- Email: [email protected]
Ventricular allorhythmia during infarct-related ventricular tachycardia
Available online at www.sciencedirect.com
Journal of Electrocardiology 45 (2012) 394 – 397 www.jecgonline.com
Ventricular allorhythmia during infarct-related ventricular tachycardia☆ Michael Peyrol, MD, a,⁎ Pascal Sbragia, MD, a Morgane Orabona, MD, a Anne-Claire Casalta, MD, a Marc Laine, MD, a Alexandre Decourt, MD, a Amandine Quatre, MD, a Alexis Jacquier, MD, b Nazirou Dodo Siddo, MD, a Franck Paganelli, MD a a
Department of Cardiology, Centre Hospitalier Universitaire Nord, Marseille, France Department of Radiology, Centre Hospitalier Universitaire Nord, Marseille, France Received 26 December 2011
b
Abstract
Ventricular allorhythmia is an electrocardiogram feature leading to a pattern of “regularly irregular” arrhythmia mainly reported during non–life-threatening organized atrial tachycardia. We report the infrequent case of a patient presenting with ventricular allorhythmia during infarct-related ventricular tachycardia. The potential mechanisms of this tachycardia are discussed. © 2012 Elsevier Inc. All rights reserved.
Keywords:
Electrocardiogram; Ventricular tachycardia; Sudden cardiac death
Case report A 78-year-old patient without known cardiac disease was referred to our intensive care unit for presyncopal wide-QRS tachycardia. Hemodynamic status was unstable, with a mean arterial pressure of 45 mm Hg. The mean heart rate was 180 beats/min. Initial electrocardiogram (ECG) showed wide-QRS tachycardia with right bundlebranch block-like configuration and left-axis deviation (Fig. 1A). QRS duration was 140 milliseconds. During tachycardia, ventricular allorhythmia due to repeated sequence of 5 “short” 320-millisecond R-R cycles followed by 1 “long” 400-millisecond R-R cycle was observed, leading to a regularly irregular tachycardia pattern (Fig. 1B). Atrioventricular dissociation in inferior leads and in precordial lead V1 was easily recognized. An R- to S-interval duration in precordial lead V4 of 110 milliseconds was noted. These previously mentioned ECG patterns were consistent with the diagnosis of ventricular tachycardia (VT). 1 Otherwise, concerning QRS morphology, monophasic R wave in lead V1 was found, which rendered the diagnosis of supraventricular tachycardia with aberrant conduction very unlikely, as reported by Wellens et al. 2 After external direct current cardioversion, the sinus rhythm ECG showed old inferior and lateral myocardial infarction (Fig. 2A). Thereafter, cardiac magnetic reso☆
Conflict of interest: None. ⁎ Corresponding author. Department of Cardiology, Centre Hospitalier Universitaire Nord, Marseille, France. E-mail address: [email protected] 0022-0736/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2012.02.006
nance imaging (MRI) was performed and confirmed the diagnosis of ischemic heart disease with transmural late enhancement of inferior, posterior, and lateral left ventricular regions (Fig. 2B, C). Left ventricular ejection fraction was severely depressed at 28%. A single-chamber implantable cardioverter-defibrillator (ICD) was performed in the present patient for secondary prevention of sudden cardiac death according to current guidelines. 3
Discussion We report here a rare case of ventricular allorhythmia occurring during infarct-related VT. Allorhythmia is an ECG feature mainly reported during regular atrial tachycardia or atrial flutter. In these cases, this ECG pattern is due to “alternating Wenckebach” conduction through the atrioventricular node. 4,5 In patients with ischemic heart disease, most VTs are due to reentry around fixed regions of infarction or conduction block. Therefore, infarct-related VTs are stable and show highly regular wide-QRS tachycardia. From an electrophysiologic standpoint, an isthmus exhibiting slow conduction velocity and located within the region of infarction is critical for the maintenance of the reentrant circuit. 3,6 The depolarization of the isthmus is not seen on the surface ECG. Indeed, the QRS complex morphology during tachycardia only indicates the location of the reentry circuit exit. At this point, the depolarization wavefront leaves the end of the isthmus and propagates through the ventricles. In the present patient, the QRS morphology remained
M. Peyrol et al. / Journal of Electrocardiology 45 (2012) 394–397
395
A
B
600
400
320
600 320
320
600 320
320
600
400
600 320
320
600 320
320
600 320
400
600 320
320
320
320
320
Fig. 1. A, Twelve-lead ECG showing wide-QRS tachycardia with right bundle-branch block-like configuration and left-axis deviation. Electrocardiogram criteria for VT were as follows: monophasic R wave in lead V1, an R- to S-interval duration in precordial lead V4 of 110 milliseconds, and atrioventricular dissociation in inferior leads and in precordial lead V1. B, Ventricular allorhythmia during tachycardia. A short R-R cycle duration was 320 milliseconds (blue), and a long R-R cycle duration was 400 milliseconds (red). Atrial activity showing sinus tachycardia, with positive P waves in leads I and II and a cycle length of 600 milliseconds, is noted (black lines).
unchanged after a short and long R-R cycle. Thus, in this case, the reentry circuit exit was stable and fixed. Therefore, to explain the long R-R cycles and, thus, R-R cycle irregularity during VT, we have to admit that there were not 1 but 2 reentry circuit entrances. The R-R cycle length depended on the importance of the slow conduction area that the depolarization wavefront had to cross to leave the isthmus. 6,7 Before the long R-R cycle, the reentry circuit entrance was more proximal and led to a substantial longer slow conduction area to cross through the isthmus for the propagating wavefront. Otherwise, according to right bundle-branch block-like configuration and left-axis deviation during VT, a left posterior fascicular origin could be discussed. Fascicular left ventricular VT usually considered as a benign entity with excellent prognostic was first recognized by Zipes et al 8 in patients exhibiting the following diagnostic triad: right bundle-branch block-like configuration and left-axis deviation during VT, induction with atrial pacing, and absence of underlying heart disease. Few years later, Belhassen et al 9 demonstrated the verapamil sensitivity of
the arrhythmia. More recently, different studies reported cases of patients with a rare form of ischemia-induced fascicular VT. 10,11 In these patients, foci of ischemiainduced heart disease in inferior and anteroseptal wall disease could be linked with the development of left posterior fascicular and anterior fascicular VT, respectively. Electrophysiologic studies were performed to validate the involvement of left bundle–Purkinje system during VT. Nevertheless, in the present patient, the fascicular origin of the VT seems very unlikely because it appears improbable, on the account of a large scar of posterior and lateral myocardial infarction on cardiac MRI images, that myocardial ischemia solely involved the left posterior perifascicular region and, thus, led to a pure reentrant fascicular mechanism during VT. 12 Lastly, in the present patient who received an ICD, the “regular irregular” arrhythmia might lead to failure in the detection of recurrent VT if stability criteria were applied. The latter has been designed to minimize inappropriate detection and ICD therapies of supraventricular tachycardia with R-R instability, mainly, atrial fibrillation. In this
396
M. Peyrol et al. / Journal of Electrocardiology 45 (2012) 394–397
A
B
C
Fig. 2. A, Twelve-lead sinus rhythm ECG with an aspect of old posterior and lateral myocardial infarction. B and C, Four-chamber and short-axis views during cardiac MRI with transmural enhancement of the posterior and lateral left ventricular regions (black arrows) consistent with old myocardial infarction.
setting, underdetection due to irregular R-R intervals can be produced by 2 mechanisms: long R-R intervals that exceed the VT detection interval and oscillations of the cycle length longer than the usually 40-millisecond programed stability. 13 This should influence discrimination algorithm adjustment of the device. Otherwise, concerning ICD therapy for spontaneous arrhythmias, antitachycardia pacing, 8-pulse burst pacing train at 88% of the VT cycle length, was reported to be very effective for termination of slow (N320-millisecond cycle length) and fast (b320millisecond cycle length) reentrant VT in the PainFREE trial. 14 The application of antitachycardia pacing for arrhythmia termination in patients with regularly irregular infarct-related VT needs to be further investigated. Conclusion In conclusion, this case demonstrates that ventricular allorhythmia, mainly reported during non–life-threatening organized atrial arrhythmia, may be observed during scarrelated VT and must not lead to misdiagnosis of such potentially lethal rhythm disorder. This ECG feature might influence discrimination algorithms and tiered therapy adjustment of the ICD. References 1. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649.
2. Wellens HJ, Bär FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978;64:27. 3. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006;48:e247. 4. Slama R, Leclercq JF, Rosengarten M, Coumel P, Bouvrain Y. Multilevel block in the atrioventricular node during atrial tachycardia and flutter alternating with Wenckebach phenomenon. Br Heart J 1979;42:463. 5. Littmann L, Svenson RH. Atrioventricular alternating Wenckebach periodicity: conduction patterns in multilevel block. Am J Cardiol 1982;49:855. 6. Stevenson WG, Friedman PL, Sager PT, et al. Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping. J Am Coll Cardiol 1997;29:1180. 7. Oreto G, Satullo G, Luzza F, Donato A, Scimone IM, Cavalli A. Irregular ventricular tachycardia: a possible manifestation of longitudinal dissociation within the reentry pathway. Am Heart J 1992;124: 1506. 8. Zipes DP, Foster PR, Troup PJ, Pedersen DH. Atrial induction of ventricular tachycardia: reentry versus triggered automaticity. Am J Cardiol 1979;44:1. 9. Belhassen B, Shapira I, Pelleg A, Copperman I, Kauli N, Laniado S. Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil: an ECG-electrophysiologic entity. Am Heart J 1984;108(4 Pt 1):1034. 10. Reithmann C, Hahnefeld A, Remp T, Steinbeck G. Ventricular tachycardia with participation of the left bundle–Purkinje system in patients with structural heart disease: identification of slow conduction during sinus rhythm. J Cardiovasc Electrophysiol 2007;18:808.
M. Peyrol et al. / Journal of Electrocardiology 45 (2012) 394–397 11. Ventura R, Steven D, Klemm HU, et al. Decennial follow-up in patients with recurrent tachycardia originating from the right ventricular outflow tract: electrophysiologic characteristics and response to treatment. Eur Heart J 2007;28:2338. 12. Jane-Wit D, Batsford W, Malm B. Ischemic etiology for adenosine-sensitive fascicular tachycardia. J Electrocardiol 2011; 44:217.
397
13. García-Alberola A, Yli-Mäyry S, Block M, et al. RR interval variability in irregular monomorphic ventricular tachycardia and atrial fibrillation. Circulation 1996;93:295. 14. Wathen MS, Sweeney MO, DeGroot PJ, et al. PainFREE Investigators. Shock reduction using antitachycardia pacing for spontaneous rapid ventricular tachycardia in patients with coronary artery disease. Circulation 2001;104:796.
Journal of Electrocardiology 45 (2012) 394 – 397 www.jecgonline.com
Ventricular allorhythmia during infarct-related ventricular tachycardia☆ Michael Peyrol, MD, a,⁎ Pascal Sbragia, MD, a Morgane Orabona, MD, a Anne-Claire Casalta, MD, a Marc Laine, MD, a Alexandre Decourt, MD, a Amandine Quatre, MD, a Alexis Jacquier, MD, b Nazirou Dodo Siddo, MD, a Franck Paganelli, MD a a
Department of Cardiology, Centre Hospitalier Universitaire Nord, Marseille, France Department of Radiology, Centre Hospitalier Universitaire Nord, Marseille, France Received 26 December 2011
b
Abstract
Ventricular allorhythmia is an electrocardiogram feature leading to a pattern of “regularly irregular” arrhythmia mainly reported during non–life-threatening organized atrial tachycardia. We report the infrequent case of a patient presenting with ventricular allorhythmia during infarct-related ventricular tachycardia. The potential mechanisms of this tachycardia are discussed. © 2012 Elsevier Inc. All rights reserved.
Keywords:
Electrocardiogram; Ventricular tachycardia; Sudden cardiac death
Case report A 78-year-old patient without known cardiac disease was referred to our intensive care unit for presyncopal wide-QRS tachycardia. Hemodynamic status was unstable, with a mean arterial pressure of 45 mm Hg. The mean heart rate was 180 beats/min. Initial electrocardiogram (ECG) showed wide-QRS tachycardia with right bundlebranch block-like configuration and left-axis deviation (Fig. 1A). QRS duration was 140 milliseconds. During tachycardia, ventricular allorhythmia due to repeated sequence of 5 “short” 320-millisecond R-R cycles followed by 1 “long” 400-millisecond R-R cycle was observed, leading to a regularly irregular tachycardia pattern (Fig. 1B). Atrioventricular dissociation in inferior leads and in precordial lead V1 was easily recognized. An R- to S-interval duration in precordial lead V4 of 110 milliseconds was noted. These previously mentioned ECG patterns were consistent with the diagnosis of ventricular tachycardia (VT). 1 Otherwise, concerning QRS morphology, monophasic R wave in lead V1 was found, which rendered the diagnosis of supraventricular tachycardia with aberrant conduction very unlikely, as reported by Wellens et al. 2 After external direct current cardioversion, the sinus rhythm ECG showed old inferior and lateral myocardial infarction (Fig. 2A). Thereafter, cardiac magnetic reso☆
Conflict of interest: None. ⁎ Corresponding author. Department of Cardiology, Centre Hospitalier Universitaire Nord, Marseille, France. E-mail address: [email protected] 0022-0736/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2012.02.006
nance imaging (MRI) was performed and confirmed the diagnosis of ischemic heart disease with transmural late enhancement of inferior, posterior, and lateral left ventricular regions (Fig. 2B, C). Left ventricular ejection fraction was severely depressed at 28%. A single-chamber implantable cardioverter-defibrillator (ICD) was performed in the present patient for secondary prevention of sudden cardiac death according to current guidelines. 3
Discussion We report here a rare case of ventricular allorhythmia occurring during infarct-related VT. Allorhythmia is an ECG feature mainly reported during regular atrial tachycardia or atrial flutter. In these cases, this ECG pattern is due to “alternating Wenckebach” conduction through the atrioventricular node. 4,5 In patients with ischemic heart disease, most VTs are due to reentry around fixed regions of infarction or conduction block. Therefore, infarct-related VTs are stable and show highly regular wide-QRS tachycardia. From an electrophysiologic standpoint, an isthmus exhibiting slow conduction velocity and located within the region of infarction is critical for the maintenance of the reentrant circuit. 3,6 The depolarization of the isthmus is not seen on the surface ECG. Indeed, the QRS complex morphology during tachycardia only indicates the location of the reentry circuit exit. At this point, the depolarization wavefront leaves the end of the isthmus and propagates through the ventricles. In the present patient, the QRS morphology remained
M. Peyrol et al. / Journal of Electrocardiology 45 (2012) 394–397
395
A
B
600
400
320
600 320
320
600 320
320
600
400
600 320
320
600 320
320
600 320
400
600 320
320
320
320
320
Fig. 1. A, Twelve-lead ECG showing wide-QRS tachycardia with right bundle-branch block-like configuration and left-axis deviation. Electrocardiogram criteria for VT were as follows: monophasic R wave in lead V1, an R- to S-interval duration in precordial lead V4 of 110 milliseconds, and atrioventricular dissociation in inferior leads and in precordial lead V1. B, Ventricular allorhythmia during tachycardia. A short R-R cycle duration was 320 milliseconds (blue), and a long R-R cycle duration was 400 milliseconds (red). Atrial activity showing sinus tachycardia, with positive P waves in leads I and II and a cycle length of 600 milliseconds, is noted (black lines).
unchanged after a short and long R-R cycle. Thus, in this case, the reentry circuit exit was stable and fixed. Therefore, to explain the long R-R cycles and, thus, R-R cycle irregularity during VT, we have to admit that there were not 1 but 2 reentry circuit entrances. The R-R cycle length depended on the importance of the slow conduction area that the depolarization wavefront had to cross to leave the isthmus. 6,7 Before the long R-R cycle, the reentry circuit entrance was more proximal and led to a substantial longer slow conduction area to cross through the isthmus for the propagating wavefront. Otherwise, according to right bundle-branch block-like configuration and left-axis deviation during VT, a left posterior fascicular origin could be discussed. Fascicular left ventricular VT usually considered as a benign entity with excellent prognostic was first recognized by Zipes et al 8 in patients exhibiting the following diagnostic triad: right bundle-branch block-like configuration and left-axis deviation during VT, induction with atrial pacing, and absence of underlying heart disease. Few years later, Belhassen et al 9 demonstrated the verapamil sensitivity of
the arrhythmia. More recently, different studies reported cases of patients with a rare form of ischemia-induced fascicular VT. 10,11 In these patients, foci of ischemiainduced heart disease in inferior and anteroseptal wall disease could be linked with the development of left posterior fascicular and anterior fascicular VT, respectively. Electrophysiologic studies were performed to validate the involvement of left bundle–Purkinje system during VT. Nevertheless, in the present patient, the fascicular origin of the VT seems very unlikely because it appears improbable, on the account of a large scar of posterior and lateral myocardial infarction on cardiac MRI images, that myocardial ischemia solely involved the left posterior perifascicular region and, thus, led to a pure reentrant fascicular mechanism during VT. 12 Lastly, in the present patient who received an ICD, the “regular irregular” arrhythmia might lead to failure in the detection of recurrent VT if stability criteria were applied. The latter has been designed to minimize inappropriate detection and ICD therapies of supraventricular tachycardia with R-R instability, mainly, atrial fibrillation. In this
396
M. Peyrol et al. / Journal of Electrocardiology 45 (2012) 394–397
A
B
C
Fig. 2. A, Twelve-lead sinus rhythm ECG with an aspect of old posterior and lateral myocardial infarction. B and C, Four-chamber and short-axis views during cardiac MRI with transmural enhancement of the posterior and lateral left ventricular regions (black arrows) consistent with old myocardial infarction.
setting, underdetection due to irregular R-R intervals can be produced by 2 mechanisms: long R-R intervals that exceed the VT detection interval and oscillations of the cycle length longer than the usually 40-millisecond programed stability. 13 This should influence discrimination algorithm adjustment of the device. Otherwise, concerning ICD therapy for spontaneous arrhythmias, antitachycardia pacing, 8-pulse burst pacing train at 88% of the VT cycle length, was reported to be very effective for termination of slow (N320-millisecond cycle length) and fast (b320millisecond cycle length) reentrant VT in the PainFREE trial. 14 The application of antitachycardia pacing for arrhythmia termination in patients with regularly irregular infarct-related VT needs to be further investigated. Conclusion In conclusion, this case demonstrates that ventricular allorhythmia, mainly reported during non–life-threatening organized atrial arrhythmia, may be observed during scarrelated VT and must not lead to misdiagnosis of such potentially lethal rhythm disorder. This ECG feature might influence discrimination algorithms and tiered therapy adjustment of the ICD. References 1. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649.
2. Wellens HJ, Bär FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978;64:27. 3. Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006;48:e247. 4. Slama R, Leclercq JF, Rosengarten M, Coumel P, Bouvrain Y. Multilevel block in the atrioventricular node during atrial tachycardia and flutter alternating with Wenckebach phenomenon. Br Heart J 1979;42:463. 5. Littmann L, Svenson RH. Atrioventricular alternating Wenckebach periodicity: conduction patterns in multilevel block. Am J Cardiol 1982;49:855. 6. Stevenson WG, Friedman PL, Sager PT, et al. Exploring postinfarction reentrant ventricular tachycardia with entrainment mapping. J Am Coll Cardiol 1997;29:1180. 7. Oreto G, Satullo G, Luzza F, Donato A, Scimone IM, Cavalli A. Irregular ventricular tachycardia: a possible manifestation of longitudinal dissociation within the reentry pathway. Am Heart J 1992;124: 1506. 8. Zipes DP, Foster PR, Troup PJ, Pedersen DH. Atrial induction of ventricular tachycardia: reentry versus triggered automaticity. Am J Cardiol 1979;44:1. 9. Belhassen B, Shapira I, Pelleg A, Copperman I, Kauli N, Laniado S. Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil: an ECG-electrophysiologic entity. Am Heart J 1984;108(4 Pt 1):1034. 10. Reithmann C, Hahnefeld A, Remp T, Steinbeck G. Ventricular tachycardia with participation of the left bundle–Purkinje system in patients with structural heart disease: identification of slow conduction during sinus rhythm. J Cardiovasc Electrophysiol 2007;18:808.
M. Peyrol et al. / Journal of Electrocardiology 45 (2012) 394–397 11. Ventura R, Steven D, Klemm HU, et al. Decennial follow-up in patients with recurrent tachycardia originating from the right ventricular outflow tract: electrophysiologic characteristics and response to treatment. Eur Heart J 2007;28:2338. 12. Jane-Wit D, Batsford W, Malm B. Ischemic etiology for adenosine-sensitive fascicular tachycardia. J Electrocardiol 2011; 44:217.
397
13. García-Alberola A, Yli-Mäyry S, Block M, et al. RR interval variability in irregular monomorphic ventricular tachycardia and atrial fibrillation. Circulation 1996;93:295. 14. Wathen MS, Sweeney MO, DeGroot PJ, et al. PainFREE Investigators. Shock reduction using antitachycardia pacing for spontaneous rapid ventricular tachycardia in patients with coronary artery disease. Circulation 2001;104:796.