Acquired Tricuspid Valve Stenosis Associated with Two Ventricular Endocardial Pacing Leads in a Dog

Introduction

Acquired tricuspid valve stenosis (TVS) has been reported in humans as a rare complication of transvenous endocardial pacemaker placement due to lead infection, tricuspid valve leaflet perforation, a loop in the right ventricle interfering with tricuspid valve function, or multiple endocardial pacing leads.^1–7 Acquired TVS secondary to endocardial pacing lead placement has been reported in one dog previously due to excessive lead redundancy.⁸ The authors report the first canine case of acquired TVS associated with two ventricular endocardial pacing leads.

Case Report

An 11 yr old spayed female terrier weighing 9.27 kg presented for pacemaker re-evaluation. Approximately 10 yr prior, the dog had a permanent transvenous pacemaker implanted (a single right ventricular endocardial lead, ventricular pacing, ventricular sensing, inhibition response and rate-adaptive programming) for third-degree atrioventricular block of unknown etiology. Seven years later, a second surgery was performed to replace a battery-depleted pulse generator. Following replacement, interrogation of the pacing system revealed abnormally low lead impedance, suspected to be due to an accidental iatrogenic lead insulation break during the surgery. Consequently, repeated output increases were necessary to maintain ventricular capture, which ultimately led to accelerated battery depletion. Due to the suspected lead insulation break causing the low impedance, a new lead and generator were implanted 6 mo prior to the current presentation. The previously implanted lead was left in place because its tip was presumably fixed by fibrosis at its ventricular insertion point and because its presence was not deemed to be problematic. Consequently, two endocardial pacing leads were present at the time of re-evaluation.

The dog was presented to the authors' institution for abdominal distension. Physical examination revealed a heart rate of 100 beats/min with poor pulse quality. Rectal temperature was normal, the dog was eupneic, and abdominal distension was evident with a palpable fluid wave. Two-view thoracic radiographs revealed mild right-sided cardiac enlargement, appropriate positioning of the endocardial pacing leads in the ventricular myocardium, and no evidence of pulmonary edema or pleural effusion. There was a loop evident in the original endocardial pacing lead, suspected to be crossing the tricuspid annulus. Echocardiography revealed mild dilation of the left ventricle and right ventricle and moderate dilation of the right atrium. There was hyperechoic tissue associated with the pacing leads as they crossed the tricuspid valve annulus (Figure 1). Mild tricuspid regurgitation was identified on color Doppler interrogation, and spectral Doppler interrogation (Figure 2) revealed an elevated peak inflow velocity of approximately 3 m/sec through the tricuspid valve consistent with TVS. A brief ultrasound examination of the abdomen revealed distended hepatic veins and ascites. Abdominocentesis was performed, and the abdominal effusion was consistent with a modified transudate and was otherwise unremarkable. A diagnosis of right-sided congestive heart failure secondary to acquired TVS was made. The primary differential diagnoses were thrombosis, fibrosis, or infection of the pacing leads.

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A complete blood count revealed a mature neutrophilia (13,940 neutrophils/uL; reference range 3,000–11,500 neutrophils/uL) but was otherwise unremarkable. The serum biochemical profile was normal. Consequently, pacemaker lead infection was considered less likely, and the dog was prescribed aspirin^a [0.5 mg/kg per os (PO) q 24 hr] for possible thrombosis of the pacing leads. In addition, furosemide^b (1.3 mg/kg PO q 12 hr) and pimobendan^c (0.25 mg/kg PO q 12 hr) were prescribed for the management of right-sided congestive heart failure.

Over the following 6 wk, despite upward titration of diuretic therapy, the dog continued to suffer recurrent severe ascites requiring regular abdominocentesis. The dog was ultimately euthanized 6 wk after diagnosis of TVS and right-sided congestive heart failure. The owner declined a necropsy.

Discussion

It is postulated that either lead loop redundancy or multiple endocardial pacing leads causes “whiplash” injury to the valve apparatus, which has been supported by imaging studies in human patients.^3,7 It is believed that chronic repeated injury to the tricuspid valve apparatus is necessary for the development of fibrous tissue, precipitating acquired TVS, because all previously reported cases in human patients were characterized by long implant durations, ranging from 7 to 33 yr.^1–7 The only previous veterinary report of pacemaker associated acquired TVS was in a dog where an excessive loop of the endocardial pacemaker lead was hypothesized to precipitate fibrous tissue development and TVS 5.5 yr after initial placement.⁸ In the dog reported herein, the original endocardial pacing lead was placed 10 yr previously and the second endocardial pacing lead was placed 6 mo prior to the development of acquired TVS. The dog had an excessive loop in the original lead; however, the acquired TVS only developed after placement of the second endocardial pacing lead. Evaluation prior to placement of the second endocardial pacing lead failed to identify echocardiographic abnormalities consistent with TVS. As such, the authors cannot rule out subclinical TVS was developing in the dog but remain undetected prior to placement of the second endocardial pacing lead. Therefore, it is uncertain if the initial lead or a combination of multiple leads incited the development of the TVS in this dog. Because necropsy was not performed, the authors were unable to determine if the TVS was due to fibrous tissue development or pacemaker-associated thrombus, the latter having been reported in the cranial vena cava in dogs.^8,10–13

In humans with acquired TVS associated with endocardial pacing leads, many of the leads' insulation were made of silicone.^1–7 A silicone-insulated lead was used in the dog described in this case as well as the other canine case of acquired TVS.⁸ The tricuspid apparatus may be more reactive to silicone, which may contribute to the development of TVS.⁹ In addition, silicone is the most common material utilized for pacemaker lead insulation, which may also explain why it is more commonly reported with pacemaker associated TVS cases.¹⁴ The association of the pacing lead insulation material with the development of acquired TVS requires further investigation.

The diagnosis of TVS in human medicine is made primarily through continuous-wave spectral Doppler interrogation as quantification of tricuspid valve orifice area and pressure half time are not standardized.¹⁵ The echocardiographic diagnosis of TVS in humans is based on an increase in transvalvular velocity recorded by continuous-wave Doppler as peak inflow velocity through a normal tricuspid valve rarely exceeds 0.7 m/sec.¹⁵ In humans with TVS, it is common to record peak velocities exceeding 1–2 m/sec.¹⁵ In dogs, peak tricuspid inflow velocity rarely exceeds 1 m/sec, and the dog reported herein demonstrated inflow velocities as high as 3 m/sec, consistent with acquired TVS.¹⁶

Management of acquired TVS in people involves surgical valve replacement, surgical valvuloplasty, or percutaneous balloon valvuloplasty.^3,5,6 Balloon valvuloplasty has only been reported in isolated case reports in dogs with congenital tricuspid stenosis.^16,17 Due to the invasiveness, as well as uncertain efficacy of balloon valvuloplasty for acquired TVS, the owner declined further therapy. The long-term survival in this case was poor, which is similar to the previous veterinary case report that was also managed medically.⁸ As such, it suggests that medical management is ineffective for pacemaker-associated acquired TVS and that more aggressive therapy is indicated when this rare complication is identified.

Conclusion

In conclusion, the authors report a rare complication of multiple endovascular pacemaker lead implantation in a dog. Clinicians should be aware of this rare condition and consider more aggressive therapy as medical management appears ineffective.