Patent Ductus Arteriosus Ligation and Pulmonary Artery Banding in a Kitten

Introduction

Ventricular septal defect (VSD) is one of the most common forms of feline congenital heart disease.¹ Interestingly, patent ductus arteriosus (PDA) is less frequently reported in cats than in dogs.¹ Typical therapy in an affected cat would involve surgical closure of the PDA and either medical management or pulmonary artery banding of the VSD, depending on shunt magnitude and its hemodynamic significance. In cats, low body weights preclude open-heart surgery for primary closure of VSDs.

The purpose of this report is to illustrate the diagnostic and therapeutic challenges faced when dealing with such small, immature animals presenting with congenital heart disease and congestive heart failure. To the authors’ knowledge, this is the first published report of concurrent PDA and VSD in a kitten.

Case Report

A 2-month-old, 0.9-kg, male intact domestic shorthaired kitten was presented to the Veterinary Hospital of the University of Pennsylvania with a history of respiratory distress, exercise intolerance, decreased appetite, and poor weight gain compared with its siblings. The kitten was in poor body condition with dull mentation. It was tachypneic at rest and had markedly increased respiratory efforts. On auscultation, lung sounds were harsh in all fields. The mucous membranes were pink and moist, and the capillary refill time was prompt. Femoral arterial pulses were bounding. The heart rate was 200 beats per minute (bpm), and the rhythm was regular. A grade IV/V harsh systolic murmur was heard loudest over the left heart base, and it radiated widely over both the left and right parasternum. A grade III/V diastolic murmur was also audible and was loudest over the left heart base.

Thoracic radiographs revealed predominantly left-sided enlargement of the cardiac silhouette. The vertebral heart size was 12.0, which was significantly larger than the reported reference values (reference range 8.0) for kittens of similar age.² There was dilatation of the descending aorta, consistent with a ductal aneurysm in the ventrodorsal view. A diffuse, interstitial-alveolar pulmonary pattern was consistent with moderate pulmonary edema. Both the pulmonary arteries and veins appeared engorged. An electrocardiogram revealed a sinus rhythm with a heart rate of 180 bpm. The QRS duration was prolonged (0.06 seconds; reference range 0.04 seconds), and R wave amplitude was increased (1.3 mV; reference range 0.9 mV), which were suggestive of left ventricular enlargement.³

An echocardiogram revealed severe left atrial and left ventricular dilatation. The left ventricular systolic function was decreased. A moderate-sized (4 mm in diameter), peri-membranous VSD was confirmed from repeated measurements made in two-dimensional mode from both the right parasternal short-axis and long-axis views. Doppler echocardiography revealed a left-to-right flow direction across the VSD. The peak flow velocity was 3.0 meters per second, equivalent to a 36-mm Hg pressure gradient using the modified Bernoulli equation.⁴ Every effort was made to ensure that optimal alignment was achieved when examining the VSD flow, to ensure that poor alignment was not the cause for the low transventricular Doppler-estimated pressure gradient. The echocardiogram also revealed a large PDA shunting blood from left to right. The pulmonary artery flow profile at the level of the pulmonic valve was laminar. There was no tricuspid or pulmonic insufficiency to enable indirect measurement of pulmonary artery pressures. The aortic flow profile was laminar. There was mild mitral regurgitation.

Because of the kitten’s low body weight and unstable cardiovascular status, it was not possible to accurately quantify the contributions of each cardiac defect to the overall shunt volume using invasive hemodynamic studies. Therefore, based on the initial echocardiographic findings of a moderate-sized VSD (relative to the aortic root diameter of 7 mm) and a large PDA, both pulmonary artery banding (to decrease left-to-right blood flow across the VSD) and PDA ligation were recommended. The kitten was hospitalized and treated with furosemide^a (2 mg/kg intravenously [IV] q 12 hours).

The following day, a thoracotomy was performed through the left fifth intercostal space under isoflurane anesthesia. The PDA was dissected and ligated as previously described.⁵⁶ A segment of latex tubing was placed around the aorta distal to the PDA. Extrapericardial dissection of the PDA and visualization of right-angled forceps placed around the PDA from cranial to caudal was facilitated by elevation of the aorta with the latex tubing. Two, 3-0 silk ligatures^b were passed around the PDA and tied on the aortic and pulmonary artery ends of the PDA, respectively.

A horizontal incision was made in the pericardium ventral to the phrenic nerve. Sutures of 4-0 silk^c were placed from the pericardium to the thoracotomy incision, elevating the heart in a pericardial basket. The left atrium was retracted caudally with a moistened cotton-tip applicator. The main pulmonary artery was dissected in a cranial-to-caudal direction using arrowhead tip surgical eye spears^d and right-angled forceps. A 1.5 mm-width silastic band^e was placed around the main pulmonary artery just distal to the pulmonic valve. The circumference of the main pulmonary artery was decreased by 30%, and the band was clamped with a mosquito hemostat. Two sutures of 4-0 prolene^f were placed through the ends of the band to hold it in place [see Figure]. The ends of the silastic band were cut distal to the Prolene sutures, and the pericardium was closed with 4-0 polydioxanone.^g The ribs were apposed with interrupted sutures of 4-0 polydioxanone. Prior to tightening the last suture, the lungs were gently inflated to remove air from the pleural space. The remaining thoracic musculature, subcutaneous tissue, and skin were closed in a routine manner. The kitten recovered uneventfully from general anesthesia.

The next day, the kitten was alert and responsive. The femoral pulse pressure was normal. The heart rate was 160 bpm, and the rhythm was regular. A grade III/V systolic murmur of equal intensity was heard over both the left and right parasternum. There was no diastolic murmur. The respiratory rate was 40 breaths per minute, with only a mild increase in respiratory effort. The lung sounds were less harsh than those ausculted before surgery. Thoracic radiographs revealed a decrease in both heart size and the pulmonary interstitial-alveolar pattern. The pulmonary vasculature was still prominent. The pulmonary artery band was visible above the pulmonic valve. An echocardiogram confirmed successful surgical ligation of the PDA. The peak flow velocity across the VSD was unchanged. There was no increase in the peak flow velocity across the region of the band, suggesting that the band was not restrictive at that time. The left atrial and left ventricular chamber sizes were slightly decreased compared with the preoperative echocardiogram measurements. The kitten was discharged on the following day on furosemide (2 mg/kg per os [PO] q 12 hours) because of the persistent tachypnea and residual pulmonary edema.

The kitten was reexamined 1, 3, 6, and 12 months after surgery. Over this time period, the kitten showed marked clinical improvement, with above-average weight gain and increased exercise tolerance. At 6 months of age, the kitten was larger than his littermates. Cardiac medications were discontinued 4 months postoperatively based on radiographic resolution of the left-sided congestive heart failure. Thoracic radiographs demonstrated a significant decrease in heart size. The vertebral heart size was 8.5 at 1 year after surgery. The pulmonary arteries and veins remained prominent.

Echocardiography showed a progressive decrease in the left atrial and left ventricular chamber sizes over the 12-month postoperative period. The fractional shortening, used as an indication of the left ventricular systolic function, improved and stabilized. The VSD size remained stable at 4 mm in diameter. The Doppler-derived transventricular pressure gradient increased to 80 mm Hg within the first month following surgery, and then it remained stable between the 1- and 12-month postoperative evaluations. Minimal restriction across the pulmonary artery band was noted at the 12-month evaluation.

Discussion

This case report describes successful surgical correction of PDA and pulmonary artery banding for VSD in a kitten. Prior reports exist in the veterinary literature of PDA ligation and pulmonary artery banding as palliative treatments for left-to-right shunting of VSDs in cats; however, there are no published reports describing the use of both surgical procedures to treat this combination of congenital cardiac defects in cats.^5–9

Patent ductus arteriosus ligation results in substantial hemodynamic benefits by alleviating left-to-right blood shunting and by decreasing both pulmonary overcirculation and left heart volume overload.¹⁰ In this kitten, the actual contribution from the VSD to the pulmonary and left heart overcirculation was difficult to determine preoperatively because of the coexistence of the large left-to-right PDA. Evaluating the contribution of the VSD was further complicated by the animal’s low body weight and unstable cardiovascular status, which made invasive hemodynamic studies impossible. The authors’ decision to perform pulmonary banding was based on the initial echocardiographic findings and the desire to optimize the animal’s clinical outcome.

Two factors determine the functional hemodynamic disturbance caused by a left-to-right VSD.¹¹ The first is the size of the defect, as measured relative to the aortic valve cross-sectional area. A small VSD results in restricted flow and a small volume shunt. A large VSD that exceeds the cross-sectional area of the aortic root is termed nonrestrictive.¹¹ Nonrestrictive VSDs present less resistance to blood flow than the aorta and, therefore, result in a large volume of left-to-right flow.¹¹ This kitten had a moderate-sized VSD prior to surgery (approximately 50% to 66% of the aortic root diameter). In theory, a VSD this large would result in a hemodynamically significant shunt volume.

The second determining factor is the relative right ventricular outflow impedance compared with left ventricular outflow impedence.¹¹ In the absence of pulmonic stenosis, the right ventricular outflow impedance should reflect the pulmonary arterial systolic pressure.¹¹ The preoperative echocardiographic evaluation of this kitten revealed a decreased peak flow velocity across the VSD. One possibility for this low transventricular Doppler-estimated gradient was poor echocardiographic probe alignment, although efforts were made to ensure proper alignment by taking repeated measurements from both the right parasternal short-axis and long-axis views. An alternative explanation is that in the absence of pulmonic stenosis, this low transventricular Doppler-estimated gradient was secondary to an increase in both the right ventricular and pulmonary arterial systolic pressures. The authors were unable to confirm the suspicion of pulmonary hypertension, as there was no detectable pulmonary insufficiency or tricuspid regurgitation to enable indirect Doppler measurements of right ventricular or pulmonary artery pressures.⁴ Chronic, severe pulmonary overcirculation can result in pulmonary vascular damage and pulmonary hypertension, which may be irreversible; therefore, the aim of surgery was to intervene prior to the onset of irreversible pulmonary vascular damage.¹¹

The purpose of pulmonary artery banding was to create pulmonic stenosis and thus increase right ventricular outflow impedance and right ventricular pressure. This impedance decreases the pressure gradient across the VSD and subsequent shunt fraction.⁸ It is recommended that the diameter of the main pulmonary artery be decreased to 33% of the pulmonic valve annulus.⁸ However, since this kitten was only 2 months old at the time of surgery, it was decided that the band should be minimally restrictive to allow room for growth. A silastic band was used rather than umbilical tape, in the hope that the band would expand and stretch as the kitten grew and be less likely to cause a life-threatening pulmonic stenosis. Over-zealous banding in a growing animal can result in severe pulmonic stenosis, right ventricular myocardial failure, and right-sided congestive heart failure.⁸

During the 12 months following surgery, the velocity of blood flow across the pulmonary artery band region increased from 1.2 meters per second (equivalent to 6 mm Hg pressure gradient) to 2.6 meters per second (equivalent to 27 mm Hg pressure gradient). Considering the significant increase in body weight and growth during this time period, the degree of pulmonic stenosis at the 12-month evaluation was mild. It should be noted, however, that the silastic material chosen for the pulmonary artery band had considerable elastic properties, and the band may have stretched over time to accommodate the growing pulmonary artery and protect the cat from progressive pulmonic stenosis.

The data collected over the 12 months following surgery suggested that the PDA was the more hemodynamically significant lesion of the two. The follow-up echocardiographic information obtained from the cat suggested that the hemodynamic and clinical improvements arose from the PDA ligation and that, in hindsight, the pulmonary artery banding procedure was probably not necessary. However, as previously emphasized, the low body weight and unstable cardiovascular status made preoperative invasive hemodynamic studies virtually impossible, so the clinical decision was based on the initial echocardiographic findings.

The increase in the pressure gradient across the VSD to 80 mm Hg, 1 month after surgery, was consistent with a significant decrease in the right ventricular pressure. Although pulmonary hypertension was never actually documented in this cat, it was probable that ligation of the PDA resulted in a significant decrease in the pulmonary artery and right ventricular pressures, because of reversal of flow-related pulmonary hypertension. It was this decrease in pulmonary artery pressure after PDA ligation that revealed the true nature of the VSD as a restrictive lesion. It is also possible that with growth, the VSD became more restrictive relative to the aortic size (aortic root diameter at the 12-month evaluation was 10 mm). An alternative explanation is that alignment with flow across the VSD was better at follow-up examinations than at the initial examination.

Conclusion

Surgical ligation of a PDA and pulmonary banding for a concurrent VSD were performed in a 2-month-old kitten with evidence of left heart failure. The kitten subsequently became clinically normal over the 12-month postoperative period, with echocardiographic evidence of improved left ventricular function. The contribution of the pulmonary artery banding to the cat’s clinical improvement could not be definitively assessed, and ligation of the PDA may have been responsible for the improved hemodynamic function of the heart.