A 5-year-old intact male German Shepherd Dog was referred to the James L. Voss Veterinary Teaching Hospital at Colorado State University for evaluation of microbial culture-negative aortic valve endocarditis. The dog had a 5-month history of progressive lethargy, poor appetite, weight loss, and congestive heart failure. The suspected origin of the valvular endocarditis was a tooth root abscess. At the time of the initial evaluation, the dog was being treated with furosemide (1.7 mg/kg [0.8 mg/lb], PO, every morning and 1.2 mg/kg [0.5 mg/lb], PO, every evening), spironolactone (0.53 mg/kg [0.24 mg/lb], PO, q 24 h), enalapril (0.5 mg/kg [0.23 mg/lb], PO, q 12 h), cephalexin (23 mg/kg [10.5 mg/lb], PO, q 12 h), famotidine (0.25 mg/kg [0.11 mg/lb], PO, q 24 h), and metoclopramide (0.25 mg/kg, PO, q 8 h).
On physical examination, the dog had a body condition score of 2/9, bounding femoral and carotid arterial pulses, grade 3/6 systolic ejection and diastolic decrescendo murmurs at the left cardiac base, and periodontal disease. The dog weighed 43.2 kg (95.0 lb). A vegetative lesion consistent with aortic valve endocarditis was observed via 2-dimensional echocardiography. Severe AVI was confirmed via color flow and spectral Doppler echocardiography. The half-time of the AVI velocity profile was 130 milliseconds. The peak aortic ejection velocity was 4.0 m/s (predicted range, 1.0 to 1.4 m/s). The calculated peak systolic pressure gradient across the aortic valve was 64 mm Hg (predicted range, 4 to 8 mm Hg). Left atrial diameter was 48.1 mm (predicted range, 27.4 to 30.6 mm); the left atrial-to-aortic diameter ratio was 1.89 (predicted range, 0.8 to 1.1). Left ventricular diameter during diastole was 63.6 mm (predicted range, 40.2 to 42 mm) and during systole was 42.9 mm (predicted range, 25.4 to 27 mm). Left ventricular fractional shortening was 32.5% (predicted range, 33.0% to 46.0%). The mitral valve appeared structurally normal and a mild to moderate centrally located jet was detected, which suggested functional mitral valve regurgitation secondary to ventricular dilation. Systolic arterial blood pressure was 124 mm Hg (predicted range, 90 to 150 mm Hg). Sinus rhythm was identified via ECG. Results of serum biochemical analyses indicated that BUN and creatinine concentrations were mildly high (36 mg/dL [reference range, 7 to 32 mg/dL] and 1.6 mg/dL [reference range, 0.4 to 1.5 mg/dL], respectively). The nucleated blood cell count was mildly high (16.1 × 103 cells/μL; reference range, 4.5 to 15 × 103 cells/μL).
Heterotopic implantation of a porcine bioprosthetic heart valve into the descending aorta was performed in an effort to palliate cardiac volume overload associated with the dog's severe AVI. Premedication consisted of methadone (0.7 mg/kg [0.32 mg/lb], SC) and glycopyrrolate (0.01 mg/kg [0.005 mg/lb], SC). Anesthesia was induced with fentanyl (10 μg/kg [4.5 μg/lb], IV), midazolam (0.2 mg/kg [0.09 mg/lb], IV), lidocaine (2.0 mg/kg [0.9 mg/lb], IV), and etomidate (0.14 mg/kg [0.06 mg/lb], IV) and maintained with infusions of fentanyl (10 to 20 μg/kg/h [4.5 to 9.1 μg/lb/h], IV) and lidocaine (50 μg/kg/min [22.7 μg/lb/min], IV) and inhalation of isoflurane (0.2% to 1%) in oxygen. Ventilation was supported by use of a pressure-limited ventilator with inspiratory pressures of 12 to 15 cm H2O. Neuromuscular blockade was induced with intermittent bolus administration of atracurium (0.2 mg/kg, IV). Arterial catheters were placed in a forelimb and a hind limb to monitor systemic blood pressure cranial and caudal to the planned valve implantation site. Before surgery, systolic, diastolic, and mean arterial blood pressures were 120, 43 (predicted range, 60 to 100 mm Hg), and 65 (predicted range, 70 to 100 mm Hg) mm Hg, respectively. Blood gas analysis was performed periodically during the procedure; non–lactic acid metabolic acidemia was treated with sodium bicarbonate (30 mEq, IV) on 2 occasions. Permissive hypothermia was allowed during surgery until the time of aortic clamp release, whereupon active rewarming was initiated. Esophageal temperature reached a nadir of 32.1°C (89.8°F).
A valved conduit was constructed at the surgery table from a 19-mm porcine bioprosthetic heart valvea and 20-mm PTFE vascular graftb just prior to surgery (Figure 1). The thoracic cavity was opened via a thoracotomy at the left fourth intercostal space. Positive end-expiratory pressure of 2.5 cm of H2O was added to the airway. A portion of descending aorta just distal to the left subclavian artery was isolated, and 2 umbilical tapes were passed around it. A bolus of heparin (100 U/kg [45.5 U/lb], IV) was administered. The descending aorta was occluded by use of 2 straight vascular forceps and divided transversely between the forceps. End-to-end anastomoses were performed between the ends of the divided aorta and valved conduit by use of 5-0 PTFE suturec in a simple continuous suture pattern. The vascular forceps were removed. Aortic occlusion time was 16 minutes and 45 seconds. The anastomotic sites were packed with surgical sponges and compressed for 5 minutes to control hemorrhage. A small leak in the proximal anastomosis was closed with a buttressed mattress suture of 4-0 polypropylene.
Illustrations of heterotopic implantation of a porcine bioprosthetic heart valve in the descending aorta of a dog with aortic valve endocarditis and severe AVI. A—Prior to the start of surgery, a valved conduit was constructed from an 19-mm porcine bioprosthetic heart valve and 20-mm PTFE stretch vascular graft. B—The descending aorta distal to the left subclavian artery was isolated. C—That portion of the descending aorta was clamped with vascular forceps and divided. The valved conduit was sutured between the cut ends of the aorta with PTFE suture in a simple continuous pattern. D—The aortic clamps were removed.
Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.727
Illustrations of heterotopic implantation of a porcine bioprosthetic heart valve in the descending aorta of a dog with aortic valve endocarditis and severe AVI. A—Prior to the start of surgery, a valved conduit was constructed from an 19-mm porcine bioprosthetic heart valve and 20-mm PTFE stretch vascular graft. B—The descending aorta distal to the left subclavian artery was isolated. C—That portion of the descending aorta was clamped with vascular forceps and divided. The valved conduit was sutured between the cut ends of the aorta with PTFE suture in a simple continuous pattern. D—The aortic clamps were removed.
Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.727
Illustrations of heterotopic implantation of a porcine bioprosthetic heart valve in the descending aorta of a dog with aortic valve endocarditis and severe AVI. A—Prior to the start of surgery, a valved conduit was constructed from an 19-mm porcine bioprosthetic heart valve and 20-mm PTFE stretch vascular graft. B—The descending aorta distal to the left subclavian artery was isolated. C—That portion of the descending aorta was clamped with vascular forceps and divided. The valved conduit was sutured between the cut ends of the aorta with PTFE suture in a simple continuous pattern. D—The aortic clamps were removed.
Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.727
After the implantation of the bioprosthetic valve, systolic, diastolic, and mean arterial blood pressure was 115, 30, and 61 mm Hg, respectively, in the forelimb and 110, 62, and 77 mm Hg, respectively, in the hind limb. Mannitol (0.5 g/kg, IV) and 1 unit of DEA 1.1-positive packed RBCs were administered after aortic occlusion. A thoracostomy tube was placed, and the thoracic cavity was closed in a routine fashion. After closure of the thoracic cavity, positive end-expiratory pressure was removed from the breathing circuit and neuromuscular blockade was reversed via administration of edrophonium (0.25 mg/kg, IV). Supportive treatments in the perioperative period included administration of furosemide (1.0 mg/kg [0.45 mg/lb], IV [2 doses]), hetastarch (10 mL/kg, IV), and dopamine (10 μg/kg/min, IV). During a 6-hour period after surgery, blood (477 mL) that accumulated in the pleural space was collected, placed in a cell washer,d and re-administered IV as washed RBCs (240 mL). An infusion of fentanyl (1.0 to 4.0 μg/kg/min [0.45 to 1.8 μg/lb/min], IV) was administered for 48 hours after surgery to provide analgesia. Cefazolin (2.38 mg/kg [1.08 mg/lb], IV, q 8 h) was administered for 4 days after surgery. Anticoagulation treatment with heparin (100 U/kg, SC, q 8 h) was initiated 22 hours after surgery and continued for 4 days. Warfarin (0.05 mg/kg [0.023 mg/lb], PO, q 24 h) was also administered 3 days after surgery and was continued for 3 months. The dose of warfarin was adjusted on the basis of periodic measurement of the prothrombin time and calculation of the international normalized ratio.1 The target international normalized ratio was 2 to 3. Aspirin (0.8 mg/kg [0.36 mg/lb], PO, q 24 h) was administered from the time of surgery.
Clinical signs improved gradually following surgery. After 3 months, the dog's appetite was apparently normal and its body condition score had improved to 4/9. The femoral pulses were considered normal, but carotid pulses were still bounding. Echocardiographic indices were similar to preoperative values. Metoprolol (0.07 mg/kg [0.032 mg/lb], PO, q 12 h) was added to the treatment protocol. Seven months after surgery, the dog was still clinically improving and gaining weight. Systolic, diastolic, and mean arterial blood pressures (determined via an oscillometric method) were 121, 40, and 65.6 mm Hg, respectively, in the forelimb and 115, 55.6, and 83.6 mm Hg, respectively, in the hind limb. Echocardiographic indices of cardiac size remained similar to preoperative values. The half-time of the AVI velocity profile had increased to 210 milliseconds, suggesting that the severity of AVI had diminished. The dog was anesthetized to perform transesophageal echocardiography of the bioprosthetic valve. Bioprosthetic valve leaflets were thin with apparently normal leaflet motion and no insufficiency (Figure 2). By 12 months after surgery, bounding carotid pulses were no longer evident. The dog's weight had increased to 50.3 kg (111 lb). The dosage of furosemide (0.5 mg/kg, PO, q 12 h) had been decreased to 40% of the preoperative dosage, and the dosage of metoprolol had been gradually increased to 0.5 mg/kg, PO, every 12 hours. At 24 months after surgery, the dog was alive, able to engage in vigorous levels of activity and exercise, and had not had an episode of congestive heart failure since surgery.
Transesophageal echocardiographic views obtained during systole (A) and diastole (B) of the bioprosthetic heart valve and vascular graft in the descending aorta of the dog of this report 7 months after surgery. Valve leaflet motion appeared normal. Color flow Doppler echocardiography revealed that the valve prosthesis was competent. There was no evidence of thrombus formation or valve leaflet thickening.
Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.727
Transesophageal echocardiographic views obtained during systole (A) and diastole (B) of the bioprosthetic heart valve and vascular graft in the descending aorta of the dog of this report 7 months after surgery. Valve leaflet motion appeared normal. Color flow Doppler echocardiography revealed that the valve prosthesis was competent. There was no evidence of thrombus formation or valve leaflet thickening.
Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.727
Transesophageal echocardiographic views obtained during systole (A) and diastole (B) of the bioprosthetic heart valve and vascular graft in the descending aorta of the dog of this report 7 months after surgery. Valve leaflet motion appeared normal. Color flow Doppler echocardiography revealed that the valve prosthesis was competent. There was no evidence of thrombus formation or valve leaflet thickening.
Citation: Journal of the American Veterinary Medical Association 231, 5; 10.2460/javma.231.5.727
Discussion
Severe AVI secondary to aortic valve endocarditis often results in congestive heart failure because of severe left ventricular volume overload. Once heart failure occurs, the course is invariably progressive and death usually occurs in a short period after the diagnosis.2,3 Treatment options for dogs with aortic valve endocarditis are generally limited to medical management of heart failure and administration of antimicrobials. Neither of these treatments addresses the underlying hemodynamic overload that causes progressive heart failure.
Orthotopic aortic valve replacement to correct the underlying hemodynamic overload is the treatment of choice for humans with severe AVI.4 Options for aortic valve replacement are mechanical prosthetic heart valves,5 bioprosthetic heart valves,6 and cryopreserved valve allografts.7 Mechanical prosthetic heart valves are constructed of inert biomaterials, such as pyrolytic carbon, and individuals with an implant require lifetime administration of anticoagulants to prevent thrombosis of the prosthesis. Bioprosthetic heart valves are constructed from animal (eg, pig) tissues and are fixed with glutaraldehyde to prevent tissue rejection. A principle advantage of bioprosthetic heart valves over mechanical valves is that administration of anticoagulants is only required for 3 months after surgery.
Heterotopic implantation of a valve prosthesis to correct AVI in humans was first reported by Hufnagel et al8 in 1954, before the advent of the heart-lung machine (ie, cardiopulmonary bypass). With the descending aorta clamped yet maintaining blood flow to the head and heart, the prosthesis was implanted into the aorta just distal to the origin of the left subclavian artery in that procedure. The prosthesis was a cage-and-ball–type mechanical prosthesis. The procedure reportedly decreased AVI by 75% and dramatically improved clinical signs.9 However, the procedure was largely abandoned in favor of orthotopic aortic valve replacement after the development of cardiopulmonary bypass surgery. The effectiveness of heterotopic aortic valve replacement was reaffirmed many years later in a report of 4 humans who were considered poor candidates for standard orthotopic aortic valve replacement.4
On the basis of indirect and direct evidence, it appears that substantial palliation of AVI was achieved in the dog in this report via implantation of a bioprosthetic valve and PTFE vascular graft into its descending aorta. The rapidly progressive worsening of the dog's condition before surgery (characterized by weight loss, weakness, and rapid escalation of the effective dosage of furosemide) was typical of dogs with severe AVI. Severity of left ventricular dilation and systolic dysfunction, strongly bounding arterial pulses, and short AVI velocity half-time10 all suggested that the magnitude of the hemodynamic overload was considerable before surgery. The dog's gradual but clear clinical improvement during a 24-month period after surgery was considered unlikely had it not received considerable hemodynamic benefit from the surgical procedure. The immediate correction of the diastolic arterial blood pressure abnormality distal to the bioprosthesis provided evidence that the implanted valve had unloaded diastolic retrograde flow from the caudal aorta. Less expected was the gradual disappearance over time of bounding pulses cranial to the prosthesis. The gradual increase in the AVI velocity half-time over a 12-month period also suggested that the severity of AVI continued to improve with time after surgery. The reason for this gradual improvement was not clear. Left ventricular dimensions did not change further after surgery and remained abnormal. Similar failure of left ventricular dimension abnormalities to resolve completely has been detected in dogs after mitral valve surgery11,12 and likely reflects both the severity of AVI before surgery and the fact that heterotopic valve implantation does not completely correct AVI.
To our knowledge, this is the first report of a dog with severe naturally occurring AVI that underwent heterotopic aortic valve implantation. As our experience with the dog of this report has illustrated, it is feasible to perform heterotopic aortic valve implantation without the aid of cardiopulmonary bypass and the procedure can provide substantial palliation of clinical signs for dogs with severe AVI.
ABBREVIATIONS
| AVI | Aortic valve insufficiency |
| PTFE | Polytetrafluoroethylene |
Mosaic 305, Medtronic Inc, Minn.
GORE-TEX stretch vascular graft, WL Gore & Associates Inc, Flagstaff, Ariz.
GORE-TEX suture, WL Gore & Associates Inc, Flagstaff, Ariz.
Didaco cell washer and 125-mL surgical wash set, COBE Cardiovascular, Arvada, Colo.
References
- 1↑
Triplett DA. Current recommendations for warfarin therapy. Cardiol Clin Ann Drug Ther 1998;2:141–149.
- 2
Sisson D, Thomas WP. Endocarditis of the aortic valve in the dog. J Am Vet Med Assoc 1984;184:570–577.
- 4↑
Cale AR, Sang CT & Campanella C, et al. Hufnagel revisited: a descending thoracic aortic valve to treat prosthetic valve insufficiency. Ann Thorac Surg 1993;55:1218–1221.
- 5↑
Shanmugam G, MacArthur K, Pollock J. Mechanical aortic valve replacement: long-term outcomes in children. J Heart Valve Dis 2005;14:166–171.
- 6↑
David TE, Ivanov J & Armstrong S, et al. Late results of heart valve replacement with the Hancock II bioprosthesis. J Thorac Cardiovasc Surg 2001;121:268–277.
- 7↑
Yap CH, Yii M. Allograft aortic valve replacement in the adult: a review. Heart Lung Circ 2004;13:41–51.
- 8↑
Hufnagel CA, Harvey WP & Rabil PJ, et al. Surgical correction of aortic insufficiency. Surgery 1954;35:673–683.
- 9↑
Hufnagel CA, Gomes MN. Late follow-up of ball-valve prostheses in the descending thoracic aorta. J Thorac Cardiovasc Surg 1976;72:900–909.
- 10↑
Heinle SK. Quantitation of valvular regurgitation: beyond color flow mapping. In:Ottto CM, ed.The practice of clinical echocardioraphy. 2nd ed. Philadelphia: WB Saunders Co, 2002;367–388.
- 11
Griffiths LG, Orton EC, Boon JA. Evaluation of techniques and outcomes of mitral valve repair in dogs. J Am Vet Med Assoc 2004;224:1941–1945.
- 12
Orton EC, Hackett TB & Mama K, et al. Technique and outcome of mitral valve replacement in dogs. J Am Vet Med Assoc 2005;226:1508–1511.
