The Use of an Implantable Cardioverter Defibrillator in a Boxer Dog to Control Clinical Signs of Arrhythmogenic Right Ventricular Cardiomyopathy

Abstract

A 2-year-old, male, intact Boxer Dog presented to the Washington State University Veterinary Teaching Hospital's Emergency Service for acute onset of vomiting and lethargy. Physical examination identified weakness, pale mucous membranes, prolonged capillary refill time (.3 seconds), weak peripheral pulses, marked tachycardia (.250 bpm), and hypother-mia (96uF). The remainder of the physical examination was considered unremarkable. An ECG disclosed sustained ventricular tachycardia (VT) with a heart rate of 280 bpm. A lidocaine a bolus (2 mg/kg IV) converted the VT to sinus rhythm for a short time. A lidocaine constant rate infusion (CRI) at 25 mg/kg/min was used to maintain sinus rhythm, and mexiletine b was initiated at 5 mg/kg PO q8h. CBC, serum biochemistry panel, urinalysis, and thoracic radiographs were unremarkable. The dog responded quickly to drug therapy, and clinical signs resolved. The dog was discharged the next day on oral mexiletine but was returned 9 days later with sustained VT at approximately 300 bpm. The VT appeared to be of left ventricular origin (right bundle-branch block appearance). The same lidocaine dose and CRI were used as described above. The dog converted quickly to sinus rhythm and clinical signs again resolved. A routine echocardiogram (ECG) was performed approximately 18 hours after resolution of VT. The echocardiogram disclosed evidence of mild tricuspid valve dysplasia (considered incidental), normal cardiac chamber sizes, and normal global left ventricular function. A minimum database was reevaluated, and abdominal ultrasonography was performed to screen for metabolic causes of VT. No abnormalities were identified. Idiopathic ventricular arrhythmia or arrhythmo-genic right ventricular cardiomyopathy with right bundle-branch block appearing VT was the working diagnosis. 1 Medical therapy was changed from mexile-tine to sotalol, c 1.2 mg/kg PO q12h. The dog presented similarly on several occasions (day 20, day 24, day 45). At each presentation, rapid, sustained VT was noted and converted to sinus rhythm with lidocaine. The dog was hospitalized on continuous ECG monitoring, and a lidocaine CRI or multiple lidocaine boluses were administered. On each presentation , medical therapy was adjusted, initially by increasing the sotalol dosage (2.4 mg/kg PO q12h), then by changing the protocol to oral atenolol d (0.4 mg/kg PO q12h, increasing to 0.8 mg/kg PO q12h) and mexiletine (6 mg/kg PO q8h, increasing to 8 mg/kg PO q8h), in combination as has been described. 2 Routine imaging and laboratory evaluations were repeated and found unremarkable. Because of the poor response to medical therapy, it was felt that the long-term prognosis was poor, and sudden cardiac death was likely to occur. The decision to implant an implantable cardioverter-defibrillator (ICD) was made after consultation with the owner. The technique of implantation of the ICD was similar to pacemaker implantation. The ICD system consists of a pulse generator and a high-voltage conducting lead placed transvenously into the right ventricle. Similar to a pacemaker, the lead serves as a vehicle for current flow and senses local electrograms. The technique for pacemaker placement has been described elsewhere. 3,4 The lead used in this dog was an active fixation endocardial lead 75 cm in length. e The left jugular vein was used to access the right ventricle, and the site of lead placement in the ventricle was analyzed with an implantable antiarrhythmic device programmer. f Lead impedance, R-wave amplitude, and T-wave amplitude were analyzed at each site, because it was critical that the ICD could sense the appropriate waveform for determining therapy. The relative difference between the R-wave and the T-wave amplitude in this dog was fairly minor in many sites tested. We felt the risk of oversensing T waves and ''double counting'' the heart rate could pose a problem. Because the R wave must differ in amplitude by 3-fold to avoid T-wave over-sensing, each potential placement in this dog was tested and the lead was continually moved until an appropriate sensing location was found. In this dog, it appeared that securing a lead in the apical portion of the right ventricular outflow tract provided the best sensing for differentiating the R and T waves. The lead was secured to the left jugular vein and surrounding tissues with a lead sheath after adequate positioning was verified. The remainder of the lead was tunneled subcutaneously (SQ) over the point of the shoulder to the left thoracic region. The ICD generator g was placed in a subcutane-ous pocket created over the left thorax at the region of the left ventricular apex. The lead was tunneled into the pocket and connected to the generator. The ICD generator placement was chosen because of the bulki-ness of the generator and because it allowed the generator to be used as one of the electrodes of