Fixed subaortic stenosis as a congenital heart defect has been reported in a relatively small number of cases. The classic description of feline subaortic stenosis reflects the presence of a fibrous ring just underneath the aortic valve. The present case has a unique morphological aspect, analogous with a rare human stenosis. A 15-month-old, ESH female presented with an anamnesis consisting of respiratory distress, apathy, and anorexia. The clinical examination displayed a patient with lethargy and severe dyspnea, whilst lung auscultation identified generalized bilateral pulmonary crackles. A systolic IV/VI parasternal murmur was identified on the left thorax, while the murmur intensity on the right side was III/VI. Electrocardiogram showed a sinus rhythm interrupted by ventricular ectopic beats. Two-dimensional (2D) echocardiography revealed a concentric hypertrophy of the left ventricle, with severe left atrium enlargement and mild pleural and pericardial effusion. A subaortic, hyperechoic structure was seen from the right parasternal five-chamber view, accompanied by post-stenotic aortic dilatation. The aortic peak velocity was 5.2 m/s, a feature that characterizes the severe form of aortic stenosis. The cat died shortly after presentation and necropsy was performed. Subaortic stenosis was confirmed on gross examination. The structure that induced stenosis of the left ventricle outflow tract (LVOT) had the appearance of a rudimental valve with moderator bands attached. Microscopically, it contains fibrous and smooth muscular tissue and cardiac conduction fibers. This type of subaortic stenosis resembles the cushion-like pseudovalve type described only in human cardiology. This is the first case describing clinical signs, ECG, echocardiography, and histopathological findings in a cat with cushion-like pseudovalve subaortic stenosis. Fixed subaortic stenosis is a rare congenital disease in cats, which should be taken into consideration in young cats with dyspnea and left ventricular hypertrophy.

Subvalvular aortic stenosis (SAS) is the most common congenital heart disease (CHD) in dogs and is also prevalent in human children. A fibrous ridge below the aortic valve narrows the left ventricular outflow tract (LVOT) and increases blood flow velocity, leading to devastating side effects in diseased patients. Due to the similarities in presentation, anatomy, pathophysiology, cardiac development, genomics, and environment between humans and dogs, canine SAS patients represent a critical translational model of human SAS. Potential adverse outcomes of SAS include arrhythmias, left-sided congestive heart failure, endocarditis, exercise intolerance, syncope, and sudden cardiac death. The greatest divergence between canine and human SAS clinical research has been the standard of care regarding treatment of these outcomes, with pharmacological intervention dominating best practices in veterinary medicine and surgical intervention comprising the standard practice for human SAS patients. Regardless of the species, the field has yet to identify a treatment option to prevent disease progression or permanently remove the fibrous ridge, but historical leaps in SAS research support a continued translational approach as the most promising method for achieving this goal.