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Intermittent capture of the right ventricular outflow tract by atrial pacing in a patient with a dual-chamber pacemaker
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Journal of Electrocardiology 45 (2012) 787 – 789 www.jecgonline.com
Intermittent capture of the right ventricular outflow tract by atrial pacing in a patient with a dual-chamber pacemaker Julio Daniel Pastori, MD, a,⁎ Hugo Ariel Garro, MD, a Adrián Baranchuk, MD, b Pablo Ambrosio Chiale, MD a a
División Cardiología, Centro de Arritmias Cardíacas de la Ciudad Autónoma de Buenos Aires, Hospital General de Agudos J.M. Ramos Mejía, Buenos Aires, Argentina b Heart Rhythm Service, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada Received 7 May 2012
Abstract
We describe a previously unreported phenomenon of intermittent outflow right ventricular tract capture from the atrial lead of a dual-chamber pacemaker. This was more obvious at slower paced atrial rates and disappeared by decreasing the atrial pulses voltage. Electroanatomical mapping showed that the onset of activation was nearly simultaneous at the insertion site of the atrial lead and at an intermediate level of the right ventricular outflow tract. This exceptional finding might be erroneously diagnosed as due to pseudo-pseudo fusion beats. © 2012 Elsevier Inc. All rights reserved.
Keywords:
Cardiac pacemakers; Atrial lead; Ventricular pacing
Introduction In patients with dual-chamber pacemakers, right ventricular pacing from the atrial lead usually results from dislodgment and displacement of the atrial lead into the right ventricle, which is accompanied by a characteristic sequence of electrocardiographic findings. 1 In this article, we describe a previously unreported phenomenon of intermittent right ventricular outflow capture from the atrial lead placed in the anterior and medial right atrium. Case description A 58-year-old woman with Chagas heart disease and symptomatic sinus node dysfunction underwent dualchamber DDDR pacemaker (Axios 04 Biotronik - Woermannkehre 1, D - 12359, Berlin, Germany) implantation. Six years after implantation, an elevation of the atrial stimulation threshold was detected during her last visit. This happened at anytime during the previous 6 months, as it was not detected in her prior visits. The atrial threshold (0.6 V at implantation) varied between 1.2 and 1.4 V and rose to 2.0 V in the last ⁎ Corresponding author. Centro de Arritmias Cardíacas de la Ciudad Autónoma de Buenos Aires, División Cardiología, Hospital General de Agudos J.M. Ramos Mejía, General Urquiza 609, 1221 Buenos Aires, Argentina. E-mail addresses: [email protected], centrodearritmias@fibertel.com.ar 0022-0736/$ – see front matter © 2012 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jelectrocard.2012.06.018
visit. Consequently, the atrial stimulation voltage (in bipolar mode) was reprogrammed from 2.5 to 4.0 V. Two months later, the patient was referred to our clinic due to atypical chest pain. The electrocardiogram showed some atrial stimuli capturing the ventricle (Fig. 1). The paced QRS complexes displayed a “left bundle branch block pattern” with AQRS at +50º and transition in the precordial leads between V3 and V4, suggesting that the site of origin was at a not-too-high level of the right ventricular outflow tract. The presence of ventricular stimuli with a shortened AV interval (110 milliseconds) into the wide QRS complexes was considered to be “safety pacing.” Pseudofusion (Fig. 1A) and fusion (Fig. 1B) beats due to simultaneous propagation by the conduction system and the ventricular apex pacing were also observed. The intermittent ventricular capture by atrial stimuli was more frequently observed at slower paced atrial rates. An increase in pacing rate was provoked (Fig. 1B) to exclude the possibility that the wide QRS complexes coinciding with atrial stimuli could be due to automatic ventricular activity. This abnormality disappeared by reducing the atrial pulses voltage. Pacemaker reprogramming with a shorter AV interval than that showed in Fig. 1 (120 milliseconds) evoked QRS complexes with the typical electrocardiographic pattern of right ventricular apical pacing (not shown). A chest x-ray depicted the atrial electrode lead in an anterior and medial position rather than in the right appendage. The atrial electrode
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J.D. Pastori et al. / Journal of Electrocardiology 45 (2012) 787–789
Fig. 1. A,Twelve-lead electrocardiogram (ECG) recording obtained during DDD pacing at a basic rate of 40 beats/min with an AV interval of 200 milliseconds. Ventricular pseudo fusion beats are observed in the first and third beats. In beats 2, 4, and 5, atrial stimuli are followed by wide QRS complexes without a discernible latency period. The electrocardiographic pattern of these ectopic ventricular beats suggests a right ventricular outflow tract origin. A stimulus is also apparent within the QRS complexes with a shorter AV interval (“safety pacing”). B, Twelve-lead ECG recording obtained after increasing the paced atrial rate to 60 beats/min and shortening the AV interval to 150 milliseconds. The sequence of events persists as in panel A, but the first, fourth, and seventh beats show fusion QRS complexes caused by excitatory waves arising from normal AV conduction and from right ventricular apical pacing (compare with panel A).
impedance and sensitivity were normal, and the atrial electrogram did not exhibit prominent far-field ventricular potentials (Fig. 2). To understand the activation sequence, an electroanatomical mapping of activation of the right cardiac chambers was performed with the EnSite NavX system (St Jude Medical, ST Paul, MN, USA) after appropriate adjustments of atrial voltage. In those beats whose ventricular depolarization was elicited by the atrial stimuli, the onset of activation was nearly simultaneous at the level of the atrial lead insertion site and at an intermediate level of the right ventricular outflow tract. Noteworthy, propagation of ventricular excitatory wave was faster toward its upper area than toward the apex (Fig. 3).
Discussion The existence of “pseudo-pseudo fusion” beats, a coincidence between atrial stimuli and ventricular ectopic beats, 2 was disregarded because the abnormal findings reported in this article persisted at different paced atrial rates and disappeared when atrial stimuli voltage was decreased. An accessory myocardial connection between the atrial stimulation site and the right ventricle, with intermittent conduction, can be also ruled out because of the following reasons: 1. The virtual inexistence of a discernible interval between the atrial stimulus and the onset of premature right ventricular activation
Fig. 2. Atrial and ventricular electrograms and marker channels during atrial stimulation with 1:1 atrioventricular conduction. A indicates atrial pacing; R, ventricular sensing. The atrial electrogram exhibits a very small far-field ventricular potential, which is not detected and does not induce any annotation in the atrial channel.
J.D. Pastori et al. / Journal of Electrocardiology 45 (2012) 787–789
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Fig. 3. Electroanatomic activation mapping of the right atrium (RA) and ventricle (RV) during right atrial pacing causing premature ventricular beats, in a left anterior oblique view at approximately 30º. The color code indicates, from white to purple, the propagation of the activation process. It initiates in the right atrium (white) and immediately propagates to the atrial adjacent tissue and the right ventricular outflow tract (red) with faster activation of the high right ventricular outflow tract (yellow) than of the apical region (green, blue, and purple). RAA indicates right atrial appendage; SVC, superior vena cava.
2. The consistent suppression of right ventricular outflow tract premature activation when the voltage of the atrial stimuli was decreased The latter leads to speculate on the possible role of premature stimulation of the right ventricular outflow tract because of an excitatory field of greater magnitude caused by the rise of the output voltage in the atrial channel. However, the presence of an enhanced excitability area in the site of the right ventricle simultaneously activated with atrial stimulation cannot be completely ruled out. The electroanatomical mapping confirmed that the right ventricular activation was faster toward the upper part of the right ventricular outflow tract than toward its apical region. This could be due to dissimilar regional electrophysiologic properties of the right ventricular myocardium caused, to some extent, by Chagas disease right ventricular involvement. 3
Acknowledgments We are indebted to Dr Javier Banchs, MD, for his useful comments and suggestions to the manuscript. This work was supported, in part, by the Fundación de Investigaciones Cardiológicas Einthoven and the Consejo de Investigación en Salud, Ministry of Health, Government of Buenos Aires City. References 1. Kiviniemi MS, Pirnes MA, Eramen HJ, et al. Complications related to permanent pacemaker therapy. Pacing Clin Electrophysiol 1999;22:711. 2. Levine PA, Seltzer JP. Fusion, pseudofusion, pseudo-pseudofusion and confusion: normal rhythms associated with atrioventricular sequential DVI pacing. Clin Prog Pacing and Electrophysiol 1983;1:70. 3. Rosenbaum MB. Chagasic myocardiopathy. Prog Cardiovasc Dis 1964; 7:199.
Journal of Electrocardiology 45 (2012) 787 – 789 www.jecgonline.com
Intermittent capture of the right ventricular outflow tract by atrial pacing in a patient with a dual-chamber pacemaker Julio Daniel Pastori, MD, a,⁎ Hugo Ariel Garro, MD, a Adrián Baranchuk, MD, b Pablo Ambrosio Chiale, MD a a
División Cardiología, Centro de Arritmias Cardíacas de la Ciudad Autónoma de Buenos Aires, Hospital General de Agudos J.M. Ramos Mejía, Buenos Aires, Argentina b Heart Rhythm Service, Kingston General Hospital, Queen's University, Kingston, Ontario, Canada Received 7 May 2012
Abstract
We describe a previously unreported phenomenon of intermittent outflow right ventricular tract capture from the atrial lead of a dual-chamber pacemaker. This was more obvious at slower paced atrial rates and disappeared by decreasing the atrial pulses voltage. Electroanatomical mapping showed that the onset of activation was nearly simultaneous at the insertion site of the atrial lead and at an intermediate level of the right ventricular outflow tract. This exceptional finding might be erroneously diagnosed as due to pseudo-pseudo fusion beats. © 2012 Elsevier Inc. All rights reserved.
Keywords:
Cardiac pacemakers; Atrial lead; Ventricular pacing
Introduction In patients with dual-chamber pacemakers, right ventricular pacing from the atrial lead usually results from dislodgment and displacement of the atrial lead into the right ventricle, which is accompanied by a characteristic sequence of electrocardiographic findings. 1 In this article, we describe a previously unreported phenomenon of intermittent right ventricular outflow capture from the atrial lead placed in the anterior and medial right atrium. Case description A 58-year-old woman with Chagas heart disease and symptomatic sinus node dysfunction underwent dualchamber DDDR pacemaker (Axios 04 Biotronik - Woermannkehre 1, D - 12359, Berlin, Germany) implantation. Six years after implantation, an elevation of the atrial stimulation threshold was detected during her last visit. This happened at anytime during the previous 6 months, as it was not detected in her prior visits. The atrial threshold (0.6 V at implantation) varied between 1.2 and 1.4 V and rose to 2.0 V in the last ⁎ Corresponding author. Centro de Arritmias Cardíacas de la Ciudad Autónoma de Buenos Aires, División Cardiología, Hospital General de Agudos J.M. Ramos Mejía, General Urquiza 609, 1221 Buenos Aires, Argentina. E-mail addresses: [email protected], centrodearritmias@fibertel.com.ar 0022-0736/$ – see front matter © 2012 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jelectrocard.2012.06.018
visit. Consequently, the atrial stimulation voltage (in bipolar mode) was reprogrammed from 2.5 to 4.0 V. Two months later, the patient was referred to our clinic due to atypical chest pain. The electrocardiogram showed some atrial stimuli capturing the ventricle (Fig. 1). The paced QRS complexes displayed a “left bundle branch block pattern” with AQRS at +50º and transition in the precordial leads between V3 and V4, suggesting that the site of origin was at a not-too-high level of the right ventricular outflow tract. The presence of ventricular stimuli with a shortened AV interval (110 milliseconds) into the wide QRS complexes was considered to be “safety pacing.” Pseudofusion (Fig. 1A) and fusion (Fig. 1B) beats due to simultaneous propagation by the conduction system and the ventricular apex pacing were also observed. The intermittent ventricular capture by atrial stimuli was more frequently observed at slower paced atrial rates. An increase in pacing rate was provoked (Fig. 1B) to exclude the possibility that the wide QRS complexes coinciding with atrial stimuli could be due to automatic ventricular activity. This abnormality disappeared by reducing the atrial pulses voltage. Pacemaker reprogramming with a shorter AV interval than that showed in Fig. 1 (120 milliseconds) evoked QRS complexes with the typical electrocardiographic pattern of right ventricular apical pacing (not shown). A chest x-ray depicted the atrial electrode lead in an anterior and medial position rather than in the right appendage. The atrial electrode
788
J.D. Pastori et al. / Journal of Electrocardiology 45 (2012) 787–789
Fig. 1. A,Twelve-lead electrocardiogram (ECG) recording obtained during DDD pacing at a basic rate of 40 beats/min with an AV interval of 200 milliseconds. Ventricular pseudo fusion beats are observed in the first and third beats. In beats 2, 4, and 5, atrial stimuli are followed by wide QRS complexes without a discernible latency period. The electrocardiographic pattern of these ectopic ventricular beats suggests a right ventricular outflow tract origin. A stimulus is also apparent within the QRS complexes with a shorter AV interval (“safety pacing”). B, Twelve-lead ECG recording obtained after increasing the paced atrial rate to 60 beats/min and shortening the AV interval to 150 milliseconds. The sequence of events persists as in panel A, but the first, fourth, and seventh beats show fusion QRS complexes caused by excitatory waves arising from normal AV conduction and from right ventricular apical pacing (compare with panel A).
impedance and sensitivity were normal, and the atrial electrogram did not exhibit prominent far-field ventricular potentials (Fig. 2). To understand the activation sequence, an electroanatomical mapping of activation of the right cardiac chambers was performed with the EnSite NavX system (St Jude Medical, ST Paul, MN, USA) after appropriate adjustments of atrial voltage. In those beats whose ventricular depolarization was elicited by the atrial stimuli, the onset of activation was nearly simultaneous at the level of the atrial lead insertion site and at an intermediate level of the right ventricular outflow tract. Noteworthy, propagation of ventricular excitatory wave was faster toward its upper area than toward the apex (Fig. 3).
Discussion The existence of “pseudo-pseudo fusion” beats, a coincidence between atrial stimuli and ventricular ectopic beats, 2 was disregarded because the abnormal findings reported in this article persisted at different paced atrial rates and disappeared when atrial stimuli voltage was decreased. An accessory myocardial connection between the atrial stimulation site and the right ventricle, with intermittent conduction, can be also ruled out because of the following reasons: 1. The virtual inexistence of a discernible interval between the atrial stimulus and the onset of premature right ventricular activation
Fig. 2. Atrial and ventricular electrograms and marker channels during atrial stimulation with 1:1 atrioventricular conduction. A indicates atrial pacing; R, ventricular sensing. The atrial electrogram exhibits a very small far-field ventricular potential, which is not detected and does not induce any annotation in the atrial channel.
J.D. Pastori et al. / Journal of Electrocardiology 45 (2012) 787–789
789
Fig. 3. Electroanatomic activation mapping of the right atrium (RA) and ventricle (RV) during right atrial pacing causing premature ventricular beats, in a left anterior oblique view at approximately 30º. The color code indicates, from white to purple, the propagation of the activation process. It initiates in the right atrium (white) and immediately propagates to the atrial adjacent tissue and the right ventricular outflow tract (red) with faster activation of the high right ventricular outflow tract (yellow) than of the apical region (green, blue, and purple). RAA indicates right atrial appendage; SVC, superior vena cava.
2. The consistent suppression of right ventricular outflow tract premature activation when the voltage of the atrial stimuli was decreased The latter leads to speculate on the possible role of premature stimulation of the right ventricular outflow tract because of an excitatory field of greater magnitude caused by the rise of the output voltage in the atrial channel. However, the presence of an enhanced excitability area in the site of the right ventricle simultaneously activated with atrial stimulation cannot be completely ruled out. The electroanatomical mapping confirmed that the right ventricular activation was faster toward the upper part of the right ventricular outflow tract than toward its apical region. This could be due to dissimilar regional electrophysiologic properties of the right ventricular myocardium caused, to some extent, by Chagas disease right ventricular involvement. 3
Acknowledgments We are indebted to Dr Javier Banchs, MD, for his useful comments and suggestions to the manuscript. This work was supported, in part, by the Fundación de Investigaciones Cardiológicas Einthoven and the Consejo de Investigación en Salud, Ministry of Health, Government of Buenos Aires City. References 1. Kiviniemi MS, Pirnes MA, Eramen HJ, et al. Complications related to permanent pacemaker therapy. Pacing Clin Electrophysiol 1999;22:711. 2. Levine PA, Seltzer JP. Fusion, pseudofusion, pseudo-pseudofusion and confusion: normal rhythms associated with atrioventricular sequential DVI pacing. Clin Prog Pacing and Electrophysiol 1983;1:70. 3. Rosenbaum MB. Chagasic myocardiopathy. Prog Cardiovasc Dis 1964; 7:199.