Subvalvular pulmonary stenosis in a kitten.

A 4-week-old, male domestic shorthair was presented to the Atlantic Veterinary College (AVC) Teaching Hospital emergency service with difficulty in breathing. The kitten and its littermate had been fostered for the past 2 wk. The caretaker noted that this kitten had an adequate appetite and was smaller than its sibling. The kitten had demonstrated normal behavior and physical activity with no obvious medical problems, prior to its presentation for dyspnea. On physical examination, the patient was depressed, but responsive, and was in good body condition. It had openmouthed breathing and cyanotic mucous membranes. The lung sounds were inaudible over a grade VI/VI systolic heart murmur. The murmur, along with a palpable thrill, was appreciated on the left side in the region of the lower 3rd or 4th intercostal space. The patient also had a green mucopurulent discharge and blepharospasm of the left eye. The patient was immediately supplemented with oxygen via a face mask, resulting in a marked improvement in the color of the mucous membranes. Single lateral radiographs revealed severe pleural effusion. The cardiac silhouette was obscured and the lungs were displaced both cranially and dorsally. Subsequent views were not taken, due to the patient's distress when restrained. The patient was maintained on oxygen via face mask. The right side of the thorax was shaved and prepared for thoracocentesis. This yielded 15 mL of reddish-pink, milky, mildly viscous fluid. A presumptive diagnosis of congestive heart failure was made. The patient was euthanized by cardiac puncture under general anaesthesia. At necropsy, the kitten weighed 483 g and appeared to be in good body condition. The thoracic cavity contained approximately 15 mL of cloudy, blood-tinged, milky fluid, suggestive of chylous effusion. The heart was enlarged weighing 5.1 g, or 1.1% of total body weight (the weight of a clinically normal 7-week-old cat's heart is 0.76% of total body weight) (1). The heart was markedly widened at the base and the right atrium was 2 to 3 times the size of the left atrium. The heart was injected with 10% buffered formalin, fixed for 24 h, and then sectioned using echoplane landmarks. The right atrium was markedly dilated. The thickness of the right ventricular wall was equal to that of the left ventricular wall (Figure 1). In the normal adult heart, the left ventricular wall is 2 to 3 times thicker than the right ventricular wall (2). The pulmonary outflow tract was markedly narrowed to 1 mm in diameter, approximately 4 mm below the pulmonary valves, which indicated subvalvular pulmonary stenosis (Figure 2). The abdominal cavity contained approximately 4 mL of blood-stained fluid. The liver was diffusely enlarged with a “nutmeg” or mottled appearance, typical of chronic passive congestion. Figure 1. Photograph of the heart transected longitudinally. The right ventricular wall is markedly thickened due to the obstruction of the pulmonary outflow tract. The right atrium is markedly dilated. Figure 2. Photograph of the right venticular outflow tract. Arrow pointing to narrowing. The crista ventricularis muscle is hypertrophied. Gross pathological diagnoses included subvalvular pulmonary outflow obstruction, right ventricular hypertrophy, right atrial dilation, chronic passive congestion in the liver, chylothorax, and ascites. Microscopic examination of the heart and liver supported the gross pathological findings. The myofibers of the right ventricle were hypertrophied. There was scant, lightly staining, eosinophilic material, suggestive of edema, and mild collagen deposition surrounding vascular structures and, occasionally, separating myofibers. Marked hepatic congestion in zone 3, with mild hepatocellular degeneration, were considered to result from right-sided heart failure. The final diagnosis was subvalvular pulmonary stenosis with right ventricular hypertrophy and right atrial dilation, acute to subacute centrilobular hepatic congestion, chylothorax, and ascites. Congenital heart disease is less common in cats than in dogs. The reported prevalence is 0.2–1.0/1000 hospital admissions (versus 6.8–8.0/1000 in dogs) (3). Congenital cardiovascular disorders comprise about 10% of clinical cardiology cases in domestic mammals and are encountered more frequently in cattle and dogs than in cats (2). No consistent breed or gender predilections have been determined in cats. Generally, a congenital heart defect is suspected when a heart murmur is detected in a young dog or cat. Other supporting clinical signs include failure to thrive, exercise intolerance, cyanosis, collapse or seizure, jugular venous distension, electrocardiographic abnormalities, and radiographic evidence of cardiac enlargement. Mitral valve anomalies are thought to be the most common cardiac anomaly in the cat (2). Ventricular septal defects, aortic stenosis, tricuspid valve dysplasia, patent ductus arteriosus, persistent common atrioventricular canal, and tetralogy of Fallot have also been reported (4,5). Pulmonary stenosis is a rare congenital heart defect in cats with only a few reports found in the literature (5,6,7). In one study, 107 cats were diagnosed with a congenital cardiac anomaly and only 2 of these had pulmonary stenosis (5). Subvalvular pulmonary stenosis is hypothesized to develop from an extension of the crista supraventricularis (7). During embryonic development, the pulmonic valve originates from 3 swellings (2 truncus swellings and 1 intercalated swelling) within the developing truncus arteriosus. Subvalvular pulmonary stenosis may result from abnormal partitioning of the bulbus cordis during ventricular septal formation, but this hypothesis remains unproven (8). An abnormal consolidation of the embryological muscle of the trabeculae carneae, or an aberrant outgrowth of the conus septum, may result in the extension of the crista supraventricularis and blockage of outflow through the pulmonic valve (7). In this case, the muscle forming the crista ventricularis was hypertrophied, and fibrous connective tissue also contributed to the subvalvular pulmonary stenosis, as shown in Figure 2. The principle hemodynamic consequence of pulmonary stenosis is increased resistance to right ventricular systolic outflow, with a proportional increase in right ventricular systolic pressure causing right ventricular hypertrophy. The extent of the cardiac muscle hypertrophy is proportional to the severity of the obstruction. Attempts to increase cardiac output resulted in right ventricular hypertrophy and an increase in size of the papillary muscles and muscle of the trabeculae carneae. The increased velocity through the stenosis generated turbulence and vibration, resulting in the VI/VI systolic murmur. Right-sided heart failure follows impedance of pulmonary circulation; this may be due to valvular abnormalities (pulmonary stenosis, tricuspid dysplasia) or secondary to either left-sided heart failure or primary pulmonary disease (cor pulmonale). The increased venous hydrostatic pressure that occurs with right-sided heart failure can result in hepatic congestion, edema, ascites, and hydrothorax. Chylothorax is a commonly diagnosed sequela to right-sided heart failure in cats (9). One hypothesis suggests that the abnormal flow and increased pressure within the thoracic duct may lead to exudation of chyle from intact but dilated thoracic lymphatic vessels. Cats that are unable to shunt the increased lymph flow into the venous circulation through alternate routes, for example, may exhibit chylous effusion. Chylous effusion is not associated with right-sided heart failure in dogs. The ability of dogs to form alternate lymphatic-venous communications has been experimentally shown by ligating the thoracic duct (10,11,12) or the cranial vena cava (13). Attempts to treat either chylothorax alone, or in association with right-sided heart failure, have been relatively unsuccessful. While the prognosis for any cat with congestive heart failure (CHF) is poor, CHF associated with chylothorax has a guarded to grave prognosis. Subvalvular pulmonary stenosis producing clinical signs and pathological changes of CHF in a 4-week-old kitten is reported. Clinicians and pathologists are reminded to carefully examine hearts from young animals with respiratory signs to assess congenital heart anomalies.

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