Now that ablation of atrial fibrillation has become an important treatment for patients who have not responded to medications, focal and maccroreentant atrial arrhythmias have complicated long-term outcomes. In some cases, reentry occurs because linear lesions create zones of slow conduction but they fail to cause a line of block. Reentry
Heart Rhythm, Vol 4, No 10, October 2007 may circulate around or through the pulmonary veins, the mitral valve annulus, or through other regions of the left atrium that were subjected to ablation.
Future directions What does the future hold for the treatment of focal and macroreentrant atrial arrhythmias? As we reflect on the progress that has been made in recent decades, it is clear that our advances have depended on animal models and painstaking observations made in clinical laboratories. There is a genuine need for better antiarrhythmic drugs to treat patients who are not optimal candidates for invasive procedures or who would prefer to avoid this approach. Nonetheless, it is difficult to predict whether the next generation of antiarrhythmic medications will appreciably alter pharmacologic treatment. It is likely that ablation techniques will continue to evolve based on improved understanding of pathophysiology and advances in mapping technology and delivery of energy for ablation of critical tissue. The most challenging patients have arrhythmias that are difficult to induce, multiple arrhythmias, or circuits that are extremely complex. ECG imaging is a novel, noninvasive tool for imaging cardiac arrhythmia and defining electrophysiological properties.26 It combines multielectrode body surface ECG recordings with three-dimensional anatomical heart-torso imaging to reconstruct an epicardial electroanatomical map. Recently, ECG imaging has been used successfully to define the origins of ventricular and atrial arrhythmias.27,28 As this technology evolves, it might be feasible to take this technology to the next level so that we could capture transient arrhythmias during ambulatory monitoring, reference the recordings to a computed tomography scan, and predict the reentrant circuit or focal origin with a high degree of accuracy. This would facilitate ablation strategies in patients whose arrhythmias are difficult to induce or sustain. It might be feasible to target critical tissue based on the results of ambulatory ECG imaging alone in patients whose arrhythmias cannot be induced. Most of our work is directed toward treatment of arrhythmias when patients develop symptoms and seek our attention. The real question is, How can we prevent these arrhythmias from developing in the first place? Although some insights may be gained from observations made during electrophysiology studies, it is more likely that the answer rests in basic science. If we could develop safe and effective measures to prevent the development of arrhythmias, the downstream cost of treating them could be averted. Perhaps this is our next frontier.
References 1. Saoudi N, Cosio F, Walso A, Chen SA, Iesaka Y, Lesh M, Saksena S, Salerno J, Schoels W. Classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanism and anatomic bases: a statement from a joint expert group from the working group of arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. J Cardiovasc Electrophysiol 2001;12:852– 866. 2. Chen SA, Chiang CE, Yang CJ, Cheng CC, Wu TJ, Wang SP, Chiang BN, Chang MS. Sustained atrial tachycardia in adult patients: electrophysiological characteristics, pharmacological response, possible mechanisms and effects of radiofrequency ablation. Circulation 1994;90:1262–1278.
Lindsay
Focal and Macroreentrant AT
3. Chen S-A, Tai C-T, Chiang C-E, Chiang C-E, Ding U-A, Chang MS. Focal atrial tachycardia: reanalysis of the clinical and electrophysiologic characteristics and prediction of successful radiofrequency ablation. J Cardiovasc Electrophysiol 1998;9:355–365. 4. Engelstein ED, Lippman N, Stein KM, Lerman BB. Mechanism-specific effects of adenosine on atrial tachycardia. Circulation 1994;89:2645–2654. 5. Markowitz SM, Stein KM, Mittal S, Slotwiner DJ, Lerman BB. Differential effects of adenosine on focal and macroreentrant atrial tachycardia. J Cardiovasc Electrophysiol 1999:10:489 –502. 6. Chiale PA, Garro HA, Schmidberg J, Sanchez RA, Acunzo RS, Lago M, Levy G, Levin M. Inappropriate sinus tachycardia may be related to an immunologic disorder involving cardiac beta andrenergic receptors. Heart Rhythm 2006;3: 1182–1186. 7. Shen WK, Low PA, Jahangir A, Munger TM, Friedman PA, Osborn MJ, Stanton MS, Packer DL, Rea RF, Hammill SC. Is sinus node modification appropriate for inappropriate sinus tachycardia with features of postural orthostatic tachycardia syndrome? Pacing Clin Electrophysiol 2001;24:217–230. 8. Kalman JM, Olgin JE, Karch MR, Hamdan M, Lee RJ, Lesh MD. “Cristal tachycardias”: origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol 1998;31:451– 459. 9. Ouyang F, Ma J, Ho SY, Bansch D, Schmidt B, Ernst S, Kuck KH, Liu S, Huang H, Chen M, Chun J, Xia Y, Satomi K, Chu H, Zhang S, Antz M. Focal atrial tachycardia originating from the non-coronary aortic sinus: electrophysiological characteristics and catheter ablation. J Am Coll Cardiol 2006;48:122–131. 10. Higa S, Tai CT, Lin YJ, Liu TY, Lee PC, Huang JL, Hsieh MH, Yuniadi Y, Huang BH, Lee SH, Ueng KC, Ding YA, Chen SA. Focal atrial tachycardia: new insight from noncontact mapping and catheter ablation. Circulation 2004; 109:84 –91. 11. Tang CW, Scheinman MM, Van Hare GF, Epstein LM, Fitzpatrick AP, Lee RJ, Lesh MD. Use of P wave configuration during atrial tachycardia to predict site of origin. J Am Coll Cardiol 1995;1315–1324. 12. Kistler PM, Roberts-Thomson KC, Haqqani HM, Fynn SP, Singarayar S, Vohra JK, Morton JB, Sparks PB, Kalman JM. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol 2006;48:1010 –1017. 13. Lewis T, Feil S, Stroud WD. Observations upon flutter and fibrillation. II. The nature of auricular flutter. Heart 1920;7:191–246. 14. Rosenblueth A, Garcia Ramos J. Studies on flutter and fibrillation: the influence of artificial obstacles on experimental auricular flutter. Am Heart J 1947;33: 677– 684. 15. Waldo AL, MacLean WA, Karp RB, Kouchoukos NT, James TN. Entrainment and interruption of atrial flutter with atrial pacing. Studies in man following open heart surgery. Circulation 1977;56:737–745. 16. Cosio FG, Lopez-Gil M, Giocolea A, Arribas F, Barroso JL. Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J Cardiol 1993;71:705–709.
1363 17. Treidman JK, Saul JP, Weindling SN, Walsh EP. Radiofrequency ablation of intra-atrial reentrant tachycardia after surgical palliation of congenital heart disease. Circulation 1995;91:707–714. 18. Baker BM, Lindsay BD, Bromberg BI, Frazier DW, Cain ME, Smith JM. Catheter ablation of clinical intraatrial reentrant tachycardias resulting from previous atrial surgery: localizing and transecting the critical isthmus. J Am Coll Cardiol 1996;28:411– 417. 19. Van Hare GF, Lesh MD, Ross BA, Perry JC, Dorostkar PC. Mapping and radiofrequency ablation of intraatrial reentrant tachycardia after the Senning or Mustard procedure for transposition of the treat arteries. Am J Cardiol 1996; 77:985–991. 20. Nakagawa H, Shah N, Matsudaira K, Overholt E, Chandrasekaran K, Beckman KJ, Spector P, Calame JD, Rao A, Hasdemir C, Otomo K, Wang Z, Lazzara R, Jackman WM. Characterization of reentrant circuit in macroreentrant right atrial tachycardia after surgical repair of congenital heart disease: isolated channels between scars allow “focal” ablation. Circulation 2001;103:699 –709. 21. Philippon F, Plumb VJ, Epstein AE, Kay GN. The risk of atrial fibrillation following radiofrequency catheter ablation of atrial flutter. Circulation 1995;92: 430 – 435. 22. Hsieh MH, Tai CT, Chiang CE, Tsai CF, Yu WC, Chen YJ, Ding YA, Chen SA. Recurrent atrial flutter and atrial fibrillation after catheter ablation of the cavotricuspid isthmus: a very long-term follow-up of 333 patients. J Interv Card Electrophysiol 2002;7:225–231. 23. Paydak H, Kall JG, Burke MC, Rubenstein D, Kopp DE, Verdino RJ, Wilber DJ, Atrial fibrillation after radiofrequency ablation of type I atrial flutter: time to onset, determinants, and clinical course. Circulation 1998;98:315–322. 24. Wazni O, Marrouche NF, Martin DO, Gillinov AM, Saliba W, Saad E, Klein A, Bhargava M, Bash D, Schweikert R, Erciyes D, Abdul-Karim A, Brachman J, Gunther J, Pisano E, Potenza D, Fanelli R, Natale A. Randomized study comparing combined pulmonary vein-left atrial junction disconnection and cavotricuspid isthmus ablation versus pulmonary vein-left atrial junction disconnection alone in patients presenting with typical atrial flutter and atrial fibrillation. Circulation 2003;108:2479 –2483. 25. Ortiz J, Niwano S, Abe H, Rudy Y, Johnson NJ, Waldo AL. Mapping the conversion of atrial flutter to atrial fibrillation and atrial fibrillation to atrial flutter: insights into mechanisms. Circ Res 1994;74:882– 894. 26. Ramanathan C, Jia P, Ghanem R, Ryu K, Rudy Y. Activation and repolarization of the normal human heart under complete physiological conditions. Proc Nat Acad Sci 2006;103:6309 – 6314. 27. Intini A, Goldstein RN, Jia P, Ramanathan C, Ryu K, Giannattasio B, Gilkeson R, Stambler BS, Brugada P, Stevenson WG, Rudy Y, Waldo AL. Electrocardiographic imaging (ECGI), a novel diagnostic modality used for mapping of focal left ventricular tachycardia in a young athlete. Heart Rhythm 2005;2: 1250 –1252. 28. Wang Y, Cuculich PS, Woodard PK, Lindsay BD, Rudy Y. Focal atrial tachycardia after pulmonary vein isolation: noninvasive mapping with electrocardiographic imaging (ECGI). Heart Rhythm 2007, in press.
Focal and macroreentrant atrial tachycardia: From bench to bedside and back to the bench again Bruce D. Lindsay, MD From the Department of Clinical Electrophysiology, Washington University School of Medicine, St. Louis, Missouri. A recent position document recommended that atrial arrhythmias be categorized as focal or macroreentrant on the basis of mechanisms and anatomic features.1 This classification reflects progress in understanding the pathophysiology of these arrhythmias and provides a practical basis for discussing their diagnostic features and treatment. Focal atrial tachycardias are characterized by a point source with concentric spread of activation from the origin. They appear to be caused by abnormal automaticity, microreentry, and triggered activity.2,3 The criteria to differentiate these mechanisms depend on the response to isoproterenol, programmed atrial stimulation, whether the onset is sudden or increases gradually, and the response to adenosine, propranolol, or other pharmacologic interventions.2–5 Triggered activity has been associated with delayed after-depolarizations recorded from monophasic action potential catheters. The diagnosis of microreentry depends on evidence of manifest and concealed entrainment. Other focal mechanisms require further study. Inappropriate sinus tachycardia and postural orthostatic tachycardia syndrome are probably caused by autonomic dysfunction. Recent evidence suggests that inappropriate sinus tachycardia is related to an immunologic disorder involving cardiac beta-receptor antibodies.6 This is an important distinction because they are often refractory to common pharmacologic interventions. Moreover, long-term outcomes are highly variable after sinus node ablation in patients with inappropriate sinus tachycardia, and the procedure is ineffective for those with postural orthostatic tachycardia.7 Multifocal atrial tachycardia is another difficult problem because it often occurs in patients with severe cardiopulmonary disease who are not candidates for electrophysiology study. Our clinical insights about the mechanisms and origins of multifocal tachycardia are limited. KEYWORDS Ablation; Atrial arrhythmias; Focal atrial tachycardia; Atrial flutter (Heart Rhythm 2007;4:1361–1363) Address reprint requests and correspondence: Bruce D. Lindsay, M.D., Professor of Medicine, Director, Clinical Electrophysiology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8086, St. Louis, MO 63110. E-mail address: [email protected].
The anatomic origin of focal atrial tachycardias is not an accurate predictor of the mechanism.3 Focal atrial tachycardias arise along the crista terminalis, in the right and left atrial appendages, within the coronary sinus, in the tissue bounded by Koch’s triangle, in the septum, in pulmonary veins, in the floor or roof of the left atrium, along the annulus of the tricuspid and mitral valves, and at the noncoronary aortic cusp.2,3,8 –10 One reason focal atrial tachycardias are attracting more attention is that they are a common cause of palpitations in patients who have undergone pulmonary vein antral isolation. In such cases, the origin may be located well outside the pulmonary vein antrum, and the severity of symptoms can necessitate a second ablation procedure. Studies have shown that the standard electrocardiogram (ECG) can predict the origin of focal atrial tachycardias.11,12 While the observations from these studies are useful, interpretation of the standard ECG is limited by several factors. Focal atrial tachycardias tend to be paroxysmal, which can make it difficult to obtain a representative recording. Even when recordings are available, the P wave may be buried within the T wave, which affects the accuracy of analysis. Under the best circumstances, there are limitations on the diagnostic accuracy of the standard ECG, and the criteria that have been developed may not be as accurate in the presence of significant underlying atrial enlargement or conduction delay. From a practical point of view, it is difficult to predict which medications will be most effective when the decision is based on ambulatory monitor recordings. Treatment with propranolol, calcium channel blockers, or other antiarrhythmic medications may be tried empirically. When medications are ineffective or poorly tolerated, many patients are referred for electrophysiology studies to determine whether the origin can be identified and ablated. The mechanism may determine how focal arrhythmias are induced, but successful ablation depends on the ability to identify the origin and reach the target. One factor limiting ablation of focal atrial tachycardias is that it may be difficult to induce the arrhythmia, which is a constraint for mapping and results in an unreliable endpoint by which the success of the procedure must be judged. Electroanatomic mapping helps the physician to navigate the catheter with greater appreci-
1547-5271/$ -see front matter © 2007 Heart Rhythm Society. All rights reserved.
doi:10.1016/j.hrthm.2007.05.024
1362 ation of the three-dimensional anatomy, but short runs of the arrhythmia or isolated beats make this approach extremely tedious. Noncontact mapping has the advantage of using a single beat to identify the origin, which is extremely useful in patients with arrhythmias that are nonsustained or difficult to induce.10 Atrial macroreentry can involve single reentrant loops or more complex figure-of-8 reentry. It is of particular historical interest that our understanding of these mechanisms dates back to the work of Lewis and coworkers,13 who were able to induce and study atrial reentry in canines. Rosenblueth and Garcia Ramos14 recognized the need for conduction block and demonstrated that the cycle length of reentry was affected by the length of a surgical incision around which their model of reentry circulated. Waldo et al’s15 seminal work in humans used entrainment to show that atrial flutter is a form of reentry with an excitable gap. Subsequent studies employed entrainment mapping to define the reentrant loop associated with common isthmus-dependent right atrial flutter, and Cosio et al16 demonstrated that this circuit could be interrupted by ablation of tissue within the isthmus. The mapping techniques and principles of entrainment that were established in these early studies have been extended to assess and treat other forms of atrial macroreentry. Other clinical studies have confirmed reentry around surgical scars in the left or right atrium in patients who have undergone operations for coronary artery disease, valvular heart disease, or reconstructive surgery required by congenital abnormalities.17–20 These circuits are referred to as lesion atrial reentry. The observations made during these studies show reentry around a region of conduction block, and it is often possible to demonstrate a zone of slow conduction within the reentrant circuit. Successful ablation depends on the use of activation and entrainment mapping to define the circuit, which is interrupted by ablation of tissue from a line of block to a conduction boundary. While this is often defined by an anatomic boundary, sometimes ablation is performed to connect adjacent scars separated by an isthmus of tissue that serves as a critical element of the circuit.20 The ability to ablate circuits associated with macroreentry has unveiled an interesting relationship between these arrhythmias and atrial fibrillation.20 –25 While in some cases atrial fibrillation is induced by macroreentry, the converse occurs frequently. Long-term follow-up of patients who have undergone ablation of typical isthmus-dependent right atrial flutter shows a propensity for them to develop atrial fibrillation. Those with a history of atrial fibrillation or structural heart disease are at greatest risk. In many cases, this becomes apparent in the laboratory or during short-term follow-up. Now that ablation of atrial fibrillation has become an important treatment for patients who have not responded to medications, focal and maccroreentant atrial arrhythmias have complicated long-term outcomes. In some cases, reentry occurs because linear lesions create zones of slow conduction but they fail to cause a line of block. Reentry
Heart Rhythm, Vol 4, No 10, October 2007 may circulate around or through the pulmonary veins, the mitral valve annulus, or through other regions of the left atrium that were subjected to ablation.
Future directions What does the future hold for the treatment of focal and macroreentrant atrial arrhythmias? As we reflect on the progress that has been made in recent decades, it is clear that our advances have depended on animal models and painstaking observations made in clinical laboratories. There is a genuine need for better antiarrhythmic drugs to treat patients who are not optimal candidates for invasive procedures or who would prefer to avoid this approach. Nonetheless, it is difficult to predict whether the next generation of antiarrhythmic medications will appreciably alter pharmacologic treatment. It is likely that ablation techniques will continue to evolve based on improved understanding of pathophysiology and advances in mapping technology and delivery of energy for ablation of critical tissue. The most challenging patients have arrhythmias that are difficult to induce, multiple arrhythmias, or circuits that are extremely complex. ECG imaging is a novel, noninvasive tool for imaging cardiac arrhythmia and defining electrophysiological properties.26 It combines multielectrode body surface ECG recordings with three-dimensional anatomical heart-torso imaging to reconstruct an epicardial electroanatomical map. Recently, ECG imaging has been used successfully to define the origins of ventricular and atrial arrhythmias.27,28 As this technology evolves, it might be feasible to take this technology to the next level so that we could capture transient arrhythmias during ambulatory monitoring, reference the recordings to a computed tomography scan, and predict the reentrant circuit or focal origin with a high degree of accuracy. This would facilitate ablation strategies in patients whose arrhythmias are difficult to induce or sustain. It might be feasible to target critical tissue based on the results of ambulatory ECG imaging alone in patients whose arrhythmias cannot be induced. Most of our work is directed toward treatment of arrhythmias when patients develop symptoms and seek our attention. The real question is, How can we prevent these arrhythmias from developing in the first place? Although some insights may be gained from observations made during electrophysiology studies, it is more likely that the answer rests in basic science. If we could develop safe and effective measures to prevent the development of arrhythmias, the downstream cost of treating them could be averted. Perhaps this is our next frontier.
References 1. Saoudi N, Cosio F, Walso A, Chen SA, Iesaka Y, Lesh M, Saksena S, Salerno J, Schoels W. Classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanism and anatomic bases: a statement from a joint expert group from the working group of arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. J Cardiovasc Electrophysiol 2001;12:852– 866. 2. Chen SA, Chiang CE, Yang CJ, Cheng CC, Wu TJ, Wang SP, Chiang BN, Chang MS. Sustained atrial tachycardia in adult patients: electrophysiological characteristics, pharmacological response, possible mechanisms and effects of radiofrequency ablation. Circulation 1994;90:1262–1278.
Lindsay
Focal and Macroreentrant AT
3. Chen S-A, Tai C-T, Chiang C-E, Chiang C-E, Ding U-A, Chang MS. Focal atrial tachycardia: reanalysis of the clinical and electrophysiologic characteristics and prediction of successful radiofrequency ablation. J Cardiovasc Electrophysiol 1998;9:355–365. 4. Engelstein ED, Lippman N, Stein KM, Lerman BB. Mechanism-specific effects of adenosine on atrial tachycardia. Circulation 1994;89:2645–2654. 5. Markowitz SM, Stein KM, Mittal S, Slotwiner DJ, Lerman BB. Differential effects of adenosine on focal and macroreentrant atrial tachycardia. J Cardiovasc Electrophysiol 1999:10:489 –502. 6. Chiale PA, Garro HA, Schmidberg J, Sanchez RA, Acunzo RS, Lago M, Levy G, Levin M. Inappropriate sinus tachycardia may be related to an immunologic disorder involving cardiac beta andrenergic receptors. Heart Rhythm 2006;3: 1182–1186. 7. Shen WK, Low PA, Jahangir A, Munger TM, Friedman PA, Osborn MJ, Stanton MS, Packer DL, Rea RF, Hammill SC. Is sinus node modification appropriate for inappropriate sinus tachycardia with features of postural orthostatic tachycardia syndrome? Pacing Clin Electrophysiol 2001;24:217–230. 8. Kalman JM, Olgin JE, Karch MR, Hamdan M, Lee RJ, Lesh MD. “Cristal tachycardias”: origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol 1998;31:451– 459. 9. Ouyang F, Ma J, Ho SY, Bansch D, Schmidt B, Ernst S, Kuck KH, Liu S, Huang H, Chen M, Chun J, Xia Y, Satomi K, Chu H, Zhang S, Antz M. Focal atrial tachycardia originating from the non-coronary aortic sinus: electrophysiological characteristics and catheter ablation. J Am Coll Cardiol 2006;48:122–131. 10. Higa S, Tai CT, Lin YJ, Liu TY, Lee PC, Huang JL, Hsieh MH, Yuniadi Y, Huang BH, Lee SH, Ueng KC, Ding YA, Chen SA. Focal atrial tachycardia: new insight from noncontact mapping and catheter ablation. Circulation 2004; 109:84 –91. 11. Tang CW, Scheinman MM, Van Hare GF, Epstein LM, Fitzpatrick AP, Lee RJ, Lesh MD. Use of P wave configuration during atrial tachycardia to predict site of origin. J Am Coll Cardiol 1995;1315–1324. 12. Kistler PM, Roberts-Thomson KC, Haqqani HM, Fynn SP, Singarayar S, Vohra JK, Morton JB, Sparks PB, Kalman JM. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol 2006;48:1010 –1017. 13. Lewis T, Feil S, Stroud WD. Observations upon flutter and fibrillation. II. The nature of auricular flutter. Heart 1920;7:191–246. 14. Rosenblueth A, Garcia Ramos J. Studies on flutter and fibrillation: the influence of artificial obstacles on experimental auricular flutter. Am Heart J 1947;33: 677– 684. 15. Waldo AL, MacLean WA, Karp RB, Kouchoukos NT, James TN. Entrainment and interruption of atrial flutter with atrial pacing. Studies in man following open heart surgery. Circulation 1977;56:737–745. 16. Cosio FG, Lopez-Gil M, Giocolea A, Arribas F, Barroso JL. Radiofrequency ablation of the inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J Cardiol 1993;71:705–709.
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