Successful balloon angioplasty of right pulmonary coarctation with left pulmonary artery interruption in a cat: a long-term outcome follow-up case report

Abstract

A 4-month-old, British Shorthair kitten was referred to our institute for evaluation of a heart murmur. Thoracic radiography and echocardiography revealed narrowing of the right pulmonary artery, accompanied by right atrial dilation and right ventricular hypertrophy. The systolic flow velocity across the stenotic lesion was 6.15 m/sec, with a pressure gradient of 151.42 mmHg. Computed tomography confirmed right pulmonary coarctation with concurrent interruption of the left pulmonary artery. Balloon angioplasty was performed, reducing the systolic flow velocity from 6.15 m/sec to 2.79 m/sec and relieving right ventricular pressure overload. One year later, thoracic radiography revealed left lung collapse and right lung hyperinflation; however, the patient remained asymptomatic. At 33 months post-diagnosis, the patient continued to thrive without any clinical signs.

Stenosis of the pulmonary trunk or branch, also known as peripheral pulmonary artery stenosis or pulmonary coarctation (PC), is a congenital anomaly characterized by one or more narrow segments in the main or peripheral branches of the pulmonary arteries [1, 13, 22]. This anomaly is rare in humans and accounts for approximately 2–3% of heart disease in neonates [3]. Pulmonary coarctation is also a rare congenital disorder in cats, reported in approximately 6% of all congenital heart diseases in one study [21]. Similar to pulmonic stenosis, this condition results in obstruction of blood flow from the right ventricle to the pulmonary artery [1, 22]. Treatment for pulmonary coarctation is considered in humans when there is increased right ventricular pressure or clinical signs attributable to stenosis [17].

Pulmonary artery interruption (PAI), previously referred to as the unilateral absence of the pulmonary artery, is a rare vascular anomaly in cats and humans characterized by a complete discontinuity between the main pulmonary artery and one of its branches [5, 8, 10, 18]. Cases of PAI have been reported in the veterinary literature [8, 13, 18, 25, 28], and a few instances describe both PC and PAI co-occurring [13, 18]. However, to date, no studies have detailed the CT features of cats with both PAI and PC, along with long-term monitoring of treatment outcomes. This article describes the CT features of PAI and PC as well as a successful balloon angioplasty procedure with long-term follow-up.

A 4-month-old male British Shorthair kitten (790 g) was referred for evaluation of a heart murmur detected during a routine examination. The patient was asymptomatic and had not received any medications. A systolic grade IV/VI murmur was auscultated with maximal intensity over the right parasternal area. The remainder of the physical examination was unremarkable, with a normal systolic blood pressure of 114 mmHg. Complete blood count, serum chemistry, and urinalysis results were within reference ranges. Thoracic radiography revealed mild cardiomegaly (vertebral heart size, 8.9) with mild right atrial enlargement and a slight leftward shift of the mediastinum (Fig. 1). The right caudal lobar pulmonary artery and vein appeared mildly dilated. Transthoracic echocardiography showed mild-to-moderate right ventricular hypertrophy and moderate right atrial dilation (Table 1). The main pulmonary artery was normal in size relative to the aortic root, and the pulmonary valve appeared normal with a standard annulus. Color Doppler examination revealed narrowing of the right pulmonic artery branch with turbulent flow. Continuous wave Doppler showed a marked increase in systolic flow velocity (peak velocity 4.93 m/sec and pressure gradient 97.2 mmHg) across the stenotic lesion. However, the left pulmonary artery was not visualized. No abnormalities were observed in the tricuspid valve, left atrium, left ventricle, or left ventricular outflow tract. The patient was re-evaluated one month later and remained asymptomatic. Repeat transthoracic echocardiography showed progressive right ventricular hypertrophy and increased stenosis of the right pulmonary artery (peak velocity 6.15 m/sec and pressure gradient 151.42 mmHg). Based on these findings, a tentative diagnosis of right PC with right ventricular hypertrophy and right atrial enlargement was made. The kitten was prescribed a daily oral dose of 0.5 mg/kg atenolol (Atenol, KyungDong Pharm., Gwacheon, Korea). Due to the severity of the stenosis and significant progressive changes in the right side of the heart, balloon angioplasty was subsequently performed.

Fig. 1.

Thoracic radiography images at initial presentation (A, B) and transthoracic echocardiography images one month after initial presentation (C, D, E). Lateral (A) and ventrodorsal (B) thoracic radiographs reveal mild cardiomegaly with mild right atrial enlargement and a slight leftward shift of the cardiac axis. Right parasternal short-axis echocardiogram (C, D) shows a focal narrowing between the main pulmonary artery (MPA) and right pulmonary artery (RPA) (arrowhead), with evidence of right ventricular hypertrophy (white arrows), dilation of the MPA, a stenotic RPA, and post-stenotic dilation. Color Doppler imaging demonstrates turbulent flow within the RPA, while the left pulmonary artery (LPA) is not visualized. (E) The maximum velocity through the stenotic region was 6.15 m/sec, corresponding to a pressure gradient (PG) of 151.42 mmHg. RVOT: right ventricular outflow tract, MPA: main pulmonary artery, Ao: aorta, RPA: right pulmonic artery.

Table 1. Echocardiographic indices of the patient at initial presentation, 1 months after presentation, 1 month after procedure, and 1 year after procedure.

	Presentation	1 month after presentation	1 month after procedure	1 year after procedure
BW (kg)	0.79	1.57	3.69	4.8
LVIDD (mm)	10.7	11.1	12.3	15.97
LVIDS (mm)	5.9	4.4	7.6	9.25
LV FS (%)	44.8	60.1	38.2	42.0
LA:Ao	1.31	1.37	1.44	1.09
LAd long (mm)	5.16	8.85	11.7	10.8
LAd short (mm)	7.15	8.14	10.81	11.42
MV E peak (m/sec)	0.76	0.95	0.93	0.78
MV E/A	1.2	1.38	1.4	1.15
TV E peak (m/sec)	0.43	0.52	0.61	0.62
TV E/A	1	0.58	0.81	1.07
TR velocity (m/sec)	None	None	None	None
TR PG (mmHg)	None	None	None	None
PV velocity (m/sec)	0.7	1.14	1.01	1.05
PS velocity (m/sec)	4.93	6.15	2.7	2.56
PS PG (mmHg)	97.2	151.42	29.1	26.29
RVIDD (mm)	5.27	7.54	5.07	4.85
RVIDDn (mm)	0.56	0.66	0.35	0.31
RV FS (%)	27.7	37.7	35.7	32.9
Ao velocity (m/sec)	1.04	1.28	0.88	0.91

BW: body weight, LVIDD: left ventricular end-diastolic internal diameter, LVIDS: left ventricular end-systolic internal diameter, LV FS: left ventricular fractional shortening, LA:Ao: left atrium to aorta ratio, LAd long: left atrial diameter (long axis), LAd short: left atrial diameter (short axis), MV E peak: mitral valve E wave peak velocity, MV E/A: mitral valve E/A ratio, TV E peak: tricuspid valve E wave peak velocity, TV E/A: tricuspid valve E/A ratio, TR velocity: tricuspid regurgitation velocity, TR PG: tricuspid regurgitation pressure gradient, PV velocity: pulmonary valve velocity, PS velocity: pulmonic stenosis velocity, PS PG: pulmonic stenosis pressure gradient, RVIDD: right ventricular end-diastolic internal diameter in diastole, RVIDDn: right ventricular end-diastolic internal diameter normalized by body weight, RV FS: right ventricular fractional shortening, Ao velocity: aortic valve velocity.

Before balloon angioplasty, thoracic computed tomography (CT) was performed to assess the right pulmonary artery branch and to evaluate the left pulmonary artery branch, which had not been visualized on transthoracic echocardiography. The CT scan utilized a 16-row multi-detector CT scanner (Somatom Emotion, Siemens Medical Systems, Forchheim, Germany) with a slice thickness of 0.75 mm, using 110 mAs and 110 kV. A contrast study was conducted following the intravenous administration of iohexol (880 mgI/kg; Omnipaque 300^®, GE Healthcare, Shanghai, China) at a rate of 3 mL/sec using a power injector (Medrad Vistron C-T Injector System, Medrad, Inc., Minneapolis, MN, USA). Post-contrast images were acquired 3 sec after injection, first from cranial to caudal and then with an additional series from caudal to cranial. On the CT images, the right PC was identified in the proximal segment of the right pulmonary artery (Fig. 2). The left pulmonary artery branch appeared markedly narrow with a very short length and could not be traced beyond the level of the 9th thoracic vertebra. No systemic collateral vessels or bronchial artery hypertrophy were observed on post-contrast CT images. The left hemithorax volume was smaller than that of the right, with cranial displacement of the left diaphragm and leftward displacement of the cranial mediastinum. Parenchymal changes were also noted in the left lung, including multiple pulmonary parenchymal bands suggestive of pseudofibrosis observed in the left cranial lung lobe, along with thickening of the bronchi and peribronchial cuffing. No obvious filling defects were observed within the pulmonary arteries, ruling out pulmonary thromboembolism. The patient was diagnosed with right-sided PC and left-sided PAI.

Fig. 2.

In the 3-dimensional (3D) reconstructed computed tomography (CT) angiogram (A, B), there is a focal narrowing of the proximal right pulmonary artery (RPA) (white star) accompanied by dilation of the main pulmonary artery (MPA). Post-stenotic dilation of the RPA branch (white arrows) is also visible. The left pulmonary artery branch is absent (blue arrows). Transverse and dorsal reconstructed CT images (C, D) reveal asymmetric lung fields with hypoinflation, along with elevation of the left hemidiaphragm and a mediastinal shift due to hypoinflation. Multiple pulmonary parenchymal bands (pseudofibrosis) are evident. MPA: main pulmonary artery, Ao: aorta, RPA: right pulmonic artery, RPA-Cr: cranial part of the right pulmonic artery, RPA-Cd: caudal part of the right pulmonic artery.

Balloon angioplasty was performed under general anesthesia. Prior to anesthesia, premedication was administered intravenously (25 mg/kg cefazolin sodium; Cefazolin Injection, Chongkundang, Seoul, Korea). For sedation and analgesia, 0.05 mg/kg hydromorphone HCl (Dilid inj., Hana Pharmaceutical Co., Ltd., Seoul, Korea) and 0.2 mg/kg midazolam (Midacum Inj., Myung Moon, Seoul, Korea) were administered intravenously. General anesthesia was induced via intravenous injection of 1% propofol (Provive Inj., Pharmbio Korea, Seoul, Korea) at a dosage of 3.5 mL per cat.. Endotracheal intubation was performed, and anesthesia was maintained using isoflurane and oxygen. A crystalloid fluid solution (Plasma Solution A; HK Inno, Seoul, Korea) was administered intravenously at a rate of 6.25 mL/hr for intraoperative fluid management. Continuous monitoring included clinical evaluation; inspiratory and expiratory fractions of CO₂, O₂, and isoflurane; pulse oximetry; direct blood pressure measurement using a 24-gauge catheter placed in the dorsal pedal artery of the right hind limb; and esophageal temperature monitoring. For the balloon angioplasty procedure, a percutaneous transvenous approach via the right jugular vein was performed using a 7-French, 4 cm long introducer sheath (Prelude, Merit Medical, South Jordan, UT, USA). A 5-French straight angiographic catheter with metallic marker bands (Marker-Straight, Infiniti Medical, Redwood, CA, USA) was advanced transorally through the esophagus to the heart level to calibrate the fluoroscopic measurement system (OEC Elite; GE, Chicago, IL, USA). A 5-French pigtail angiographic catheter (Performa PIG, Merit Medical) was introduced through the jugular vein using a 0.035-inch guidewire (Zipwire, Boston Scientific, Marlborough, MA, USA) and advanced to the right ventricle apex. An angiogram was obtained using 3 mL of a non-ionic contrast agent by rapid hand injection (Fig. 3). The angiogram revealed a focal narrowing of the right pulmonary artery, with the diameter of the right pulmonary branch around the stenotic lesion measuring between 5.3 and 5.9 mm. A 7 mm ×20 mm high-pressure balloon (Mustang; Boston Scientific, Marlborough, MA, USA) was used to achieve a balloon-to-pulmonary artery diameter ratio ranging from 1.18 to 1.32. After removing the wire, a 0.035-inch J-tip spring coil guidewire (Silverway; Asahi Intecc, Nagoya, Japan) was introduced through the angiographic catheter. Before angioplasty, the fluoroscopic projection angle was adjusted to the right anterior oblique (RAO) 40° based on the CT angiography images. A combination of spring-coil wire and angiographic catheter was positioned in the right pulmonary artery across the stenosis. Subsequently, the angiographic catheter was replaced with a balloon catheter, which was positioned across the stenotic area. Marked desaturation was observed when the balloon catheter was inserted, with arterial hemoglobin oxygen saturation (SpO₂) decreasing from 98% to 85% and mean arterial pressure dropping from 69 mmHg (systolic 94 mmHg) to 21 mmHg (systolic 33 mmHg), although the heart rate remained stable. The balloon was hand-inflated to 14 atm, and a reduction in the stenotic waist was observed. The balloon was then inflated a second time to confirm the complete elimination of the waist. After balloon dilation, the guidewire and balloon catheter were withdrawn from the pulmonary artery, and both desaturation and hypotension rapidly resolved. However, ventricular tachycardia was observed, prompting the administration of an intravenous bolus of lidocaine (0.1 mL/kg; Lidocaine in 2% lidocaine injection, Jeil Pharmaceutical Co., Ltd., Seoul, Korea). Ventricular tachycardia resolved on electrocardiography, leaving only a right bundle branch block. The introducer sheath was removed, and the jugular vein was manually compressed for 20 min. The total procedure duration was 94 min, with an anesthesia time of 131 min. The patient recovered uneventfully from anesthesia and was closely monitored post-procedure, with no adverse events observed.

Fig. 3.

In the right ventricular selective angiography performed during balloon angioplasty (A), a stenotic lesion of the right pulmonary artery (RPA) with post-stenotic dilation and main pulmonary artery (MPA) dilation is evident (arrow). In the left parasternal short-axis echocardiogram taken one month post-procedure (B, C, D), the maximum velocity through the stenotic area was measured at 2.79 m/sec, with a pressure gradient (PG) of 31.19 mmHg. The degree of right ventricular concentric hypertrophy and post-stenotic dilation appeared reduced. MPA: main pulmonary artery, RPA: right pulmonic artery, RV: right ventricle.

After the procedure, the patient was closely monitored for blood pressure and electrocardiogram changes, and no adverse events, such as pain, arrhythmia, or major hemorrhage were observed. The patient was discharged the following day. To manage post-procedural discomfort and prevent potential complications, gabapentin (10 mg/kg, twice daily; Neurontin, Viatris, Seoul, Korea) and amoxicillin-clavulanic acid twice daily (12.5 mg/kg, twice daily; Amocla, Kuhnil, Seoul, Korea) were prescribed for one week. A recheck echocardiography performed one month post-procedure showed a decrease in both the systolic maximum velocity and pressure gradient of the stenotic lesion (maximum velocity: 2.79 m/sec, pressure gradient: 31.19 mmHg). There was also a reduction in the size of the right atrium and right ventricular hypertrophy, and the murmur was less intense (grade II/VI).

One year later, thoracic radiography and echocardiographic re-evaluation were conducted as part of a pre-anesthetic examination for castration. The patient remained clinically stable and asymptomatic. The Echocardiographic showed that the systolic maximum velocity and pressure gradient remained reduced (maximum velocity: 2.56 m/sec, pressure gradient: 26.29 mmHg), and the previously observed remodeling of the right atrium resolved (Fig. 4). However, thoracic radiographs revealed that, unlike at the initial presentation, the left lung field had collapsed with a leftward shift of the mediastinum and hyperinflation of the right lung lobes. Additionally, a moderate bronchointerstitial pattern was observed throughout most of the remaining lung fields, particularly in the caudal lung lobe. Despite these findings, room air oxygen saturation remained within the normal range (98%), and no respiratory abnormalities or clinical symptoms were present. Castration was performed uneventfully at the primary veterinary hospital, and the patient survived for 991 days after the initial diagnosis with no changes in clinical symptoms.

Fig. 4.

Thoracic radiography images (A, B) and transthoracic echocardiography images (C, D, E, F) one year after the balloon angioplasty procedure. Lateral (A) and ventrodorsal (B) thoracic radiographs show collapse of the left hemithorax lung field with a leftward shift of the mediastinum and hyperinflation of the right lung fields. A moderate bronchointerstitial pattern is also observed in the most lung fields. Right parasternal long-axis (C) and short-axis (D) echocardiograms reveal a decrease in the size of the right atrium and in right ventricular hypertrophy. Left parasternal short-axis echocardiogram (E, F) with color Doppler demonstrates reduced turbulent flow within the right pulmonary artery (RPA) and a decrease in maximum velocity through the stenotic region, from 6.15 m/sec to 2.79 m/sec, corresponding to a pressure gradient (PG) of 26.29 mmHg. RV: right ventricle, RA: right atrium, LV: left ventricle, LA: left atrium, Ao: Aorta, PV: pulmonic valve, PAS: stenotic lesion of right pulmonic artery.

This case report describes a cat diagnosed with left PAI and concurrent right PC. Preoperative evaluation of the anatomical structures was conducted using CT, followed by successful balloon angioplasty. Long-term follow-up confirmed an improvement in the stenotic region and resolution of remodeling in the right ventricle and atrium. Pulmonary artery interruption, previously referred to as unilateral absence of the pulmonary artery, is a congenital anomaly resulting from abnormal development of the left and right 6th pharyngeal arch arteries, which normally form the ductus arteriosus [5]. During normal embryological development, the right ductus arteriosus regresses, while the left ductus arteriosus connects to the pulmonary trunk. Before birth, the ductus arteriosus connects the pulmonary trunk to the descending aorta, allowing oxygen-rich blood to enter the systemic circulation. In the perinatal period, the ductus arteriosus closes through muscular contraction, followed by anatomical sealing and eventual formation of a ligament [4]. An abnormal lateral connection of the ductus arteriosus to the left pulmonary artery, combined with abnormal regression timing of the right ductus arteriosus, disrupts the vascular layers of the pulmonary artery branches. These branches may then exhibit characteristics similar to the smooth muscle tissue of the ductus arteriosus. As a result, closure of the ductus arteriosus is thought to contribute to the development of coarctation or even complete interruption of the pulmonary artery. Due to this embryological mechanism, cases of pulmonary artery interruption with concurrent contralateral branch coarctation, as seen in the present case, have been reported in both human and veterinary medicine.

In this case, thoracic radiography revealed a mild leftward shift of the mediastinum due to a reduced left hemithorax volume, along with the absence of visualization of the left pulmonary artery and vein on both radiographs and transthoracic echocardiography. In humans, thoracic radiographs can show asymmetry in lung volume, with mediastinum shifting toward the affected hemithorax and hyperinflation of the contralateral lung [12]. However, the gold standard for diagnosis in humans is CT angiography, which can identify the absence of the pulmonary artery and detect mosaic parenchymal changes, systemic collateral circulation, and bronchiectasis [6]. In this case, bronchial wall thickening and parenchymal bands were detected on the initial CT scan; however, no clinical symptoms related to respiratory issues were observed. According to human review articles, bronchiectasis and interstitial changes were observed in approximately 30.2% and 14.0% of lung CT scans, respectively, in patients with isolated unilateral absence of the pulmonary artery [29]. In a previous human study, recurrent respiratory infections were significantly associated with bronchiectasis in the affected lung lobe. The proposed mechanisms include bronchoconstriction due to alveolar hypocapnia and impaired bronchial mucociliary clearance, leading to mucus trapping and bronchiectasis development [23]. In this case, although additional respiratory infection tests such as bronchoalveolar lavage were not performed; however, no associated clinical symptoms were observed, and the patient remained free of upper respiratory symptoms throughout its survival. Therefore, the bronchial and interstitial abnormalities observed on CT scans are more likely attributable to changes related to hypocapnia and fibrosis, rather than to chronic respiratory infections. In this case, using a preoperative CT scan, the right PC was clearly identified, allowing for precise three-dimensional visualization of the anatomical structures. Detailed imaging enabled selection of the optimal fluoroscopic viewing angle in advance, which was successfully used to guide the angioplasty procedure.

Although reported cases are limited in veterinary medicine, clinical signs of isolated pulmonary artery interruption (PAI) in cats include progressive exercise intolerance and dyspnea [8, 25]. When PAI is accompanied by PC in both cats and dogs, symptoms can include exercise intolerance and respiratory distress, although some cases remain asymptomatic [13, 18]. In humans, the clinical signs of isolated PAI vary and may include chest pain, pleural effusion, dyspnea, and exercise intolerance [10, 26]. In humans, isolated PAI has been frequently reported; however, cases in which PAI occurs with contralateral PC, as in this case, are relatively rare [20, 24]. In human cases, symptoms such as chest pain and cough have been noted, but patients diagnosed at a young age often present with no clinical signs other than heart murmurs. Similar to young human patients, this feline patient presented with only a heart murmur at 3 months of age, with no other clinical signs. However, echocardiography revealed significant right heart remodeling, prompting the clinician to recommend early corrective intervention. Although the PC was successfully treated, the contralateral PAI persisted, suggesting a potential risk for future clinical signs, including cough, dyspnea, and exercise intolerance. Therefore, ongoing monitoring for these symptoms is essential. Additionally, CT images in this case revealed parenchymal bands and bronchial wall thickening, suggesting the potential for irreversible lung parenchymal damage and recurrent respiratory infections in the future, warranting close monitoring.

Pulmonary hypertension has been observed in 44% of human patients with isolated PAI, likely due to the redistribution of blood flow away from the absent pulmonary artery toward the remaining artery [26]. Increased blood flow in the contralateral pulmonary artery can lead to arteriolar remodeling, resulting in heightened resistance within the pulmonary vasculature [16]. In this case, the initial echocardiogram revealed right ventricular hypertrophy and right atrial dilation, changes likely secondary to pulmonary hypertension caused by PAI, as well as pressure overload in the right ventricle due to contralateral stenosis from PC. Although direct measurement of pulmonary artery pressure was not performed during the procedure, the resolution of right heart remodeling following balloon angioplasty suggests that pulmonary hypertension was not evident.

Current treatments for pulmonary branch stenosis in humans include surgical angioplasty, simple balloon angioplasty, cutting balloon angioplasty, and stent placement [9]. However, due to the limited success rates, challenges in accessing distally located stenoses, increased risk of surgical scarring, and a high incidence of restenosis, percutaneous balloon angioplasty or stent placement has become the preferred approach for treating pulmonary branch stenosis [27]. The success rate of simple balloon angioplasty using low-pressure balloons is approximately 60%; however, the introduction of high-pressure balloons has since improved the success rate to 72%. In this case, a high-pressure balloon with a pressure of 14 atm was used to enhance the success rate and reduce the risk of restenosis. High-pressure balloons are stiffer and less compliant than low-pressure balloons. Unlike valvular pulmonic stenosis, where the obstruction is primarily at the valve, pulmonary branch stenosis or coarctation involves narrowing of the vessel media and intima, requiring greater pressure for dilation [2]. Additionally, peripheral pulmonary arteries are more elastic than the valvular region, increasing the risk of restenosis with low-pressure balloons. Thus, a high-pressure balloon was necessary to achieve optimal results in this case. Stent placement is also an option for treating pulmonary branch stenosis resistant to simple balloon angioplasty in humans. Stent placement has been shown to significantly improve the pulmonary pressure gradient and achieve a high success rate of dilation, averaging approximately 90% [9]. In one case of stent placement, a balloon-expandable stent was used for a canine with PA stenosis and contralateral PAI; however, inadvertent stent migration occurred [18]. Although the complication rate of stent placement is low (12%) in humans, potential complications include stent malposition, migration, fracture, vessel dissection, rupture, and jailing of side branches [7, 11]. In addition, small-diameter, balloon-expandable vascular stents are more expensive than high-pressure balloons. Therefore, considering the associated costs and potential complications, simple balloon angioplasty should be attempted initially. In cases of restenosis, stent placement can be considered as a subsequent intervention.

In this case, desaturation and hypotension occurred during balloon catheter insertion but resolved immediately after balloon dilation and catheter removal. Hypotension, bradycardia, and hypoxemia are the most commonly reported complications of balloon valvuloplasty for pulmonic stenosis in dogs [15]. Hypotension and hypoxemia typically result from obstruction of pulmonary outflow during catheterization and balloon inflation [14]. In this case, hypotension and desaturation developed immediately after balloon catheterization of the right pulmonary artery. Unlike typical pulmonary stenosis, the absence of the left pulmonary artery likely exacerbated these hemodynamic changes. Balanced anesthesia techniques and invasive arterial blood pressure monitoring are essential for minimizing cardiovascular depression during cardiac procedures. Persistent hypotension and desaturation can lead to inadequate oxygen transport, ventilation-perfusion mismatch, and potential organ damage [15]. Persistent hypotension may also impair myocardial contractility, increase myocardial workload and oxygen consumption, and trigger arrhythmias. Medications, such as dobutamine, dopamine, and phenylephrine, can be administered to manage hypotension, and anticholinergic drugs may be used if bradycardia accompanies these conditions [19]. In this case, however, hypotension and desaturation were transient, requiring no additional pharmacological intervention, and the patient remained stable throughout recovery from anesthesia.

This case report describes the CT features of a cat with left PAI and right PC. Simple balloon angioplasty of the PC successfully reduced the pressure gradient at the coarctation lesion and led to improvements in right heart remodeling. Additionally, one year later, a reduction in contralateral lung volume and interstitial changes due to PAI were observed. These changes may potentially lead to respiratory symptoms in the future, making careful long-term monitoring essential.

CONFLICTS OF INTEREST

The authors have nothing to disclose.