Journal of Veterinary Cardiology (2015) 17, 154e160
www.elsevier.com/locate/jvc
CASE REPORT
Permanent dual chamber epicardial pacemaker implantation in two dogs with complete atrioventricular block Christian Weder, DVM , Eric Monnet, DVM, PhD , Marisa Ames, DVM , Janice Bright, DVM* Colorado State University, United States Received 3 September 2014; received in revised form 22 October 2014; accepted 12 November 2014
KEYWORDS Bradyarrhythmia; Artificial cardiac pacing; Atrioventricular synchrony; Chylothorax; Heart failure
Abstract Between November 2013 and December 2013, two dogs with complete atrioventricular (AV) block had a permanent, dual chamber epicardial pacing system implanted. Steroid-eluting unipolar, button-type epicardial leadsa were sutured to the right atrial appendage and right ventricular wall via a right thoracotomy in both dogs. The pacemakers were programmed in VDD mode. Permanent dual chamber epicardial pacemaker implantation was successful in both dogs with no intra-operative complications. One dog had an acute onset of neurologic signs two days post-operatively that resolved within 24 h. Both dogs have had complete resolution of the clinical signs related to the bradyarrhythmia, and one dog has had complete resolution of chylothorax. One dog had a major lead complication characterized by intermittent loss of capture that resolved by increasing the pacemaker output. Based on the outcome of these two cases, implantation of permanent dual chamber epicardial pacing systems is possible in dogs providing an alternative to dual chamber transvenous systems. ª 2015 Elsevier B.V. All rights reserved.
* Corresponding author. E-mail address: [email protected] (J. Bright). http://dx.doi.org/10.1016/j.jvc.2014.11.002 1760-2734/ª 2015 Elsevier B.V. All rights reserved.
Epicardial dual chamber pacing Abbreviations ACVIM American College of Veterinary Internal Medicine AP artificial cardiac pacing AV atrioventricular
Case 1 A seven-year-old spayed female Cavalier King Charles spaniel was referred to the cardiology service at the Colorado State University Veterinary Teaching Hospital for evaluation of an approximately four-day history of lethargy, exercise intolerance, and decreased appetite with an inappropriate bradycardia (heart rate ¼ 40 bpm). Initial diagnostics included an ECG, echocardiogram, Doppler blood pressure, complete blood count, biochemical profile, thoracic radiography, and urinalysis. Testing for heartworm, Lyme disease, Anaplasma phagocytophilum, Ehrlichia canis, Ehrlichia ewingii and Anaplasma platys was also done.b The ECG showed third-degree atrioventricular (AV) block with a ventricular escape rhythm that was unresponsive to atropine (0.04 mg/kg SQ; no AV nodal conduction noted post atropine). The Doppler echocardiogram showed degenerative mitral valve disease (ACVIM stage B21), degenerative tricuspid valve disease with severe tricuspid regurgitation, severe right atrial and right ventricular dilation, and moderate pulmonary hypertension (estimated pulmonary arterial systolic pressure based on tricuspid regurgitant jet velocity was 78.0 mmHg). A definitive etiology for the pulmonary hypertension was not identified on thoracic radiographs, heartworm testing, or echocardiography although it may have been secondary to chronic left-sided heart disease. During the echocardiogram, the transducer was directed toward the abdomen and a small volume of ascites was noted which was presumed to be secondary to right-sided heart failure. An underlying etiology for the bradyarrhythmia was not identified, and no evidence of significant non-cardiac disease was found. Treatment with a permanent artificial cardiac pacemaker was advised and, due to the severe structural heart disease and heart failure present, a dual chamber pacemaker system was recommended in attempt to optimize cardiac a CapSure Epi (model 4965) pacing lead, Medtronic Inc., Minneapolis, MN, USA. b SNAP 4Dx Plus Test, IDEXX Laboratories, Westbrook, ME, USA.
155 performance by maintaining AV synchrony and intrinsic heart rate variability. Furthermore, the risk of lead dislodgement, intracardiac thrombus, and myocardial perforation were deemed considerable with transvenous pacing due to the severe right ventricular dilation. For these reasons, dual chamber pacing with epicardial lead placement was recommended. The dog was premedicated with fentanyl (1 mg/kg IV). A flow-directed, temporary transvenous pacing leadc was introduced percutaneously into the right jugular vein through a 6 Fr vascular sheathd and advanced using fluoroscopic guidance into the right ventricle. The lead was attached to a temporary transvenous pacemakere for chronotropic support during anesthesia. Anesthesia was then induced using fentanyl (1 mg/kg IV), midazolam (0.0.21 mg/kg IV), and etomidate (0.72 mg/kg IV). After induction of general anesthesia, a permanent dual chamber epicardial pacemaking system,a,f was implanted using the surgical procedure described in detail below. The pacemaker was programmed in VDD mode2 to provide atrioventricular synchrony as well as ventricular tracking of the sinus rate. Initial pacing parameters were programmed as follows: lower rate limit 100 bpm; upper tracking rate 180 bpm; sensed AV delay 110 ms; paced AV delay rate adaptive 90e140 ms; post ventricular atrial refractory period 180 ms; post ventricular atrial blanking 180 ms; ventricular refractory period 230 ms; atrial lead sensitivity 0.5 mV; ventricular lead sensitivity 2.8 mV; pulse amplitude 3.5 mV; pulse duration 0.4 ms. The dog recovered uneventfully from anesthesia and was discharged the next day. A brief echocardiogram immediately prior to discharge showed reduction of right ventricular dilation and severity of tricuspid regurgitation as well as improvement in the estimated pulmonary artery pressure (estimated pulmonary arterial systolic pressure based on tricuspid regurgitant jet velocity decreased from 78.0 mmHg to 46.4 mmHg). The dog was rechecked at one month post-implantation where T-waves were frequently misidentified as P-waves on pacemaker interrogation. The T-wave amplitude measured from the ventricular lead was 0.6 mV, and the P-wave amplitude measured from the atrial lead was 2 mV. Therefore, the atrial lead
c
Swan-Ganz bipolar pacing catheter (model 970-120-5F), Edwards Lifesciences, Irvine, CA, USA. d FAST-CATH, St. Jude Medical, Plymouth, MN, USA. e Single chamber temporary pacemaker (model 5248), Medtronic Inc, Minneapolis, MN, USA. f Adapta ADDRL1 pacing generator, Medtronic Inc, Minneapolis, MN, USA.
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Figure 1 Thoracic radiographs from case 1 showing correct position of the epicardial leads and the pacemaker generator. The left lateral image (A) shows the atrial lead on the cranial surface of the cardiac silhouette at the level of the right auricle with the ventricular lead more caudal and ventral over the right ventricular apex. The ventrodorsal image (B) shows the atrial lead cranially at the level of the right auricle with the ventricular lead more caudal on the right ventricle. In both views the generator is located at the right craniolateral aspect of the abdominal wall.
sensitivity was reduced from 0.5 mV to 1 mV resolving the erroneous identification of T-waves by the atrial lead. The dog was rechecked again at 7 months postimplantation and the owners reported complete resolution of clinical signs and an increase in the dog’s activity. Interrogation of the pacemaker at this time showed appropriate atrial and ventricular sensing as well as appropriate pacing and capture. No pacemaker settings were changed. Thoracic radiographs obtained at this visit confirmed correct position of both leads (Fig. 1). An echocardiogram showed mild right atrial and right ventricular dilation, persistent severe tricuspid regurgitation, and an estimated pulmonary arterial systolic pressure of 43.6 mmHg.
Case 2 A ten year-old castrated male Shiba Inu presented to the cardiology service for evaluation of thirddegree AV block of at least 10 months duration and chylothorax. The dog had been lethargic and had multiple episodes of syncope during the month prior to presentation. An ECG performed at presentation confirmed third-degree AV block and a multifocal ventricular escape rhythm that was unresponsive to atropine (0.04 mg/kg IM; no AV nodal conduction post atropine). Degenerative mitral valve disease (ACVIM stage B11) and mild pleural effusion were identified on echocardiography. Thoracocentesis was performed and the fluid analysis was consistent with chylothorax. Additional diagnostics included a complete blood count, biochemical profile,
infectious disease testing,b abdominal ultrasound, and thoracic radiography. An underlying etiology for the bradyarrhythmia was not identified, and no evidence of significant non-cardiac disease was found. Given that mesothelioma could not be ruled out solely from analysis of the pleural effusion, a pleural biopsy was recommended in addition to implantation of a permanent dual chamber pacemaker. A dual chamber epicardial pacemaker was recommended because of the requirement to enter the thoracic cavity to obtain the biopsies and due to the presence of degenerative AV valve disease. The dog was judged to be stable and was discharged to return in two days for the procedures. The dog was premedicated with hydromorphone (0.1 mg/kg SQ) and atropine (0.04 mg/kg SQ). A temporary transvenous pacemaker was placed prior to induction of anesthesia as in case 1. General anesthesia was then induced with fentanyl (10 mg/kg IV), midazolam (0.21 mg/kg IV), and etomidate (0.25 mg/kg IV). After induction of anesthesia, thoracoscopy was performed with the dog positioned in dorsal recumbency. Samples of the pleura and parietal pericardium were obtained and submitted for histopathologic analysis. Following thoracoscopy, the dog was placed in left lateral recumbency and epicardial pacemaker implantation was performed in the same manner as the dog in case 1.a,g Although lateral thoracotomy was originally planned for both biopsy and pacemaker implantation, thoracoscopic biopsy was chosen by the
g Sensia SEDR01 pacing generator, Medtronic Inc, Minneapolis, MN, USA.
Epicardial dual chamber pacing surgeon at the onset of the procedure. Despite this change in biopsy technique (open versus thoracoscopic), the dog was already in the operating room for the thoracoscopic biopsy and was simply repositioned for lateral thoracotomy rather than transporting to the fluoroscopy suite (for placement of a transvenous pacing system). Also, the surgeon was comfortable with placement of a dual chamber epicardial pacing system having previously performed successful implantation as described in case 1. The dog recovered uneventfully from anesthesia and was discharged the next day. Histopathology and immunohistochemistry of the pleural and pericardial samples were consistent with reactive mesothelium without evidence of neoplasia. Two days following discharge, the dog represented to the urgent care service for acute onset ataxia with systemic hypertension identified (systolic pressure 190e200 mmHg). Neurolocalization was confined to the right lobe of the cerebellum with the primary differential of a vascular event although neoplasia, infectious/inflammatory, and intoxication could not be ruled out. The dog was hospitalized and was treated with amlodipine (0.14 mg/kg PO BID) and benazepril (0.54 mg/kg PO q 24h), and the clinical signs improved dramatically over the next 24 h. Based on the dramatic improvement over 24 h, a vascular event potentially secondary to systemic hypertension was considered the most likely etiology although a cause of the hypertension was not determined. While the dog was in the hospital, the pacemaker was interrogated and sensing and threshold were appropriate. The dog was discharged two days later with treatment for systemic hypertension consisting of amlodipine (0.14 mg/kg PO q 12h) and benazepril (0.54 mg/kg PO q 24h). The dog had persistent systemic hypertension (170 mmHg) 5 days after discharge and the dose of amlodipine was increased to 0.4 mg/kg PO q24h. Subsequent follow-up was performed by another cardiologist, and 2 months postimplantation the owners reported resolution of all clinical signs, an increase in activity, and resolution of chylothorax while sensing and capture were considered appropriate on pacemaker interrogation. The dog presented approximately 4 months post-implantation for evaluation of syncope where intermittent loss of capture was noted on pacemaker interrogation. The lead impedance was similar to implantation values; so the ventricular pacing amplitude was increased from 3.5 V to 6.0 V, and the pulse duration was increased from 0.4 ms to 0.52 ms which resulted in consistent capture. The leads appeared to be in
157 appropriate position on thoracic radiographs, although no immediate post-operative radiographs were available for comparison. Ten months postimplantation, the owner reported that the dog was doing very well with no episodes of collapse and had an excellent quality of life with appropriate sensing and capture identified from pacemaker interrogation.
Implantation procedure The dogs were placed in left lateral recumbency and an approximately 15 cm skin incision was made over the right fifth intercostal space. The cutaneous trunci and latissimus dorsi muscles were incised. The scalenus muscle was located and incised at its attachment on the fifth rib, allowing approach to the fifth intercostal space. The muscle bellies of the serratus ventralis were separated dorsally over the fifth intercostal space. The internal and external intercostal muscles were incised. The pleura was then incised providing access to the thoracic cavity. Finocietto retractors were used to facilitate proper visualization. The right cranial and middle lung lobes were retracted caudally and dorsally to expose the pericardium. A subphrenic pericardiotomy was performed and the incised pericardial edges temporarily pexied to the surrounding towels to allow visualization of the right side of the heart. A steroid eluting unipolar epicardial leada was sutured to the right atrial appendage with 4-0 polypropylene. A second lead was sutured to the midright ventricular epicardium in the same fashion in a location to avoid any major coronary arteries (Fig. 2). Unipolar leads were used based on availability and surgeon preference. Although bipolar leads can be used, unipolar leads require only one electrode-epicardial interface. An approximately 5 cm incision was made roughly 3 cm caudal to the last rib over the lateral aspect of the abdomen. The incision was extended through the external abdominal oblique muscle using electrocautery. The leads were tunneled through the tenth intercostal space using grasping forceps and then advanced under the subcutis before entering the incision/pocket created in the external abdominal oblique. The leads were attached to the pacemaker generatorf,g and tightened. Proper pacing and capture were confirmed, and the generator was placed in the pocket under the muscle. The incisions were closed routinely but the pericardium was left open. A 12-Fr chest tube was placed in standard fashion and secured with a Chinese finger trap.
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Figure 2 A schematic illustration of lead placement for a dual chamber epicardial pacemaker. One lead is sutured to the right atrial appendage while the second lead is sutured to the right ventricular epicardium. Both leads are tunneled through the tenth intercostal space and subcutis prior to placement within the incision/pocket created in the external abdominal oblique muscle (shown in inset).
Discussion Permanent artificial cardiac pacing (AP) has become the standard of care in veterinary medicine for animals with symptomatic bradyarrhythmias.3 The most common indications for AP are third-degree and high-grade second-degree atrioventricular block, sick sinus syndrome, and atrial standstill.3 The first reported implantation of a permanent pacemaker for clinical use in a dog was in 1967.4 Since that time, various technologic advances adapted from human medicine have allowed the safe implantation of more sophisticated devices in dogs resulting in improved survival time and high rates of owner satisfaction with a relatively low complication rate.3,5,6
Single chamber AP systems have traditionally been implanted in veterinary medicine, and the technique has been well described.7 Single lead transvenous endocardial pacing with the lead positioned at the right ventricular apex is most commonly used.6 The use of single chamber epicardial pacing systems has also been described in veterinary medicine, particularly as an alternative for animals considered unsuitable for permanent transvenous pacing, and are most commonly implanted via a transdiaphragmatic approach.8,9 Single chamber transvenous or epicardial pacing systems are typically programmed in VVI or VVIR mode.2 Dual chamber AP may provide superior cardiac performance and more favorable hemodynamics
Epicardial dual chamber pacing by restoring AV synchrony and allowing variable pacing rates. In humans, dual chamber pacing has been shown to improve cardiac output, blood pressure and quality of life while reducing the risk of atrial fibrillation and stroke compared to single chamber pacing.10e12 Furthermore, “pacemaker syndrome”, a constellation of clinical signs and symptoms reported in humans resulting from single chamber ventricular pacing, is mostly avoided with dual chamber pacing systems.13 Given the vague and often non-specific signs reported by people with pacemaker syndrome, this adverse response to single chamber pacing cannot be clearly identified in dogs. While some studies of human patients have shown a reduction in mortality and the signs and symptoms of heart failure with dual chamber pacing compared to single chamber pacing, other larger prospective studies have failed to show a significant improvement in survival.11,14e16 Regardless of the conflicting data, dual chamber pacing has now become the most common form of AP in human medicine.17 The use of transvenous dual chamber pacemaker systems has been reported in veterinary medicine in various publications.6,18,19 The use of a dual chamber single lead VDD system has been shown to significantly improve hemodynamics and neurohormonal parameters with a complication rate comparable to single chamber ventricular pacing in dogs.18,19 There are currently no available long-term survival data on dogs with dual chamber systems. The implantation of transvenous, dual chamber pacing systems may not be possible for small dogs and may be inappropriate for those with significant right-sided heart disease. Dual chamber epicardial pacing using two unipolar leads placed via partial or complete sternotomy has been described in neonatal children for treatment of congenital heart block.20 In these children, one lead is sutured to the epicardial surface on the midportion of the right atrium and the second lead is placed on the epicardium of the high right ventricular outflow tract.20 The pacemaker generator is placed in a submuscular bilateral rectus sheath pocket.21 Experiences from human medicine have shown that implantation of dual chamber epicardial pacemakers in neonates is technically feasible and provides a stable, acute and chronic pacing system that preserves AV synchrony and normal chronotropic response.22,23 This report describes the use of epicardial dual chamber cardiac pacing in two dogs and describes the surgical procedure used for implantation. Based on immediate and mid-term follow-up of the two dogs, dual chamber epicardial pacing provides a means of dual chamber pacing for dogs the
159 authors judged as unsuitable for tranvenous AP. One dog (case 1) had echocardiographic improvement in structural heart disease and estimated systolic pulmonary arterial pressure. While the other dog continues to do well, lead complications were encountered. The exact cause for the loss of capture remains unknown; however differentials include lead fracture, insulation break, and dislodgement, all of which were considered unlikely given normal and relatively unchanged impedance on interrogation and appropriate lead position on radiographs. Exit block due to scar tissue formation at the lead/epicardium interface is considered most likely in spite of reduced scarring associated with modern steroid eluting leads.22 The current pacemaker output is set at the maximum value and surgical intervention with lead replacement may be necessary in the future if capture is lost. Issues with capture threshold may represent a limitation of this technique; however exit block is a complication recognized with both transvenous and epicardial leads, and this report only describes two dogs.6,24 Potential additional limitations of this technique include the possible increased anesthesia time required for implantation of a dual chamber versus a single chamber epicardial system as well as the increased anesthesia time and more invasive nature with required technical expertise associated with implantation of an epicardial pacing system compared to a transvenous system. Longer term follow up of these two dogs as well as data from additional dogs are needed to determine the complication rate and long-term outcome of dual chamber epicardial pacemaker implantation in dogs.
Conflict of interest None.
References 1. Atkins C, Bonagura J, Ettinger S, Gordon S, Haggstrom J, Hamlin R, Keene B, Luis-Fuentes V, Stepien R. Guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med 2009;23:1142e1150. 2. Berstein AD, Daubert JC, Fletcher RD, Hayes DL, Luderitz B, Reynolds DW, Schoenfeld MH, Sutton R. The revised NASPE/ BPEG generic code for antibradycardia, adaptive-rate, and multisite pacing. J Pacing Clin Electrophys 2002;25:260e264. 3. Wess G, Thomas WP, Berger DM, Kittleson MD. Applications, complications, and outcomes of transvenous pacemaker implantation in 105 dogs (1997e2002). J Vet Intern Med 2006;20:877e884. 4. Buchanan JW. First pacemaker in a dog: a historical note. J Vet Intern Med 2003;17:713e714.
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5. Schrope DP, Kelch WJ. Signalment, clinical signs, and prognostic indicators associated with high-grade second degree or third-degree atrioventricular block in dogs: 124 cases (January 1, 1997eDecember 31, 1997). J Am Vet Med Assoc 2006;11:1710e1717. 6. Oyama MA, Sisson DD, Lehmkuhl LB. Practices and outcomes of artificial cardiac pacing in 154 dogs. J Vet Intern Med 2001;15:229e239. 7. Petrie JP. Permanent transvenous cardiac pacing. Clin Tech Small Anim Pract 2005;20:164e172. 8. Fingeroth JM, Birchard SJ. Transdiaphragmatic approach for permanent cardiac pacemaker implantation in dogs. Vet Surg 1986;15:329e333. 9. Fox PR, Matthiesen DT, Purse D, Brown NO. Ventral abdominal, transdiaphragmatic approach for implantation of cardiac pacemakers in the dog. J Am Vet Med Assoc 1986; 189:1303e1308. 10. Lind-Edelstam C, Nordlander R, Uden AL. Quality of life in patients with atrioventricular synchronous pacing compared to rate modulated ventricular pacing: a long-term, doubleblind, crossover study. Pacing Clin Electrophysiol 1992;15: 1467e1476. 11. Kerr CR, Connolly SJ, Abdollah H, Roberts RS, Gent M, Yusuf S, Gillis AM, Tang AS, Talajic M, Klein GJ, Newman DM. Canadian trial of physiological pacing (CTOPP): effects of physiological pacing during long-term follow-up. Circulation 2004;109:357e362. 12. Anderson HR, Nielson JC, Thomsen PEB, Thuesen L, Mortensen PT, Vesterlung T, Pedersen AK. Long-term follow-up of patients from a randomised trial of atrial versus ventricular pacing for sick sinus syndrome. Lancet 1997; 350:1210e1216. 13. Chalvidan D, Deharo JC, Djiane P. Pacemaker syndromes. Ann Cardiol Angeiol (Paris) 2000;49:224e229. 14. Lamas GA, Pashos CL, Normand SLT, McNeil B. Permanent pacemaker selection and survival in elderly medicare pacemaker recipients. Circulation 1995;91:1063e1069.
15. Lamas GA, Lee KL, Sweeny MO, Silverman R, Leon A, Yee R, Marinchak RA, Flaker G, Schron E, Orav J, Hellkamp AS, Greer S, McAnulty J, Ellenbogen K, Ehlert F, Freedman RA, Estes M, Greenspon A, Goldman L. Ventricular pacing or dual chamber pacing for sinus node dysfunction. New Eng J Med 2002;346:1854e1862. 16. Toff WD, Camm JA, Skehan DS. Single-chamber versus dual chamber pacing for high-grade second atrioventricular block. New Eng J Med 2005;353:145e155. 17. Lamas GA, Ellenbogen KA. Evidence base for pacemaker mode selection: from physiology to randomized trials. Circulation 2004;109:443e451. 18. Hildebrandt N, Stertmann WA, Wehner M, Schneider I, Neu H, Schneider M. Dual chamber pacemaker implantation in dogs with atrioventricular block. J Vet Intern Med 2009; 23:31e38. 19. Bulmer BJ, Sisson DD, Oyama MA, Solter PF, Grimm KA, Lamont L. Physiologic VDD versus nonphysiologic VVI pacing in canine 3rd degree atrioventricular block. J Vet Intern Med 2006;20:257e271. 20. Kelle AM, Backer CL, Tsao S, Stewart RD, Franklin WH, Deal BJ, Mavroudis C. Dual-chamber epicardial pacing in neonates with congenital heart block. J Thorac Cardiovas Surg 2007;134:1188e1192. 21. DeLeon SY, Ilbawi MN, Idriss FS. Pacemaker implantation in infants and children: a simplified approach. Ann Thorac Surg 1980;30:599e601. 22. Kubus P, Materna O, Gebauer RA, Matejka T, Gebauer R, Tlaskal T, Janaousek J. Permanent epicardial pacing in children: long-term results and factors modifying outcome. Europace 2012;14:509e514. 23. Cohen MI, Bush DM, Vetter VL, Tanel RE, Wieand TS, Gaynor JW, Rhodes LA. Permanent epicardial pacing in pediatric patients. Circulation 2001;103:2585e2590. 24. Sisson D, Thomas WP, Woodfield J, Pion PD, Luethy M, DeLellis LA. Permanent transvenous pacemaker implantation in forty dogs. J Vet Intern Med 1991;5:322e331.
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CASE REPORT
Permanent dual chamber epicardial pacemaker implantation in two dogs with complete atrioventricular block Christian Weder, DVM , Eric Monnet, DVM, PhD , Marisa Ames, DVM , Janice Bright, DVM* Colorado State University, United States Received 3 September 2014; received in revised form 22 October 2014; accepted 12 November 2014
KEYWORDS Bradyarrhythmia; Artificial cardiac pacing; Atrioventricular synchrony; Chylothorax; Heart failure
Abstract Between November 2013 and December 2013, two dogs with complete atrioventricular (AV) block had a permanent, dual chamber epicardial pacing system implanted. Steroid-eluting unipolar, button-type epicardial leadsa were sutured to the right atrial appendage and right ventricular wall via a right thoracotomy in both dogs. The pacemakers were programmed in VDD mode. Permanent dual chamber epicardial pacemaker implantation was successful in both dogs with no intra-operative complications. One dog had an acute onset of neurologic signs two days post-operatively that resolved within 24 h. Both dogs have had complete resolution of the clinical signs related to the bradyarrhythmia, and one dog has had complete resolution of chylothorax. One dog had a major lead complication characterized by intermittent loss of capture that resolved by increasing the pacemaker output. Based on the outcome of these two cases, implantation of permanent dual chamber epicardial pacing systems is possible in dogs providing an alternative to dual chamber transvenous systems. ª 2015 Elsevier B.V. All rights reserved.
* Corresponding author. E-mail address: [email protected] (J. Bright). http://dx.doi.org/10.1016/j.jvc.2014.11.002 1760-2734/ª 2015 Elsevier B.V. All rights reserved.
Epicardial dual chamber pacing Abbreviations ACVIM American College of Veterinary Internal Medicine AP artificial cardiac pacing AV atrioventricular
Case 1 A seven-year-old spayed female Cavalier King Charles spaniel was referred to the cardiology service at the Colorado State University Veterinary Teaching Hospital for evaluation of an approximately four-day history of lethargy, exercise intolerance, and decreased appetite with an inappropriate bradycardia (heart rate ¼ 40 bpm). Initial diagnostics included an ECG, echocardiogram, Doppler blood pressure, complete blood count, biochemical profile, thoracic radiography, and urinalysis. Testing for heartworm, Lyme disease, Anaplasma phagocytophilum, Ehrlichia canis, Ehrlichia ewingii and Anaplasma platys was also done.b The ECG showed third-degree atrioventricular (AV) block with a ventricular escape rhythm that was unresponsive to atropine (0.04 mg/kg SQ; no AV nodal conduction noted post atropine). The Doppler echocardiogram showed degenerative mitral valve disease (ACVIM stage B21), degenerative tricuspid valve disease with severe tricuspid regurgitation, severe right atrial and right ventricular dilation, and moderate pulmonary hypertension (estimated pulmonary arterial systolic pressure based on tricuspid regurgitant jet velocity was 78.0 mmHg). A definitive etiology for the pulmonary hypertension was not identified on thoracic radiographs, heartworm testing, or echocardiography although it may have been secondary to chronic left-sided heart disease. During the echocardiogram, the transducer was directed toward the abdomen and a small volume of ascites was noted which was presumed to be secondary to right-sided heart failure. An underlying etiology for the bradyarrhythmia was not identified, and no evidence of significant non-cardiac disease was found. Treatment with a permanent artificial cardiac pacemaker was advised and, due to the severe structural heart disease and heart failure present, a dual chamber pacemaker system was recommended in attempt to optimize cardiac a CapSure Epi (model 4965) pacing lead, Medtronic Inc., Minneapolis, MN, USA. b SNAP 4Dx Plus Test, IDEXX Laboratories, Westbrook, ME, USA.
155 performance by maintaining AV synchrony and intrinsic heart rate variability. Furthermore, the risk of lead dislodgement, intracardiac thrombus, and myocardial perforation were deemed considerable with transvenous pacing due to the severe right ventricular dilation. For these reasons, dual chamber pacing with epicardial lead placement was recommended. The dog was premedicated with fentanyl (1 mg/kg IV). A flow-directed, temporary transvenous pacing leadc was introduced percutaneously into the right jugular vein through a 6 Fr vascular sheathd and advanced using fluoroscopic guidance into the right ventricle. The lead was attached to a temporary transvenous pacemakere for chronotropic support during anesthesia. Anesthesia was then induced using fentanyl (1 mg/kg IV), midazolam (0.0.21 mg/kg IV), and etomidate (0.72 mg/kg IV). After induction of general anesthesia, a permanent dual chamber epicardial pacemaking system,a,f was implanted using the surgical procedure described in detail below. The pacemaker was programmed in VDD mode2 to provide atrioventricular synchrony as well as ventricular tracking of the sinus rate. Initial pacing parameters were programmed as follows: lower rate limit 100 bpm; upper tracking rate 180 bpm; sensed AV delay 110 ms; paced AV delay rate adaptive 90e140 ms; post ventricular atrial refractory period 180 ms; post ventricular atrial blanking 180 ms; ventricular refractory period 230 ms; atrial lead sensitivity 0.5 mV; ventricular lead sensitivity 2.8 mV; pulse amplitude 3.5 mV; pulse duration 0.4 ms. The dog recovered uneventfully from anesthesia and was discharged the next day. A brief echocardiogram immediately prior to discharge showed reduction of right ventricular dilation and severity of tricuspid regurgitation as well as improvement in the estimated pulmonary artery pressure (estimated pulmonary arterial systolic pressure based on tricuspid regurgitant jet velocity decreased from 78.0 mmHg to 46.4 mmHg). The dog was rechecked at one month post-implantation where T-waves were frequently misidentified as P-waves on pacemaker interrogation. The T-wave amplitude measured from the ventricular lead was 0.6 mV, and the P-wave amplitude measured from the atrial lead was 2 mV. Therefore, the atrial lead
c
Swan-Ganz bipolar pacing catheter (model 970-120-5F), Edwards Lifesciences, Irvine, CA, USA. d FAST-CATH, St. Jude Medical, Plymouth, MN, USA. e Single chamber temporary pacemaker (model 5248), Medtronic Inc, Minneapolis, MN, USA. f Adapta ADDRL1 pacing generator, Medtronic Inc, Minneapolis, MN, USA.
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Figure 1 Thoracic radiographs from case 1 showing correct position of the epicardial leads and the pacemaker generator. The left lateral image (A) shows the atrial lead on the cranial surface of the cardiac silhouette at the level of the right auricle with the ventricular lead more caudal and ventral over the right ventricular apex. The ventrodorsal image (B) shows the atrial lead cranially at the level of the right auricle with the ventricular lead more caudal on the right ventricle. In both views the generator is located at the right craniolateral aspect of the abdominal wall.
sensitivity was reduced from 0.5 mV to 1 mV resolving the erroneous identification of T-waves by the atrial lead. The dog was rechecked again at 7 months postimplantation and the owners reported complete resolution of clinical signs and an increase in the dog’s activity. Interrogation of the pacemaker at this time showed appropriate atrial and ventricular sensing as well as appropriate pacing and capture. No pacemaker settings were changed. Thoracic radiographs obtained at this visit confirmed correct position of both leads (Fig. 1). An echocardiogram showed mild right atrial and right ventricular dilation, persistent severe tricuspid regurgitation, and an estimated pulmonary arterial systolic pressure of 43.6 mmHg.
Case 2 A ten year-old castrated male Shiba Inu presented to the cardiology service for evaluation of thirddegree AV block of at least 10 months duration and chylothorax. The dog had been lethargic and had multiple episodes of syncope during the month prior to presentation. An ECG performed at presentation confirmed third-degree AV block and a multifocal ventricular escape rhythm that was unresponsive to atropine (0.04 mg/kg IM; no AV nodal conduction post atropine). Degenerative mitral valve disease (ACVIM stage B11) and mild pleural effusion were identified on echocardiography. Thoracocentesis was performed and the fluid analysis was consistent with chylothorax. Additional diagnostics included a complete blood count, biochemical profile,
infectious disease testing,b abdominal ultrasound, and thoracic radiography. An underlying etiology for the bradyarrhythmia was not identified, and no evidence of significant non-cardiac disease was found. Given that mesothelioma could not be ruled out solely from analysis of the pleural effusion, a pleural biopsy was recommended in addition to implantation of a permanent dual chamber pacemaker. A dual chamber epicardial pacemaker was recommended because of the requirement to enter the thoracic cavity to obtain the biopsies and due to the presence of degenerative AV valve disease. The dog was judged to be stable and was discharged to return in two days for the procedures. The dog was premedicated with hydromorphone (0.1 mg/kg SQ) and atropine (0.04 mg/kg SQ). A temporary transvenous pacemaker was placed prior to induction of anesthesia as in case 1. General anesthesia was then induced with fentanyl (10 mg/kg IV), midazolam (0.21 mg/kg IV), and etomidate (0.25 mg/kg IV). After induction of anesthesia, thoracoscopy was performed with the dog positioned in dorsal recumbency. Samples of the pleura and parietal pericardium were obtained and submitted for histopathologic analysis. Following thoracoscopy, the dog was placed in left lateral recumbency and epicardial pacemaker implantation was performed in the same manner as the dog in case 1.a,g Although lateral thoracotomy was originally planned for both biopsy and pacemaker implantation, thoracoscopic biopsy was chosen by the
g Sensia SEDR01 pacing generator, Medtronic Inc, Minneapolis, MN, USA.
Epicardial dual chamber pacing surgeon at the onset of the procedure. Despite this change in biopsy technique (open versus thoracoscopic), the dog was already in the operating room for the thoracoscopic biopsy and was simply repositioned for lateral thoracotomy rather than transporting to the fluoroscopy suite (for placement of a transvenous pacing system). Also, the surgeon was comfortable with placement of a dual chamber epicardial pacing system having previously performed successful implantation as described in case 1. The dog recovered uneventfully from anesthesia and was discharged the next day. Histopathology and immunohistochemistry of the pleural and pericardial samples were consistent with reactive mesothelium without evidence of neoplasia. Two days following discharge, the dog represented to the urgent care service for acute onset ataxia with systemic hypertension identified (systolic pressure 190e200 mmHg). Neurolocalization was confined to the right lobe of the cerebellum with the primary differential of a vascular event although neoplasia, infectious/inflammatory, and intoxication could not be ruled out. The dog was hospitalized and was treated with amlodipine (0.14 mg/kg PO BID) and benazepril (0.54 mg/kg PO q 24h), and the clinical signs improved dramatically over the next 24 h. Based on the dramatic improvement over 24 h, a vascular event potentially secondary to systemic hypertension was considered the most likely etiology although a cause of the hypertension was not determined. While the dog was in the hospital, the pacemaker was interrogated and sensing and threshold were appropriate. The dog was discharged two days later with treatment for systemic hypertension consisting of amlodipine (0.14 mg/kg PO q 12h) and benazepril (0.54 mg/kg PO q 24h). The dog had persistent systemic hypertension (170 mmHg) 5 days after discharge and the dose of amlodipine was increased to 0.4 mg/kg PO q24h. Subsequent follow-up was performed by another cardiologist, and 2 months postimplantation the owners reported resolution of all clinical signs, an increase in activity, and resolution of chylothorax while sensing and capture were considered appropriate on pacemaker interrogation. The dog presented approximately 4 months post-implantation for evaluation of syncope where intermittent loss of capture was noted on pacemaker interrogation. The lead impedance was similar to implantation values; so the ventricular pacing amplitude was increased from 3.5 V to 6.0 V, and the pulse duration was increased from 0.4 ms to 0.52 ms which resulted in consistent capture. The leads appeared to be in
157 appropriate position on thoracic radiographs, although no immediate post-operative radiographs were available for comparison. Ten months postimplantation, the owner reported that the dog was doing very well with no episodes of collapse and had an excellent quality of life with appropriate sensing and capture identified from pacemaker interrogation.
Implantation procedure The dogs were placed in left lateral recumbency and an approximately 15 cm skin incision was made over the right fifth intercostal space. The cutaneous trunci and latissimus dorsi muscles were incised. The scalenus muscle was located and incised at its attachment on the fifth rib, allowing approach to the fifth intercostal space. The muscle bellies of the serratus ventralis were separated dorsally over the fifth intercostal space. The internal and external intercostal muscles were incised. The pleura was then incised providing access to the thoracic cavity. Finocietto retractors were used to facilitate proper visualization. The right cranial and middle lung lobes were retracted caudally and dorsally to expose the pericardium. A subphrenic pericardiotomy was performed and the incised pericardial edges temporarily pexied to the surrounding towels to allow visualization of the right side of the heart. A steroid eluting unipolar epicardial leada was sutured to the right atrial appendage with 4-0 polypropylene. A second lead was sutured to the midright ventricular epicardium in the same fashion in a location to avoid any major coronary arteries (Fig. 2). Unipolar leads were used based on availability and surgeon preference. Although bipolar leads can be used, unipolar leads require only one electrode-epicardial interface. An approximately 5 cm incision was made roughly 3 cm caudal to the last rib over the lateral aspect of the abdomen. The incision was extended through the external abdominal oblique muscle using electrocautery. The leads were tunneled through the tenth intercostal space using grasping forceps and then advanced under the subcutis before entering the incision/pocket created in the external abdominal oblique. The leads were attached to the pacemaker generatorf,g and tightened. Proper pacing and capture were confirmed, and the generator was placed in the pocket under the muscle. The incisions were closed routinely but the pericardium was left open. A 12-Fr chest tube was placed in standard fashion and secured with a Chinese finger trap.
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Figure 2 A schematic illustration of lead placement for a dual chamber epicardial pacemaker. One lead is sutured to the right atrial appendage while the second lead is sutured to the right ventricular epicardium. Both leads are tunneled through the tenth intercostal space and subcutis prior to placement within the incision/pocket created in the external abdominal oblique muscle (shown in inset).
Discussion Permanent artificial cardiac pacing (AP) has become the standard of care in veterinary medicine for animals with symptomatic bradyarrhythmias.3 The most common indications for AP are third-degree and high-grade second-degree atrioventricular block, sick sinus syndrome, and atrial standstill.3 The first reported implantation of a permanent pacemaker for clinical use in a dog was in 1967.4 Since that time, various technologic advances adapted from human medicine have allowed the safe implantation of more sophisticated devices in dogs resulting in improved survival time and high rates of owner satisfaction with a relatively low complication rate.3,5,6
Single chamber AP systems have traditionally been implanted in veterinary medicine, and the technique has been well described.7 Single lead transvenous endocardial pacing with the lead positioned at the right ventricular apex is most commonly used.6 The use of single chamber epicardial pacing systems has also been described in veterinary medicine, particularly as an alternative for animals considered unsuitable for permanent transvenous pacing, and are most commonly implanted via a transdiaphragmatic approach.8,9 Single chamber transvenous or epicardial pacing systems are typically programmed in VVI or VVIR mode.2 Dual chamber AP may provide superior cardiac performance and more favorable hemodynamics
Epicardial dual chamber pacing by restoring AV synchrony and allowing variable pacing rates. In humans, dual chamber pacing has been shown to improve cardiac output, blood pressure and quality of life while reducing the risk of atrial fibrillation and stroke compared to single chamber pacing.10e12 Furthermore, “pacemaker syndrome”, a constellation of clinical signs and symptoms reported in humans resulting from single chamber ventricular pacing, is mostly avoided with dual chamber pacing systems.13 Given the vague and often non-specific signs reported by people with pacemaker syndrome, this adverse response to single chamber pacing cannot be clearly identified in dogs. While some studies of human patients have shown a reduction in mortality and the signs and symptoms of heart failure with dual chamber pacing compared to single chamber pacing, other larger prospective studies have failed to show a significant improvement in survival.11,14e16 Regardless of the conflicting data, dual chamber pacing has now become the most common form of AP in human medicine.17 The use of transvenous dual chamber pacemaker systems has been reported in veterinary medicine in various publications.6,18,19 The use of a dual chamber single lead VDD system has been shown to significantly improve hemodynamics and neurohormonal parameters with a complication rate comparable to single chamber ventricular pacing in dogs.18,19 There are currently no available long-term survival data on dogs with dual chamber systems. The implantation of transvenous, dual chamber pacing systems may not be possible for small dogs and may be inappropriate for those with significant right-sided heart disease. Dual chamber epicardial pacing using two unipolar leads placed via partial or complete sternotomy has been described in neonatal children for treatment of congenital heart block.20 In these children, one lead is sutured to the epicardial surface on the midportion of the right atrium and the second lead is placed on the epicardium of the high right ventricular outflow tract.20 The pacemaker generator is placed in a submuscular bilateral rectus sheath pocket.21 Experiences from human medicine have shown that implantation of dual chamber epicardial pacemakers in neonates is technically feasible and provides a stable, acute and chronic pacing system that preserves AV synchrony and normal chronotropic response.22,23 This report describes the use of epicardial dual chamber cardiac pacing in two dogs and describes the surgical procedure used for implantation. Based on immediate and mid-term follow-up of the two dogs, dual chamber epicardial pacing provides a means of dual chamber pacing for dogs the
159 authors judged as unsuitable for tranvenous AP. One dog (case 1) had echocardiographic improvement in structural heart disease and estimated systolic pulmonary arterial pressure. While the other dog continues to do well, lead complications were encountered. The exact cause for the loss of capture remains unknown; however differentials include lead fracture, insulation break, and dislodgement, all of which were considered unlikely given normal and relatively unchanged impedance on interrogation and appropriate lead position on radiographs. Exit block due to scar tissue formation at the lead/epicardium interface is considered most likely in spite of reduced scarring associated with modern steroid eluting leads.22 The current pacemaker output is set at the maximum value and surgical intervention with lead replacement may be necessary in the future if capture is lost. Issues with capture threshold may represent a limitation of this technique; however exit block is a complication recognized with both transvenous and epicardial leads, and this report only describes two dogs.6,24 Potential additional limitations of this technique include the possible increased anesthesia time required for implantation of a dual chamber versus a single chamber epicardial system as well as the increased anesthesia time and more invasive nature with required technical expertise associated with implantation of an epicardial pacing system compared to a transvenous system. Longer term follow up of these two dogs as well as data from additional dogs are needed to determine the complication rate and long-term outcome of dual chamber epicardial pacemaker implantation in dogs.
Conflict of interest None.
References 1. Atkins C, Bonagura J, Ettinger S, Gordon S, Haggstrom J, Hamlin R, Keene B, Luis-Fuentes V, Stepien R. Guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med 2009;23:1142e1150. 2. Berstein AD, Daubert JC, Fletcher RD, Hayes DL, Luderitz B, Reynolds DW, Schoenfeld MH, Sutton R. The revised NASPE/ BPEG generic code for antibradycardia, adaptive-rate, and multisite pacing. J Pacing Clin Electrophys 2002;25:260e264. 3. Wess G, Thomas WP, Berger DM, Kittleson MD. Applications, complications, and outcomes of transvenous pacemaker implantation in 105 dogs (1997e2002). J Vet Intern Med 2006;20:877e884. 4. Buchanan JW. First pacemaker in a dog: a historical note. J Vet Intern Med 2003;17:713e714.
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5. Schrope DP, Kelch WJ. Signalment, clinical signs, and prognostic indicators associated with high-grade second degree or third-degree atrioventricular block in dogs: 124 cases (January 1, 1997eDecember 31, 1997). J Am Vet Med Assoc 2006;11:1710e1717. 6. Oyama MA, Sisson DD, Lehmkuhl LB. Practices and outcomes of artificial cardiac pacing in 154 dogs. J Vet Intern Med 2001;15:229e239. 7. Petrie JP. Permanent transvenous cardiac pacing. Clin Tech Small Anim Pract 2005;20:164e172. 8. Fingeroth JM, Birchard SJ. Transdiaphragmatic approach for permanent cardiac pacemaker implantation in dogs. Vet Surg 1986;15:329e333. 9. Fox PR, Matthiesen DT, Purse D, Brown NO. Ventral abdominal, transdiaphragmatic approach for implantation of cardiac pacemakers in the dog. J Am Vet Med Assoc 1986; 189:1303e1308. 10. Lind-Edelstam C, Nordlander R, Uden AL. Quality of life in patients with atrioventricular synchronous pacing compared to rate modulated ventricular pacing: a long-term, doubleblind, crossover study. Pacing Clin Electrophysiol 1992;15: 1467e1476. 11. Kerr CR, Connolly SJ, Abdollah H, Roberts RS, Gent M, Yusuf S, Gillis AM, Tang AS, Talajic M, Klein GJ, Newman DM. Canadian trial of physiological pacing (CTOPP): effects of physiological pacing during long-term follow-up. Circulation 2004;109:357e362. 12. Anderson HR, Nielson JC, Thomsen PEB, Thuesen L, Mortensen PT, Vesterlung T, Pedersen AK. Long-term follow-up of patients from a randomised trial of atrial versus ventricular pacing for sick sinus syndrome. Lancet 1997; 350:1210e1216. 13. Chalvidan D, Deharo JC, Djiane P. Pacemaker syndromes. Ann Cardiol Angeiol (Paris) 2000;49:224e229. 14. Lamas GA, Pashos CL, Normand SLT, McNeil B. Permanent pacemaker selection and survival in elderly medicare pacemaker recipients. Circulation 1995;91:1063e1069.
15. Lamas GA, Lee KL, Sweeny MO, Silverman R, Leon A, Yee R, Marinchak RA, Flaker G, Schron E, Orav J, Hellkamp AS, Greer S, McAnulty J, Ellenbogen K, Ehlert F, Freedman RA, Estes M, Greenspon A, Goldman L. Ventricular pacing or dual chamber pacing for sinus node dysfunction. New Eng J Med 2002;346:1854e1862. 16. Toff WD, Camm JA, Skehan DS. Single-chamber versus dual chamber pacing for high-grade second atrioventricular block. New Eng J Med 2005;353:145e155. 17. Lamas GA, Ellenbogen KA. Evidence base for pacemaker mode selection: from physiology to randomized trials. Circulation 2004;109:443e451. 18. Hildebrandt N, Stertmann WA, Wehner M, Schneider I, Neu H, Schneider M. Dual chamber pacemaker implantation in dogs with atrioventricular block. J Vet Intern Med 2009; 23:31e38. 19. Bulmer BJ, Sisson DD, Oyama MA, Solter PF, Grimm KA, Lamont L. Physiologic VDD versus nonphysiologic VVI pacing in canine 3rd degree atrioventricular block. J Vet Intern Med 2006;20:257e271. 20. Kelle AM, Backer CL, Tsao S, Stewart RD, Franklin WH, Deal BJ, Mavroudis C. Dual-chamber epicardial pacing in neonates with congenital heart block. J Thorac Cardiovas Surg 2007;134:1188e1192. 21. DeLeon SY, Ilbawi MN, Idriss FS. Pacemaker implantation in infants and children: a simplified approach. Ann Thorac Surg 1980;30:599e601. 22. Kubus P, Materna O, Gebauer RA, Matejka T, Gebauer R, Tlaskal T, Janaousek J. Permanent epicardial pacing in children: long-term results and factors modifying outcome. Europace 2012;14:509e514. 23. Cohen MI, Bush DM, Vetter VL, Tanel RE, Wieand TS, Gaynor JW, Rhodes LA. Permanent epicardial pacing in pediatric patients. Circulation 2001;103:2585e2590. 24. Sisson D, Thomas WP, Woodfield J, Pion PD, Luethy M, DeLellis LA. Permanent transvenous pacemaker implantation in forty dogs. J Vet Intern Med 1991;5:322e331.
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