Acquired mitral stenosis in a cat with hypertrophic cardiomyopathy

A seven-year-old castrated male domestic shorthair cat was diagnosed with hypertrophic cardiomyopathy (HCM) and suspected mitral stenosis (MS) based on electrocardiography, thoracic radiographs and echocardiographic findings. Post-mortem examination of the heart revealed morphological features consistent with HCM. In addition, there was marked fibrous deposition on the surfaces of the chordae tendineae extending to both mitral valve leaflets, which caused total chordal fusion into pillars of fibrous tissue and fusion of the commissures. The present case indicates that acquired MS can occur in association with HCM in the cat.     

Dysplasia of the tricuspid valve in the dog and cat.

Dysplasia of the tricuspid valve in 14 dogs and 13 cats was studied. The clinical, electrocardiographic, radiographic, hemodynamic, angiocardiographic, and pathologic findings were reviewed in each species. Alterations of the tricuspid valve complex included long, thick septal leaflets adhered to the septum; absent or short, stout fused chordae tendineae; hypertrophic fused papillary muscles; insertion of papillary muscles directly into the lateral leaflets; incomplete development of the valvular tissue; and enlargement of the right atrium and ventricle. Additional intracardiac anomalies included malformation of the mitral valve complex (5 dogs and 3 cats), ventricular septal defect (3 dogs and 3 cats), pulmonary stenosis (1 dog and 1 cat), aortic stenosis (1 dog and 1 cat), and persistent left cranial vena cava (1 dog).     

No expression of angiotensin II receptors and angiotensin-converting enzyme in myxomatous canine mitral valve leaflets. An autoradiographic study

The renin-angiotensin system, including angiotensin (Ang) II and angiotensin-converting enzyme (ACE), plays an important role in cardiac fibrous tissue formation. Since changes in valvular collagen are a central part of myxomatous mitral valve disease in the dog, we speculated that Ang II and ACE might play a role in the pathogenesis of this disease. In 10 mitral valves, five with and five without clear myxomatous changes, the presence and distribution of Ang II receptors and ACE was examined autoradiographically, using 125I-Ang II and 125I-lisinopril, respectively. At postmortem examination, diseased valves were taken from old dogs, control valves from young adult dogs. No significant level of Ang II and lisinopril binding was found in normal as well as diseased valve leaflets. Equally low, insignificant levels of 125I-Ang II binding were found in the myocardium of dogs with and without valvular disease. No significant level of myocardial 125I-lisinopril binding was found. The lack of autoradiographic evidence of Ang II receptors and ACE in normal and diseased canine mitral valve leaflets suggests that the renin-angiotensin system does not play a major role in the pathogenesis of the valvular changes.     

Clinical, echocardiographic, and Doppler imaging characteristics of mitral valve stenosis in two dogs.

Mitral stenosis was diagnosed noninvasively by echocardiography and Doppler imaging in 2 Bull Terriers. Two-dimensional echocardiography revealed severe atrial and moderate left ventricular dilatation; severely reduced mitral valve opening excursion; doming of the cranial mitral valve leaflet into the left ventricle during diastole; thickened, nodular cranial mitral valve leaflets; and reduced mitral valve orifice. M-mode echocardiographic findings additionally indicated greatly diminished mitral valve E to F slope and abnormal caudal mitral valve leaflet motion. Color flow Doppler imaging revealed bright bursts of color with aliasing originating from the stenotic mitral valve orifice, extending into the left atrium during systole, and into the left atrium during diastole. Spectral Doppler recordings revealed transvalvular mitral valve gradients and prolonged pressure half-times. Necropsy performed on 1 dog revealed extremely thickened, nodular, and stiff mitral valves with short, thickened, and fused chordae tendineae. The diagnosis of mitral valve stenosis was easily facilitated with diagnostic ultrasonography.     

Balloon valvuloplasty of congenital mitral stenosis

Radiographic, echocardiographic, fluoroscopic, and angiographic images from 2 dogs with severe congenital mitral valve stenosis that underwent cardiac catheterization and balloon valvuloplasty are presented. Both dogs displayed systolic doming of the mitral valve leaflets, increased diastolic pressure gradient across the left atrium and ventricle, and decreased mitral inflow E to F slope. Balloon valvuloplasty was performed on both dogs using atrial transeptal puncture.     

Mitral valve stenosis in three cats

Two-dimensional and M-mode echocardiography were used to diagnose mitral stenosis in two cats with heart failure. This appeared to be related to mitral valve complex malformation. Ultrasound findings included thickened mitral valve leaflets with inhibited mobility, reduced mitral valve orifice size, abnormal upward (cranial) motion of the caudal mitral leaflet during diastole and severe left atrial enlargement. Colour-flow and spectral Doppler imaging helped characterise this condition. Colour-flow Doppler mapping showed turbulence and increased mitral filling velocity (aliasing) at the site of stenosis and related jets of mitral regurgitation. Spectral Doppler recordings showed increased diastolic mitral filling velocities with spectral broadening and prolonged pressure half-time. Mitral stenosis should be included in the differential diagnosis of cats with severe left atrial enlargement when congenital or acquired mitral valve disease is detected; it may represent an advanced form of mitral valve complex malformation in some cases.     

Identification of surface morphologic changes in the mitral valve leaflets and chordae tendineae of dogs with myxomatous degeneration

OBJECTIVE: To describe structural changes in the left atrioventricular (mitral) valve complex of dogs with endocardiosis by use of scanning electron microscopy. ANIMALS: 5 clinically normal dogs and 4 dogs with mitral valve endocardiosis. PROCEDURE: The mitral valve complex from each dog was fixed and prepared for examination via scanning electron microscopy. Findings in valves from clinically normal and affected dogs were compared to identify surface changes associated with endocardiosis. RESULTS: Compared with findings in valves from clinically normal dogs, endocardiosis-affected mitral valve complexes had several morphologic abnormalities. Tissue swelling on the edge of valve leaflets, chordae tendineae, and the chordal-papillary muscle junction was evident. Damage to the valve complex endothelium was unevenly distributed; in some areas, denudation of endothelial cells had exposed the basement membrane or subendothelial valve collagen matrix. This damage was most noticeable on the leaflet edges and extended more to the ventricular aspect of the valve than the atrial side. Cell loss also extended to the chordae tendineae but was less apparent at the chordal-papillary muscle junction. The remaining endothelial cells on affected valves were arranged in less-ordered rows and had more plasmalemmal microappendages, compared with cells on unaffected valves. CONCLUSIONS AND CLINICAL RELEVANCE: Morphologic changes associated with mitral valve endocardiosis in dogs were similar to those observed in humans with mitral valve prolapse. In dogs with mitral valve endocardiosis, gross changes in the valve complex may affect hemodynamics in the heart; alterations in the leaflet and chordal endothelium may contribute to pathogenesis of this disease.     

Malformation of the canine mitral valve complex.

Twenty-nine dogs, including 13 Great Danes and 5 German Shepherd Dogs and averaging 7.3 months age, were diagnosed clinically and radiographically as having mitral regurgitation. Alterations of the mitral valve complex included enlarged anulus; short thick leaflets, with an occasional cleft; short and stout or long and thin chordae tendineae; upward malposition of atrophic or hypertrophic papillary muscles; insertion of one papillary muscle directly into one or both leaflets; and diffuse endocardial fibrosis, occasionally with jet lesions in te left atrium. Other cardiac anomalies included dysplasia of the tricuspid valve (5 dogs), patent ductus afteriosus (2 dogs), aortic stenosis (2 dogs), and ventricular septal defect (1 dog).     

Aortic valve insufficiency in a one-year-old colt

Aortic insufficiency was suspected in a thin 1-year-old colt with a grade IV/V decrescendo holodiastolic murmur and a bounding arterial pulse. Echocardiographic findings (diastolic fluttering of the septal leaflet of the mitral valve, left ventricular volume overload, and incomplete aortic valve closure) were diagnostic for aortic valve insufficiency. Moderately thick fibrotic aortic valve leaflets were found at necropsy. Fenestrations were found in the aortic and pulmonic valve cusps. Congenital valvular disease may have led to aortic valvular insufficiency in this horse.     

Mitral valve dysplasia in a cat causing reversible left ventricular hypertrophy and dynamic outflow tract obstruction

A 6-month-old male European shorthair cat was examined because of a 2/6 systolic left apical cardiac murmur. Echocardiography revealed severe concentric left ventricular hypertrophy and severe dynamic left ventricular outflow tract obstruction (pressure gradient of 85 mmHg) caused by systolic anterior motion (SAM) of the septal mitral valve leaflet. After 2 months of oral treatment with atenolol, the cardiac murmur had disappeared. Echocardiography showed only slight thickening of the interventricular septum and resolution of the pressure gradient. The cat was discharged and its owner was advised to continue atenolol lifelong. Echocardiographic findings of a combination of left ventricular concentric hypertrophy and dynamic left ventricular outflow tract obstruction can be caused by hypertrophic obstructive cardiomyopathy (HOCM) or mitral valve dysplasia in the absence of hypertension and fixed aortic stenosis. In the case of HOCM, left ventricular hypertrophy is the primary process. In the case of mitral valve dysplasia, systolic anterior motion of the mitral valve is the primary problem, which leads to dynamic left ventricular outflow tract obstruction and ultimately to left ventricular concentric hypertrophy, due to pressure overload. If the left ventricular outflow tract obstruction is reduced with an oral beta-receptor blocker the secondary left ventricular hypertrophy may resolve. This would not happen in the case of hypertrophic obstructive cardiomyopathy. To the best of the authors' knowledge, this is the first documented case of severe dynamic left ventricular outflow tract obstruction and severe left ventricular hypertrophy in a cat successfully treated with oral atenolol.     

Mitral Stenosis in 15 Dogs

Mitral stenosis was diagnosed in 15 young to middle-aged dogs. There were 5 Newfoundlands and 4 bull terriers affected, suggesting a breed predisposition for this disorder. Clinical signs included cough, dyspnea, exercise intolerance, and syncope. Soft left apical diastolic murmurs were heard only in 4 dogs, whereas 8 dogs had systolic murmurs characteristic of mitral regurgitation. Left atrial enlargement was the most prominent radiographic feature. Left-sided congestive heart failure was detected by radiographs in 11 dogs within 1 year of diagnosis. Electrocardiographic abnormalities varied among dogs and included atrial and ventricular enlargement, as well as atrial and ventricular arrhythmias. Abnormalities on M-mode and two-dimensional echocardiograms included abnormal diastolic motion of the mitral valve characterized by decreased leaflet separation, valve doming, concordant motion of the parietal mitral valve leaflet, and a decreased E-to-F slope. Increased mitral valve inflow velocities and prolonged pressure half-times were detected by Doppler echocardiography. Cardiac catheterization, performed in 8 dogs, documented a diastolic pressure gradient between the left atrial, pulmonary capillary wedge, or pulmonary artery diastolic pressures and the left ventricular diastolic pressure. Necropsy showed mitral stenosis caused by thickened, fused mitral valve leaflets in 5 dogs and a supramitral ring in another dog. The outcome in affected dogs was poor; 9 of 15 dogs were euthanatized or died by 2 1/2 years of age.     

Pneumothorax in a dog with a pulmonary abscess and suspected infective endocarditis.

Nontraumatic pneumothorax was diagnosed in a dog with a pulmonary abscess and evidence of infectious endocarditis, including fever, mitral murmur, and vegetative lesion of mitral valve leaflets. Pneumothorax persisted after 4 days of continuous thoracic drainage. At exploratory thoracotomy, the diaphragmatic lung lobe was identified as the source of air leakage and was excised. Results of culturing of blood and lung tissue for aerobic and anaerobic bacteria were negative. Antibiotics were administered because of suspected bacterial endocarditis. Pneumothorax and fever resolved after surgical and medical treatments.     

Migration of a Kirschner wire to the heart in a Yorkshire terrier

A 12-year-old, male Yorkshire terrier was presented for acute pulmonary oedema. Thoracic radiographs showed a linear metallic foreign body within the cardiac silhouette. Echocardiogram showed a hyperechoic line extending through the left ventricle, the mitral valve, leading into the left atrium. A 4 cm long Kirschner wire was surgically removed by left fourth thoracotomy. The dog died two days after surgery for acute pulmonary oedema. Necropsy showed thrombi on the mitral leaflets that impeded their movement.     

Congenital supravalvular aortic stenosis in a kitten

A three-month-old, male intact Norwegian forest cat without any clinical signs was referred to the cardiology service of the author’s teaching hospital for evaluation of a cardiac murmur. The murmur was systolic with an intensity of 4 out of 6 with the point of maximal intensity at the left heart base. Echocardiography revealed a moderate mitral valve regurgitation and a moderate dynamic left ventricular outflow tract obstruction both resulting from systolic anterior motion of the mitral valve (SAM). Moreover, left ventricular concentric hypertrophy was noted. Oral atenolol therapy was initiated. Recheck examination 3.5 months later revealed unchanged murmur characteristics in the still asymptomatic kitten. Echocardiography showed no SAM, but there was a severe fixed aortic stenosis apparent caused by a discrete supravalvular lesion, 4 mm distal to the valve, with an hourglass morphology. Supravalvular aortic stenosis is a rare congenital anomaly in cats, which has not been reported antemortem yet.     

Trifoliate left atrioventricular valve with and without intact septal structures in four dogs: echocardiographic findings and surgical repair

Trifoliate left atrioventricular (AV) valve with common atrioventricular junction is considered part of the spectrum of atrioventricular septal defect. This valve morphology is typically associated with defects in the AV septum resulting in communication at the atrial or ventricular level, but has also been described as an isolated defect in the setting of a common AV junction without AV septal defect. Trifoliate left AV valve exhibits a line of apposition between the bridging leaflets that is directed toward the inlet interventricular septum, distinguishing it from isolated mitral valve cleft in which the orientation of the bridging leaflets are toward the left ventricular outflow tract. The echocardiographic findings of four dogs with trifoliate left AV valve are described; two with intact septal structures and two with large ostium primum defects. Three dogs underwent open surgical repair using different approaches depending on the presence or absence of a septal defect. One of these underwent concurrent surgical repair for right AV valve dysplasia. One dog with intact septal structures underwent interventional closure of a concurrent patent ductus arteriosus. Current terminology associated with trileaflet left AV valve malformations is reviewed.