Permanent Transvenous Pacemaker Implantation in Forty Dogs David Sisson, DVM, William P. Thomas, DVM, Jerry Woodfield, DVM, Paul D. Pion, DVM, Michael Luethy, DVM, and Laura A. DeLellis, DVM

Permanent transvenous cardiac pacemakers were implanted in 40 dogs. Electrocardiographic diagnoses included persistent atrial standstill (3 dogs), sick sinus syndrome (8 dogs), and high-grade second-degree or third-degree atrioventricular (AV) block (29 dogs). Thirteen dogs were alive and well 4 to 42 months after pacemaker implantation (mean, 16.9 months). The mean and median survival times of the 26 dogs that died or were euthanatized during the study were 17.9 months and 13 months, respectively. Most of these dogs succumbed to problems unrelated to the arrhythmia and pacemaker implant. One dog was lost to follow-up. Complications associated with permanent transvenous pacemaker implantation included lead dislodgement, infection, hematoma formation, skeletal muscle stimulation, ventricular arrhythmia, migration of the pulse generator, and skin erosion. Lead dislodgement was the most common complication, occurring in 7 of 9 dogs paced using untined electrode leads and in 6 of 30 dogs paced using tined leads. Lead dislodgement did not occur in the only dog paced using an actively fixed endocardial lead. It was concluded that permanent transvenous cardiac pacing is a feasible, less traumatic alternative to epimyocardial pacing in dogs, but that successful use of this technique requires careful implantation technique and anticipation of the potential complications. (Journal of Veterinary Internal Medicine 1991; 5:322-331)

THE FIRST totally implantable artificial cardiac pacemakers were developed more than 30 years ago.' Since then, the equipment and techniques available to accomplish artificial cardiac pacing have changed dramatially.^-^ One of the most important technologic advances in artificial pacemaker design has been the development of durable pacing and sensing endocardial electrodes (leads) that can be introduced into the heart from a peripheral vein6-*Before the development of permanent transvenous leads, reliable artificial cardiac pacing could only be accomplished by surgical implantation of an epimyocardial electrode. Currently, transvenous

From the Department of Veterinary Clinical Medicine (Sisson, Luethy), College of Veterinary Medicine, University of Illinois, Urbana, Illinois, and the Department of Medicine (Thomas, Woodfield, Pion, DeLellis), School of Veterinary Medicine, University of California, Davis, California. Dr. Woodfield's current address is the Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia. An abstract describing the early results of permanent transvenous pacemaker implantation in 14 dogs was presented at the Fourth Annual Medical Forum of the American College of Veterinary Internal Medicine, May 1987. Reprint requests: Dr. David Sisson, Department of Veterinary Clinical Medicine, College of Veterinary Medicine, 1008 West Hazelwood Drive, Urbana, IL 6 I80 I .

cardiac pacing is the preferred method of permanent cardiac pacing in human patients with symptomatic bradyarrhythmias. According to a current national survey of pacing practices in humans, less than two percent of lead implantations for antibradyarrhythmia pacing are accomplished using surgically implanted epimyocardial leads.' Since Buchanan et al. lo implanted the first artificial cardiac pacemaker in a dog with symptomatic bradycardia more than 20 years ago, epimyocardial lead systems have almost always been used to accomplish artificial cardiac pacing in Several studies have documented a high rate of complications in dogs treated with cardiac pacemakers using surgically implanted epicardial leads. '1-13 Problems have included infection, pleural effusion, pneumonia, lead dislodgement, pulse generator migration, skeletal muscle stimulation, exit block due to myocardial fibrosis, cardiac arrhythmias, heart failure, and acute renal failure. To reduce the complications and morbidity associated with lateral thoracotomy, the caudal median sternotomy and laparotomy transdiaphragmatic approaches have been advocated for the implantation of epimyocardial leads in dogs. l5-I7 With these methods, the pulse generator is placed into the abdominal cavity and may be inaccessible for external re-

322

Vol. 5

. NO. 6, 1991

323

PACEMAKER IMPLANTATION IN FORTY DOGS

programming. Laparotomy is required to replace battery-depleted pulse generators, and the thorax must be reentered to remove infected leads or to insert new leads. Most dogs requiring pacemaker implantation are old, and they are poor surgical candidates as a result of their arrhythmia(s), coexisting myocardial or valvular heart disease, or other disease This study was done to develop the technique and evaluate the efficacy of permanent transvenous cardiac pacing in dogs as an alternative to the implantation of epimyocardial leads by surgical invasion of the thorax. Materials and Methods From January 1984 until December 1988, permanent transvenous cardiac pacemaker implantation was done in 40 dogs with symptomatic bradyarrhythmias admitted to the Veterinary Medical Teaching Hospital (VMTH), University of California, Davis, or to the VMTH, University of Illinois, Urbana. Indications for cardiac pacing included persistent atrial standstill in 3 dogs, sick sinus syndrome in 8 dogs, and intermittent or persistent high-grade second-degree or third-degree (complete) atrioventricular block in 29 dogs. Rhythm diagnoses were established by standard 7- 10 lead resting electrocardiograms in 33 dogs, and in 7 dogs, by the combined recording of a resting electrocardiogram and a continuous 24-hour ambulatory electrocardiogram. The mean age of the dogs selected for pacemaker implantation was 9.1 years (range, 8 months to 16 years). Seventeen of the dogs were males, 8 of which were castrated. Twenty-three of the dogs were females, 2 1 of which were neutered. Body weights ranged from 5.2 to 38 kg (mean, 23.2 kg). Age, sex, and breed distributions, categorized according to the diagnosed rhythm disorder, are summarized in Table 1.

History and Clinical Findings Syncope was observed on one or more occasions by the owners of 25 dogs. Lethargy or exercise intolerance was

reported by the owners of 26 dogs and was the only sign observed by the owners of 5 dogs. Abdominal distension from ascites was noticed by the owners of six dogs. The owners of five dogs reported a recent onset of coughing. One dog with complete heart block and a heart rate of 50 beatslminute was considered asymptomatic by its owner. Two dogs suffered from idiopathic seizures which predated the discovery of bradycardia. Concurrent systemic disorders documented before pacemaker implantation included hypothyroidism (3 dogs), hyperadrenocorticism ( 1 dog), chronic renal failure (2 dogs), pneumonia (1 dog), chronic colitis (1 dog), and gastrointestinal bleeding of uncertain etiology (1 dog). Four of the five dogs with ascites and eight other dogs, six of which had systolic murmurs and clinical findings typical of mitral or tricuspid regurgitation, were receiving furosemide at the time of admission. One dog with mitral and tricuspid regurgitation was being treated with hydralazine. Other drugs that were being administered at the time of admission to the hospital included isoproterenol (two dogs), propantheline bromide (four dogs), atropine (two dogs), and isopropamide iodide (one dog). All of the dogs were examined at the time of admission by one or more of the authors. Systolic murmurs, grade 216 to 416, were present in 26 dogs. The murmur was loudest at the mitral valve area in 21 dogs and of equal intensity at the mitral and tricuspid valve areas in 5 dogs. Five dogs had right heart failure at the time of initial evaluation, as evidenced by ascites and jugular distension. Four of the dogs with heart failure had systolic murmurs, two had audible third-heart sounds, and one had no abnormal heart sounds.

Pacing Equipment Pulse generators of various manufacture and model number, but all of the VVI type, were implanted in the dogs in this study. Some of the pulse generators, obtained from pacemaker distributing companies or directly from the manufacturer, were new. Others, ex-

TABLE1 . Clinical Findings in 40 Dogs Requiring Pacemaker Implantation Clinical Signs ECG Diganosis

Age (Mean)

M/F Ratio

Sick sinus syndrome (n = 8)

1-15 yrs (10.6 yrs)

Persistent atrial standstill (n = 3 ) AV block (n = 29)

Breeds (No.)

Weakness

Syncope

Ascites

Cough

117

Min. Schnauzer (6), Cocker Spaniel ( I ) , Mixed breed ( 1 )

1

7

1

0

, 7 5 4 yrs (3.7 Yrs)

310

Golden Retriever (l), Cocker Spaniel (I), Mixed breed ( 1 )

3

1

2

0

1-15 yrs (9.5 yrs)

13116

Boxer (3), Cocker Spaniel (2), English Springer Spaniel (2), Dachshund (2), Standard Poodle (2), Mixed breed ( 10)

22

17

2

5

Sick sinus syndrome includes those dogs with intermittent sinus arrest or sinus bradycardia with or without supraventriculartachyarrhythmias.

324

Journal of Veterinary Internal Medicine

SISSON ET AL.

planted from human patients, were obtained from local hospitals or as private donations, and were in used condition before implantation in dogs. The initial preset pacing rate varied from 69 to 104 beats per minute, but was most commonly 80 beats/minute (12 dogs) or 100 beats/minute (19 dogs). Pulse generator output was typically preset at a voltage of 5 V with a pulse duration of I .O msec. The usual sensitivitysetting ofthe pulse generators was 2 mV. Pacemaker leads, also of various types and manufacture, were all in new condition before implantation. With one exception, the design of the endocardial lead implanted did not permit active fixation to the myocardium. Untined leads (six unipolar, three bipolar), were implanted in nine dogs. Tined unipolar leads were implanted in the remaining 30 dogs. All leads and pulse generators were sterilized with ethylene oxide before implantation.

Patient Preparation A variety of drugs and drug combinations were used to provide anesthesia during pacemaker implantation. Anesthetic induction was most often accomplished with diazepam and either oxymorphone (1 8 dogs) or ketamine (9 dogs) administered IV. In 34 dogs, isoflurane, halothane or metofane were also used in low concentrations to maintain a surgical plane of anesthesia. In two depressed and debilitated dogs, lidocaine local anesthesia was used without additional sedation. In most dogs, arterial pressure was monitored continuously through a peripheral artery catheter. Temporary transvenous pacing, using a previously described technique,' was established in four dogs before the induction of anesthesia. Provision for emergency transvenous pacing was made in the remaining cases by ensuring the ready availability of an external pulse generator and temporary pacing lead before induction of anesthesia.

Technique of Implantation After induction of anesthesia, a one- to two-inch incision was made in the skin and subcutis over the right or left external jugular vein. An endocardial lead was introduced into the vein through a small incision and advanced, with fluoroscopicguidance, until the tip was positioned in the apex of the right ventricle. When tined leads were used, attempts were always made to wedge the tip of the lead in a location where gentle traction on the lead was met with some resistance. Threshold and sensing measurements were not made at the time of implantation of the endocardial leads. Adequate placement of the lead was presumed when regular cardiac pulsations were observed by fluoroscopy, when the arterial pulse rate increased to the preprogrammed pacing rate, and when reliable sensing and pacing functions were observed on a simultaneously recorded surface or transesophageal electrocardiogram. The lead was usually se-

cured in position using two or three nonabsorbable ligatures that encircled the lead and jugular vein. The pulse generator was placed in a subcutaneous pocket created at the site of a separate skin incision on the dorsolateral aspect of the neck, into which the lead had been tunneled. Synthetic pouches were not used, but the pulse generators were usually secured to the underlying musculature by one or two nonabsorbable sutures. Subcutaneous tissues over the pulse generator were closed with absorbable suture material, and the skin incisions were closed with nonabsorbable suture material in a routine manner.

Postoperative Evaluation Lateral and dorsoventral thoracic radiographs and a 10lead electrocardiogram were obtained in all dogs within 24 hours after operation to document lead placement and satisfactory pacemaker function (Figs. 1, 2). The electrocardiogram was monitored intermittently for at least 48 hours after implantation. Dogs free of serious complications were discharged to the care of the owner 3 to 5 days after the operation. Antibiotics, most commonly oxacillin, a cephalosporin*,f or a potentiated sulfa compound,$ were prophylacticallyadministered to 33 dogs for 3 to 14 days after pacemaker implantation. Follow-up examinations were scheduled at 10 days and 3 to 6 months post-implantation, and every 6-12 months thereafter. Long-term evaluation was accomplished by periodic reexamination of the dogs and by consultation with referring veterinarians. Owner satisfaction with the procedure was assessed by telephone interview at the end of the study and was scored as poor, fair, good, or excellent. Results

At the time of submission of this report, 13 of the 40 dogs entered in the study were alive 4 to 42 months after pacemaker implantation (mean, 16.9 months; median, 14 months). The mean and median survival times of the 26 dogs that died (10 dogs) or were euthanatized (16 dogs) were 17.9 months and 13 months, respectively. The mean age at death was 10.6 years. One dog was lost to follow-up. Reasons for euthanasia included refractory heart failure (six dogs), malignant neoplasia (four dogs), aging and general debilitation (three dogs), renal failure (one dog), recurrence of syncope (one dog), and dyspnea of uncertain cause (one dog). Of the ten dogs that died, four died suddenly at home and one died suddenly in the hospital 1 day after epicardial pacemaker implantation which was required because of recurrent endocardial lead dislodgement. Two dogs died of refractory congestive heart failure. One dog died as a result of sepsis with * Keflex, Dista Products Co., Indianapolis, IN.

t Velosef, ER Squibb and Sons Inc., Princeton, NJ.

4 Tribrissen, Burroughs Wellcome Co., Research Triangle, NC.

Vol. 5

. NO. 6, 1991

325

PACEMAKER IMPLANTATION IN FORTY DOGS

Complications Life-threatening complications or complications necessitating reoperation (lead dislodgement, lead failure or exit block, infection, migration of the pulse generator, and erosion of the overlying skin) developed in 22/40 dogs (55%). Eighteen dogs experienced no (1 3 dogs) or comparatively minor complications, including post-operative hematoma/seroma, skeletal muscle stimulation, or transient ventricular arrhythmias. Lead dislodgement and the minor complications listed occurred early after pacemaker implantation ( 1- 19 days), whereas lead failure/exit block and pulse generator migration occurred later, 2 to 3 1 months after implantation. Infections at the site of pacemaker implantation were manifested early, during the first postoperative month, or after a delay of 2 to 5 months (Table 2). Arrhythmia. Paroxysmal ventricular tachycardia was detected in two dogs before pacemaker implantation. One of these dogs experienced ventricular fibrillation twice during pacemaker implantation and was successfully defibrillated each time. After pacemaker implantation, both dogs required continuous antiarrhythmic drug treatment to restore and maintain sinus rhythm. Infrequent ventricular premature beats were detected preoperatively in two dogs, persisting in one dog after pacing. Neither dog was treated with antiarrhythmic drugs. Ventricular premature beats developed in seven dogs within 48 hours of pacemaker implantation. Five dogs were

I

111

AVFI

AVL

AVF

LEAD II

FIG. 1. Lateral (A) and dorsoventral (B) thoracic radiographs show an endocardial paclng lead properly positioned in the apex of the nght ventncle.

coexisting ventricular arrhythmias believed to be caused 1

plications resulting from attempted removal of an infected lead' One dog died as a Of 'Ystemic mastocflosis, gastrointestinal bleeding, and renal failure.

pacemaker programed to pace at a rate of 100 beats per minute. Morphology of the QRS complexes is typical for dogs paced using endocardial electrodes positioned in the right ventricle. Arrows indicate the stimulus artifact produced by pacemaker discharge. Paper speed: 50 mm/second; sensitivity: 1 .O cm/l.O mV

Journal of Veterinary

326

SISSON ET AL.

Internal Medicine

TABLE2. Complications in 40 Dogs with Permanent Transvenous Pacemakers Complication

No. of Dogs

Time of Onset

Treatment/Outcome

Ventricular arrhythmia

16

Preexisting (4 dogs) Lead dislodgement (5 dogs) 248 hours (7 dogs)

2 dogs - chronic Rx 14 dogs - resolved I dog - fibrillated: revived

Lead dislodgement

13

548 hours (7 dogs), Day 3, 9,

9 dogs - repositioned 3 dogs - epicardial lead implanted 1 death (GI bleed)

12, 13, 17, 19

Infection

6

Day 15 and 17 Month 2, 3, 3.5, 4.5

4 dogs - antibiotics I lost to follow-up 2 chronic infection I death (sepsis) 2 dogs - replaced lead and pulse generator

Pulse generator migration

5

Month 3.5 (2 dogs), 4, and 16.5

2 dogs - replaced lead and pulse generator 1 dog - explanted 1 dog - antibiotics: chronic infection 1 death (lead extract)

Skeletal muscle stimulation

5

548 hours (5 dogs)

3 dogs - resolved I dog - reprogram 1 dog - persisted

Hematomaiseroma

4

Week 1 (4 dogs)

2 dogs - migration of pulse generator 1 dog - lead twiddle

Lead failure/exit block

3

Month 11, 24, 31

2 dogs - replaced lead and pulse generator 1 death (sudden)

successfully treated with antiarrhythmic drugs, whereas two dogs with infrequent arrhythmias were not treated. Ventricular arrhythmias detected in five dogs after lead dislodgement were resolved by repositioning of the endocardial lead. Lead Dislodgement. Thirteen dogs (33%), including 7 of 9 dogs paced with untined leads and 6 of 30 dogs paced with tined leads, experienced intermittent or complete loss of pacing due to lead dislodgement. Lead dislodgement occurred within 48 hours of implantation in seven dogs and was detected on postoperative days 6,9, 12, 13, 17, and 19 in the remaining six dogs. None of these dogs experienced syncope after lead dislodgement, but rhythmic contractions of the diaphragm developed in two dogs and rhythmic twitching of cervicalor forelegmusculature developed in five dogs. Electrocardiographic evidence of lead displacement included intermittent or complete loss of pacing and sensing functions in all a 1 3 dogs and ventricular arrhythmias in 5 dogs (Fig. 3). Lead dislodgement to the right atrium, caudal vena cava, or to the inflow or outflow regions of the right ventricle was verified in each case by thoracic radiographs (Fig. 4). Repeated rotation of the pulse generator in the cervical pocket (pacemaker twiddle) with dislodgement of the lead tip to the cranial vena cava was observed in two dogs

(Fig. 5). Stable cardiac pacing was achieved by reoperation and repositioning of the endocardia1 lead in 9 of the 13 dogs. Infections developed at the site of pacemaker implantation in three of these dogs. Lead dislodgement occurred repeatedly in three dogs all of which were subsequently paced using surgically implanted epicardial leads. One dog with systemic mastocytosis, gastrointestinal hemorrhage, and renal failure died before reoperation could be done. I = A n

II

-

FIG. 3. Loss of pacing and sensing functions due to lead dislodgement was manifested on electrocardiogramsby pacemaker stimulus artifacts (solid arrows) which occurred independent of the underlying cardiac rhythm and which failed to elicit ventricular depolarization. Paper speed: 50 mm/second; sensitivity: 1.O cm/l .O mV.

Vol. 5

. NO. 6, 1991

PACEMAKER IMPLANTATION IN FORTY DOGS

327

FIG. 4. Lead dislodgement was the most common serious complication observed in this study. Loss of cardiac pacing occurred when endocardial leads were dislodged from the right ventricular apex into the inflow (A) or outflow tracts (B) ofthe right ventricle, the right atrium (C), or the caudal vena cava (D).

Skin Erosion and Pacemaker Extrusion. Ventral migration of the pulse generator, erosion of the overlying skin, and secondary infection of the pacemaker implantation site was observed in five dogs 3.5 to 16.5 months after implantation. Three dogs were successfully treated with antibiotics after removal of the contaminated pulse generator and removal or partial excision and debridement of the endocardial lead. New pulse generators and endocardial leads were implanted in two ofthese dogs with no additional complications. The third dog, whose owner declined reimplantation of a new pulse generator, was alive 1 1 months after pacemaker removal. One dog died as a result of chylothorax and cranial vena caval thrombosis, which occurred during an attempt to extract an infected lead. One dog treated only with long-term antibiotics was euthanatized 14 months postimplantation ( 1 0 months after infection), in part because of persistent in-

fection at the pacemaker site. Erosion of the skin and exposure of a ground electrode was observed in one dog 30 months postimplantation. Successful management was accomplished by administration of antibiotics and removal of the contaminated portion of the exposed electrode. Infection. Infections, unrelated to ventral migration of the pulse generator, developed at the site of pacemaker implantation in six dogs, three of which had been reoperated for lead dislodgement. Three dogs, including one dog reoperated for lead dislodgement, did not receive perioperative antibiotic therapy. Infections developed in two dogs within 1 month of operation and in four dogs 2 to 4.5 months after pacemaker implantation. Management of infected pacemaker sites included removal of the pulse generator and lead from two dogs and

328

Journal of Veterinary Internal Medicine

SISSON ET AL.

shoulder skeletal musculature, not associated with lead dislodgement, was observed in five dogs. Skeletal muscle twitching spontaneously resolved in three dogs within several weeks of implantation. One of these dogs died suddenly 2 years later and results of necropsy showed severe corrosion of the endocardial lead wire. Muscle twitching abated only after reprogramming of the pulse generator in one dog and persisted in one dog. Intermittent loss of pacing capture was documented on the electrocardiograms of two dogs, 11 months and 31 months after pacemaker implantation. In both instances, the endocardial leads appeared to be normally positioned on thoracic radiographs. Pulse generator replacement did not restore normal pacing function in either dog, suggestinglead failure or exit block as the cause of pacemaker malfunction. Both dogs were successfully managed by implantation of a new pulse generator and pacing lead (1 epicardial, 1 endocardial).

Owner Satisfaction

FIG.5. In 2 dogs, repeated rotation ofthe pulsegenerator in the subcutaneous pocket (pacemaker “twiddle”) resulted In dislodgement of the endocardial lead from the right ventricle into the cranial vena cava (A) or jugular vein (B) and loss of cardiac pacing.

antibiotic therapy in all six dogs. A new pulse generator and lead were implanted in the dogs that were reoperated. In one reoperated dog, the firmly implanted endocardial lead was initially left in place but capped. Infection reoccurred in this dog and was resolved only after removal of the capped lead by the use of continuous traction for 7 days. Of the 4 dogs treated with antibiotics alone, one dog appeared to recover completely but was lost to further follow-up 6 months later; one dog died of sepsis or from coexisting ventricular arrhythmias; and a persistent draining tract at the site of pacemaker implantation developed in two dogs. A draining tract was present in both dogs at the time of euthanasia, 9 months and 28 months after implantation. Other Complications. Large hematomas or seromas developed at the site of pacemaker implantation in four dogs. Two dogs subsequently experienced ventral migration of the pulse generator and erosion of the overlying skin, and one dog experienced pacemaker twiddle with lead dislodgement. Synchronous twitching of cervical or

Thirty-nine owners were contacted by telephone to evaluate their satisfaction with the results of the procedure. The results were rated excellent by 23 owners, good by 4 owners, fair by 5 owners, and poor by 7 owners. Six of the 7 dogs that were owned by clients ranking the results as poor were dead at the time of survey, with a mean survival time of 4.9 months (range, 2 days to 15 months). Complications in this group of dogs included lead dislodgement (four dogs) and pulse generator extrusion (one dog). The five dogs that were owned by clients ranking the results as fair were dead at the time of survey with a mean survival time of 14.6 months (range, 3-28 months). Complications in these dogs included lead dislodgement (three dogs) and pacemaker-related infection (one dog). Of the 27 dogs that were owned by clients ranking the results as good or excellent, 14 were dead with a mean survival time of 26.5 months (range, 7-57 months). One dog had died during an operation to remove an infected lead and two dogs died suddenly, 26 and 57 months after pacemaker implantation. Complications included lead dislodgement (six dogs), extrusion of the pulse generator (four dogs) and post-operative infection (five dogs). Discussion Dislodgement of the endocardial lead was the most common complication observed in the dogs of this study. Predisposing causes of lead dislodgement, identified in this study and previously reported in humans implanted with endocardial leads, included the use of untined operator ine~perience,~~-’~ enlargement of the right ~entricle,’~ and inadequate stabilization of the pulse generator resulting in pacemaker twiddle.25The smooth trabecular pattern of the right ventricle of dogs,

VOl.

5 . NO.6, 1991

PACEMAKER IMPLANTATION IN FORTY DOGS

compared with that of humans, also may have contributed to the high rate of lead dislodgement.26 Fewer instances of lead dislodgement occurred when tined leads were used and after experience with the technique of lead placement was gained. The lateral projections of tined leads permit the operator to wedge the pacing electrode more securely in the apex of the right ventricle. Of the first 20 dogs studied, lead dislodgement occurred in 7 of 9 dogs paced using untined leads and in 4 of 1 1 dogs paced using tined leads. Of the last 20 dogs studied, lead dislodgement occurred in only 2 of 19 dogs paced using tined leads. Lead dislodgement did not occur in the only dog paced using an actively fixed endocardial lead. Parsonnet et al.9322reported that frequent implanters of pacemakers ( 212 procedures per year) have fewer complications, including lead dislodgement, than infrequent implanters (< 12 per year). Using these criteria, none of the operators in this study could be considered a frequent implanter. The results of this study suggest that tined rather than untined endocardial leads should be implanted in dogs. Lead dislodgement may also be prevented by use of actively fixed endocardial lead^,^^,^^ but the expense of such leads currently precludes their implantation in all dogs requiring cardiac pacemakers. Secure fixation of the pulse generator in the neck and avoidance of tension on the lead wire are also important to stable lead placement. Pacemaker twiddle can usually be prevented if the pulse generator is securely positioned in an appropriately sized p ~ c k e t . ' ~ Pulse ? ~ ~generator migration and skin erosion also resulted, at least in part, from inadequate stabilization of the pulse generator in the neck. Other factors contributing to skin erosion may have included rejection, the use of large pulse generators relative to the size of the dog, and the lack of adequate subcutaneous fat to pad the pulse generat~r.~'Possible solutions to these problems include the use of smaller pulse generators, the use of synthetic pouches, the creation of smaller subcutaneous pockets, more meticulous placement of the stabilizing sutures, and placement of the generator in a deeper, more caudal or more dorsal lo~ation.~~-~' Infections not related to pulse generator migration and skin erosion developed in six dogs in this study. Reoperation to reposition a dislodged lead appeared to be an important contributing cause of infection in this study, as reported in human^.^^.^^ Operator inexperience may also have been a contributing factor, since operating time is usually longer when a new technique is being learned.9,21,22,30 The facilities in which pacemaker implantations are done may also be an important factor influencing the prevalence of pacemaker infection^.^' All implants in this study were completed with the aid of fluoroscopy in the radiology departments of the teaching hospitals. In contrast, most permanent transvenous pacemaker procedures in human patients are done in an

329

operating room equipped with a fluoro~cope.~ Miller et al.34 have shown that pacemaker implantation can be done with equivalent safety in the catheterization laboratory as in the operating room when appropriate precautions are observed. Strict adherence to an aseptic protocol in the performance of pacemaker implantation is important. The prophylactic use of perioperative antibiotics for pacemaker implantation or repositioning is c o n t r o v e r ~ i a l . ~In ~ , this ~ ~ - study, ~~ postoperative infections developed in 3 of 33 dogs (10%) receiving antibiotics at the time of pacemaker implantation, and in 3 of 7 dogs (43%)that did not receive antibiotics. We believe that antibiotic use is warranted when transvenous pacemakers are implanted under the circumstances described. The management of pacemaker infections, whether primary or secondary to skin erosion, is also controversia1.30-33,37-41 Antibiotic therapy, guided by the results of culture and sensitivity testing, is indicated in all cases of pacemaker infection. Removal of the pulse generator is simple and is also recommended in all cases of inf e ~ t i o n . ~ ~If- ~the I lead is not tightly adhered to the right ventricular endocardium, it should also be remOVed.30-33,37-41 Wh en the infection is limited to the pulse generator pocket, a tightly adhered lead may be cut off below the infected area, sealed, and left in pla~e.~'.~' If the infection involves the intravascular portion of the lead, removal of the lead by continuous traction or by thoracotomy and excision from the right ventricle is rec~ m m e n d e d . ~ ~ ,Vigorous ~ ' , ~ ~ , ~attempts ~ to extract a tightly adhered lead may result in serious arrhythmias, damage to the tricuspid valve, inversion of the right ventricle, and death.45-46A less traumatic method for severing and removing the intravascular portion of endocardial leads has recently been described.44 Two dogs with well-positioned endocardial leads experienced loss of pacing in spite of normally functioning pulse generators. Although the leads were not rigorously tested for electrical integrity, both leads appeared to be intact and undamaged. Pacing leads have been shown to elicit an inflammatory tissue reaction in the myocardium of experimentally paced dog^.^^,^^ Inflammation and fibrosis surrounding the electrode tip can result in exit block of the pacing stimulus. Modifications in the design and composition of the pacing electrode should minimize the prevalence of this c ~ m p l i c a t i o n . ~ ~ , ~ ~ The overall prevalence of serious complications observed in this study was higher than we anticipated and was comparable to the complication rates reported by other investigators using epimyocardial lead systerns' 1-13.15 or endocardial leads5' In a reported study of transvenous cardiac pacing in 19 dogs and 1 cat, Darke et al" reported complications similar to those we observed in the last 19 dogs paced using tined leads. They reported lead dislodgement in 2 of 18 dogs paced with tined endocardial leads, the development of serous effu-

330

SISSON ET AL.

sion around the pulse generator in 6 dogs, and infection in 3 dogs-results that were similar to those we observed. Despite these complications, the authors believe that permanent transvenous endocardial pacing will become the preferred method of cardiac pacing in dogs, when fluoroscopy is available. The problems that must be solved before this method of pacing can be considered safe and reliable in the dog have been identified. The authors believe that lead dislodgement, infection, migration of the pulse generator, and skin erosion can be minimized by meticulous attention to technique. Associated problems such as heart failure due to coexisting valvular or myocardial disease are more difficult to prevent or to remedy. The high incidence of valvular and myocardial disease in this study and in prior rePorts’ 1-15,50 suggests that conduction disturbances in dogs are often an indication of a generalized myocardial disease process rather than an isolated conduction-system lesion. In view of the high incidence of valvular insufficiency, myocardial disease and congestive heart failure in dogs with symptomatic bradyanhythmias, the routine use of physiologically responsive, dual atrial and ventricular pacemakers can be anti~ipated.~’,~’ These pacing modalities offer the well-documented hemodynamic advantages of sequential atrial and ventricular c ~ n t r a c t i o n . ~ * ~Successful ’-~~ application of these and other technologic advances in pacemaker design requires that the current obstacles to reliable permanent transvenous cardiac pacing be surmounted. References 1. Chardack WM, Gage AA, Greatbatch W. A transistorized selfcontained implantable pacemaker for the long-term correction of complete heart block. Surgery 1960; 48:643-654. 2. Lillehei RC, Romero LH, Beckman CB, et al. A new solid-state long-life, lithium-powered pulse generator. Ann Thorac Surg 1974; 18:479-489. 3. Hunter SW, Bolduc L, Long V, et al. A new myocardial pacemaker lead (sutureless). Chest 1973; 63:430-433. 4. Parsonnet V, Furman S, Smyth NPD. Implantable cardiac pacemakers: Status report and resource guideline. Report of the International Society Commission for Heart Disease Resources. Am J Cardiol 1974; 34:487-500. 5. Parsonnet V, Bernstein AD. Cardiac pacing in the 1980s: Treatment and techniques in transition. J Am Coll Cardiol 1983; 1:339-354. 6. Harthorne JW, DeSanatis RW, Sulit YO, et al. Epicardial versus endocardial pacemakers: Analysis of 109 cases. Ann Thorac Surg 1968; 6:417-423. 7. Mond H, Sloman G. The small-tined pacemaker lead-absence of dislodgement. PACE 1980; 3:171-177. 8. Littleford PO, Parsonnet V, Spector SD. Method for the rapid atraumatic insertion of permanent endocardial pacemaker electrodes through the subclavian vein. Am J Cardiol 1979; 43:980-982. 9. Parsonnet V, Bernstein AD, Galasso D. Cardiac pacing practices in the United States in 1985. Am J Cardiol 1988; 62:71-77. 10. Buchanan JW, Dear MG, Pyle RL. Medical and pacemaker therapy of complete heart block and congestive heart failure in a dog. J Am Vet Med Assoc 1968; 152:1099-1109. I I . Yoshioka MM, Tilley LP, Harvey HJ, et al. Permanent pacemaker implantation in the dog. J Am Animal Hosp Assoc 1981; 17~746-750. 12. Lombard CW, Tilley LP, Yoshioka M. Pacemaker implantation in

13. 14.

15.

16. 17. 18. 19. 20. 2 1. 22. 23. 24. 25. 26.

27.

28. 29. 30. 31. 32. 33. 34.

35. 36.

Journal of Veterinary Internal Medicine

the dog: Survey and literature review. J Am Anim Hosp Assoc 1981; 171751-758. Bonagura JD, Helphrey ML, Muir WW. Complications associated with permanent pacemaker implantation in the dog. J Am Vet Med Assoc 1983; 182:149-155. Musselman EE, Rouse GP, Parker AJ. Permanent pacemaker implantation with transvenous electrode placement in a dog with complete atrioventricular heart block, congestive heart failure and Stokes-Adams Seizures. J Small Anim Pract 1976; 17:149162. Fox PR, Matthiesen DT, Purse D, et al. Ventral abdominal, transdiaphragmatic approach for implantation of cardiac pacemakersin the dog. J Am Vet Med Assoc 1986; 189:1303-1308. Fingeroth JM, Birchard SJ. Transdiaphragmatic approach for permanent cardiac pacemaker implantation in dogs. Vet Surg 1986; 15:329-333. Helphrey ML, Schollmeyer M. Pacemaker therapy. In: Kirk RW, ed. Current Veterinary Therapy VIII. Philadelphia: WB Saunders Co, 1983; 373-376. Furman S, Pannizzo F, Campo I. Comparison of active and passive leads for endocardial pacing-11. PACE 1981; 4:78-83. Holmes DR, Gersh BJ, Maloney JD, et al. Follow-up experience with permanent endocardial tined pacemaker electrodes. J Thorac Cardiovasc Surg 1980; 79565-569. Perrins EJ, Sutton R, Kalebic B, et al. Modern atrial and ventricular leads for permanent cardiac pacing. Br Heart J 1981; 46:196-201. Furman S, Fisher JD. Cardiac paceing and pacemakers. V. Technical aspects of implantation and equipment. Am Heart J 1977; 94:250-259. Parsonnet V, Crawford CC, Bernstein AD. The 198 1 United States survey of pacing practices. J Am Coll Cardiol 1984; 3:13211332. Parsonnet V, Bernstein AD, Lindsay B. Pacemaker-implantation complication rates: an analysis of some contributing factors. J Am Coll Cardiol 1989; 13:9 17-92 1. Greaow J. Goodluck P. Effect of cardiothoracic ratio on early lead failure following initial transvenous permanent pacemaker implant (Abstr). PACE 1979; 2:A-37. Weiss D, Lorber A. Pacemaker twiddler’s syndrome. Int J Cardiol 1987; 15~357-360. Cummings JR, Gelok R, Grace JL, et al. Long-term evaluation in large dogs and sheep of a series of new fixed-rate and ventricular synchronous pacemakers. J Thorac Cardiovasc Surg 1973; 66:645-652. Bisping M, Kruezer J, Birkenheier H. Three-year clinical experience with a new endocardial screw-in lead with introduction protection for use in the atria and ventricle. PACE 1980; 3:424-435. Robicsek F, T a j a n P, Harbold NB, et al. Self-anchoring endocardial pacemaker leads. Current spectrum of types, advances in design and clinical results. Am Heart J 1981; 102:775-782. Hill PE. Complications of permanent transvenous cardiac pacing: A 14-year review of all transvenous pacemakers inserted at one community hospital. PACE 1987; 10:564-570. Mond HG. Pacing side effects. In: Mond HG. The Cardiac Pacemaker Function and Malfunction. New York: Grune and Stratton, 1983; 393-424. Kirk AJ, Turner MA. Surgical aspects of permanent cardiac pacemakers. Life Support Syst 1987; 5:223-231. Choo MH, Holmes DR, Gersh BJ, et al. Permanent pacemaker infections: characterization and management. Am J Cardid 1981; 481559-564. Kennelly BM, Piller LW. Management of infected transvenous permanent pacemakers. Br Heart J 1974; 36:1133-I 140. Miller GB, Leman RB, Kratz JM, et al. Comparison of lead dislodgement and pocket infection rates after pacemaker implantation in the operating room versus the catheterization laboratory. Am Heart J 1988; 115:l048-105l. Smyth NPD. Cardiac pacemaking (collective review). Ann Thorac Surg 1969; 8:166-190. Harstein AI, Jackson J, Gilbert DN, et al. Prophylactic antibiotics and the insertion of permanent transvenous cardiac pacemakers. J Thorac Cardiovasc Surg 1978; 75:219-223.

Vol. 5

. No. 6, 1991

PACEMAKER IMPLANTATION IN FORTY DOGS

37. Siddons H, Nowak K. Surgical complications of implanting pacemakers. Br J Surg 1975; 62:929-935. 38. Choo MH, Holmes DR, Gersh BJ, et al. Infected epicardial pacemaker systems. Partial versus total removal. J Thorac Cardiovasc Surg 1981; 82:794-796. 39. Lewis AB, Hayes DL, Holmes DR, et al. Update on infections involving permanent pacemakers. J Thorac Cardiovasc Surg 1985; 89:758-763. 40. Mansour KA, Kauten JR, Hatcher CR. Management of the infected pacemaker: explanation, sterilization, and reimplantation. Ann Thorac Surg 1985; 40:617-619. 41, Holswade GR. Conservative operative procedures for extruding and/or infected pacemakers. PACE 1979; 2:A-37. 42. Hoover EL, Hsu HK, Toporoff B, et al. Use of traction for removing transvenous pacing electrodes in the presence of infection. J Tenn Med Assoc 1988; 81:504-507. 43. Yarnoz MD, Attai LA, Furman S. Infection of pacemaker electrode and removal with cardiopulmonary bypass. J Thorac Cardiovasc Surg 1974; 68:43-46. 44. Witte J, Munster W. Percutaneous pacemaker lead-transecting catheter. PACE 1988; 11:298-301. 45. Imparato AM, Kim GE. The trapped endocardial electrode. Removal by prolonged graded skin traction. Ann Thorac Surg 1972; 14:605-608. 46. Lee ME, Chaux A, Matloff JM. Avulsion ofa tricuspid valve leaflet during traction of an infected, entrapped endocardial pace-

47. 48. 49.

50. 5 1. 52. 53. 54. 55.

33 1

maker electrode. The role ofelectrode design. J Thorac Cardiovasc Surg 1977; 74:433-435. Fishbein MC, Tan KS, Beazell JW. Cardiac pathology of transvenous pacemakers in dogs. Am Heart J 1977; 93:73-81. Radovsky AS, Van Fleet JE. Effects of dexamethasone elution on tissue reaction around stimulation electrodes of endocardial pacing leads in dogs. Am Heart J 1989; 117:1288-1298. Mond H, Stokes K, Helland J, et al. The porous titanium steroid electrode: A double blind study assessingthe stimulation threshold effects of steroid. PACE 1988; 1I :2 14-2 19. Darke PGG, McAreavey D, Been M. Transvenous cardiac pacing in 19 dogs and one cat. J Small Anim Pract 1989; 30:491-499. Darke PGG, Been M, Marks A. Use of a programmable “physiological” cardiac pacemaker in a dog with total atrioventricular block. J Small Anim Pract 1985; 26:295-303. Zhou JT, Yu GY. Hemodynamic findings during sinus rhythm, atrial and AV sequential pacing compared to ventricular pacing in a dog model. PACE 1987; 10:118-124. Samet P, Castillo C, Bernstein WH. Hemodynamic sequelae of atrial, ventricular and sequential atrioventricular pacing in cardiac patients. Am Heart J 1966; 72:725-726. Reiter MJ, Hindman MC. Hemodynamic effects ofacute atrioventricular sequential pacing in patients with left ventricular dysfunction. Am J Cardiol 1982; 49:687-692. Yashar JJ, Kitzes DL, Anf M, et al. Atrioventricular sequential pacemakers: indications, complications, and long-term followup. Ann Thorac Surg 1980; 29:91-98.

STATEMENT O F OWNERSHIP, MANAGEMENT AND CIRCULATION (Act of August 12, 1970: Section 3685. Title 39 United States Code) Date of Filing-October I , 1991 ; Title of Publication-Journal of Veterinary Internal Medicine; Publication No.-08916640; Frequency of Issue-Bi-plonthly; Annual Subscription Pnce-$40.00 Location of Known Office of Publication- 100 Insurance Way, Suite 1 14, Hagerstown, MD 2 1740; Location of the Headquarters or General Business Offices of the Publisher-J.B. Lippincott Company, 227 East Washington Square, Philadelphia, PA 19 106; Publisher-American College of Veterinary Internal Medicine, 620 N. Main St., Blacksburg, VA 24060; Editor-Alfred M. Legendre, DVM, 9037 Shallowford Road, Knoxville, TN 37923; Managing Editor-Linda Krumpholz, 227 East Washington Square, Philadelphia, PA 19106; Owner-The American College of Veterinary Internal Medicine, 620 N. Main St., Blacksburg, VA 24060; Known Bondholders, Mortgagees, and other security holders owning or holding 1 percent or more of total amount of bonds, mortgages, or other securities-None. A. Total no. copies printed (net press run), average 5,350, actual 4,100; B. Paid circulation I . Sales through dealers and camers, street vendors and counter sales, average none, actual none; 2. Mail subscriptions, average 3,782, actual 3,704; C. Total paid circulation, average 3,782, actual 3,704; D. Free distribution by mail, camer or other means. Samples complimentary, and other free copies, average 142, actual 134; E. Total distribution (sum of C and D),average 3,924, actual 3,838; F. Copies not distributed 1. Office use, leftover, unaccounted, spoiled after printing, average 1,426, actual 262. 2. Returns from news agents, none; G. Total (sum of E and F-should equal net press runs shown in A), average 5,350, actual 4,100. I certify that the statements made by me above are correct and complete. J. W. Lippincott, Publisher.