An “Irritating” Magnet Test ROMAIN CASSAGNEAU, M.D., MIKAEL HANNINEN, M.D., ZACHARY LAKSMAN, M.D., JAIMIE MANLUCU, M.D., and RAYMOND YEE, M.D. From the Department of Medicine, Western University, London, Ontario, Canada
cardiac pacing, ventricular tachycardia, magnet test
Case Presentation A 77-year-old man was referred to our institution for dual-chamber pacemaker implantation for sinus node dysfunction. His presenting rhythm was sinus bradycardia at 45 beats/min, PR interval was 230 ms, and QRS width was normal. He had no previous history of coronary artery disease or cardiovascular risk factors and had a structurally normal heart on echocardiography. Preoperative bloodwork (including electrolytes) was unremarkable and he was not receiving any antiarrhythmic agents. During device implantation, poor R-wave sensing (below 4 mV) was noted at multiple sites in the right ventricle (RV; including the apical septum, mid-septal region, and RV outflow tract) despite an appropriate current of injury pattern and slew rate >0.75 V/s at these sites. After testing a total of 10 sites in the RV, an appropriate position in the RV apex was found where the Medtronic 5076 active-fixation RV lead (Medtronic Inc., Minneapolis, MN, USA) was placed. Final RV lead parameters consisted of a sensed R wave of 9 mV, a capture threshold of 0.50 V, and an impedance of 560 . The atrial lead (Medtronic 5076) was easily implanted in the septal aspect of the right atrial appendage with acceptable parameters and a Medtronic Advisa DR MRI SureScan device was connected to the leads. The rest of the procedure was unremarkable and the pacemaker was programmed in AAIR ⇔ DDDR (MVP ) mode (lower tracking rate = 50/min, upper tracking rate = 120/min, paced atrioventricular delay (AVD) = 180 ms, sensed AVD = 150 ms, A&V outputs = 3.5 v/0.5 ms with unipolar pacing, bipolar sensing). The postoperative chest x-ray confirmed appropriate atrial and ventricular lead positions and there was no excessive slack or loops noted in either leads. Postoperative 12-lead R
R
R
R
Conflicts of Interest: The authors have no conflicts of interest to declare. Address for reprints: Romain Cassagneau, M.D., London Health Science Centre, 339 Windermere Road, London, Ontario, Canada N6G5L5. Fax: +15196633782; e-mail: [email protected] Received October 27, 2013; revised December 3, 2013; accepted December 29, 2013. doi: 10.1111/pace.12355
electrocardiogram showed atrial paced rhythm followed by sensed QRS and long intrinsic atrioventricular (AV) intervals (240 ms), normal corrected QT interval (400 ms). Immediately and consistently with each magnet application, runs of nonsustained ventricular tachycardia (NSVT) were observed with a QRS morphology similar to the RV-paced morphology (Fig. 1). The same phenomenon was observed during RV threshold testing through the device in DDD mode with atrial and ventricular pacing, but not during VVI pacing. These events persisted with variable AV delays that allowed ventricular pacing, from 230 ms to 90 ms. How can AV-synchronized pacing induce ventricular arrhythmias when asynchronous RV pacing does not? Discussion This case highlights the potential proarrhythmic effects of ventricular pacing. Lethal arrhythmias occurring shortly after pacemaker implantation have been previously described,1 but the specific condition (namely AV synchronous pacing) required to elicit tachycardia in our case is highly unusual. There are three possible mechanisms that may account for our unusual case. Mechanical irritation of the endocardium is a common cause of premature ventricular contractions and NSVT during an implant procedure, but it is difficult to explain why only atrialsynchronous (and not VVI) pacing would lead to consistent irritation of the endocardium at the lead attachment site. Another possibility involves local reentry near the site of the pacing electrode. Although our patient did not have overt cardiac disease, the poor R-wave sensing observed throughout the RV endocardium raises the possibility of a subclinical infiltrative condition or diffuse fibrosis that could promote reentry. A possible explanation as to why NSVT is observed only during atrial-synchronous pacing would involve the presence of multiple conduction pathways (possibly separated by scar) with concealed fusion of an antegrade wave front with the retrograde paced stimulus, resulting in wave front collision and unidirectional block in one conduction pathway. AV-dissociated (VVI)
©2014 Wiley Periodicals, Inc. PACE, Vol. 38
January 2015
151
CASSAGNEAU, ET AL.
R pacemakers, Figure 1. Twelve-lead electrocardiogram with magnet application. In Medtronic magnet application provides a DOO mode at 85 beats/min. Runs of nonsustained ventricular tachycardia were immediately and consistently observed.
pacing or pure atrial pacing would not allow wave front collision or the development of unidirectional block. Management options for this unusual case include lead repositioning, pure atrial pacing, and dyssynchronous RV pacing. In our case, multiple lead positions had been tried and were inadequate, so we decided against repositioning the RV lead
once again. The patient’s pacing indication was for sinus node dysfunction and he had reasonable 1:1 AV conduction with rapid atrial pacing despite baseline PR prolongation, so we elected to pace AAI in order to avoid the deleterious effects of chronic RV pacing and the possible development of pacemaker syndrome with VVI pacing.
Reference 1. Nurnberg M, Pottler A, Frohner K, Kofler K, Podczeck A, Stellwag ¨ ¨ C, Steinbach K. Sudden death in pacemaker patients. Clin Prog Electrophys Pacing 1985; 3:477–480.
152
January 2015
PACE, Vol. 38
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
cardiac pacing, ventricular tachycardia, magnet test
Case Presentation A 77-year-old man was referred to our institution for dual-chamber pacemaker implantation for sinus node dysfunction. His presenting rhythm was sinus bradycardia at 45 beats/min, PR interval was 230 ms, and QRS width was normal. He had no previous history of coronary artery disease or cardiovascular risk factors and had a structurally normal heart on echocardiography. Preoperative bloodwork (including electrolytes) was unremarkable and he was not receiving any antiarrhythmic agents. During device implantation, poor R-wave sensing (below 4 mV) was noted at multiple sites in the right ventricle (RV; including the apical septum, mid-septal region, and RV outflow tract) despite an appropriate current of injury pattern and slew rate >0.75 V/s at these sites. After testing a total of 10 sites in the RV, an appropriate position in the RV apex was found where the Medtronic 5076 active-fixation RV lead (Medtronic Inc., Minneapolis, MN, USA) was placed. Final RV lead parameters consisted of a sensed R wave of 9 mV, a capture threshold of 0.50 V, and an impedance of 560 . The atrial lead (Medtronic 5076) was easily implanted in the septal aspect of the right atrial appendage with acceptable parameters and a Medtronic Advisa DR MRI SureScan device was connected to the leads. The rest of the procedure was unremarkable and the pacemaker was programmed in AAIR ⇔ DDDR (MVP ) mode (lower tracking rate = 50/min, upper tracking rate = 120/min, paced atrioventricular delay (AVD) = 180 ms, sensed AVD = 150 ms, A&V outputs = 3.5 v/0.5 ms with unipolar pacing, bipolar sensing). The postoperative chest x-ray confirmed appropriate atrial and ventricular lead positions and there was no excessive slack or loops noted in either leads. Postoperative 12-lead R
R
R
R
Conflicts of Interest: The authors have no conflicts of interest to declare. Address for reprints: Romain Cassagneau, M.D., London Health Science Centre, 339 Windermere Road, London, Ontario, Canada N6G5L5. Fax: +15196633782; e-mail: [email protected] Received October 27, 2013; revised December 3, 2013; accepted December 29, 2013. doi: 10.1111/pace.12355
electrocardiogram showed atrial paced rhythm followed by sensed QRS and long intrinsic atrioventricular (AV) intervals (240 ms), normal corrected QT interval (400 ms). Immediately and consistently with each magnet application, runs of nonsustained ventricular tachycardia (NSVT) were observed with a QRS morphology similar to the RV-paced morphology (Fig. 1). The same phenomenon was observed during RV threshold testing through the device in DDD mode with atrial and ventricular pacing, but not during VVI pacing. These events persisted with variable AV delays that allowed ventricular pacing, from 230 ms to 90 ms. How can AV-synchronized pacing induce ventricular arrhythmias when asynchronous RV pacing does not? Discussion This case highlights the potential proarrhythmic effects of ventricular pacing. Lethal arrhythmias occurring shortly after pacemaker implantation have been previously described,1 but the specific condition (namely AV synchronous pacing) required to elicit tachycardia in our case is highly unusual. There are three possible mechanisms that may account for our unusual case. Mechanical irritation of the endocardium is a common cause of premature ventricular contractions and NSVT during an implant procedure, but it is difficult to explain why only atrialsynchronous (and not VVI) pacing would lead to consistent irritation of the endocardium at the lead attachment site. Another possibility involves local reentry near the site of the pacing electrode. Although our patient did not have overt cardiac disease, the poor R-wave sensing observed throughout the RV endocardium raises the possibility of a subclinical infiltrative condition or diffuse fibrosis that could promote reentry. A possible explanation as to why NSVT is observed only during atrial-synchronous pacing would involve the presence of multiple conduction pathways (possibly separated by scar) with concealed fusion of an antegrade wave front with the retrograde paced stimulus, resulting in wave front collision and unidirectional block in one conduction pathway. AV-dissociated (VVI)
©2014 Wiley Periodicals, Inc. PACE, Vol. 38
January 2015
151
CASSAGNEAU, ET AL.
R pacemakers, Figure 1. Twelve-lead electrocardiogram with magnet application. In Medtronic magnet application provides a DOO mode at 85 beats/min. Runs of nonsustained ventricular tachycardia were immediately and consistently observed.
pacing or pure atrial pacing would not allow wave front collision or the development of unidirectional block. Management options for this unusual case include lead repositioning, pure atrial pacing, and dyssynchronous RV pacing. In our case, multiple lead positions had been tried and were inadequate, so we decided against repositioning the RV lead
once again. The patient’s pacing indication was for sinus node dysfunction and he had reasonable 1:1 AV conduction with rapid atrial pacing despite baseline PR prolongation, so we elected to pace AAI in order to avoid the deleterious effects of chronic RV pacing and the possible development of pacemaker syndrome with VVI pacing.
Reference 1. Nurnberg M, Pottler A, Frohner K, Kofler K, Podczeck A, Stellwag ¨ ¨ C, Steinbach K. Sudden death in pacemaker patients. Clin Prog Electrophys Pacing 1985; 3:477–480.
152
January 2015
PACE, Vol. 38
This document is a scanned copy of a printed document. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material.
