Dynamic obstruction of the left ventricular outflow tract in four young dogs

Four young dogs presented for evaluation of left-sided systolic heart murmurs all showed echocardiographic changes consistent with dynamic left ventricular outflow tract (LVOT) obstruction and subjective evidence of concentric left ventricular hypertrophy. In three of the dogs, abnormal mitral valve apparatus and systolic anterior motion of the anterior mitral valve leaflet with associated mitral insufficiency were also detected. All dogs were medicated with a beta1-adrenergic antagonist. Subsequent examinations showed that the dynamic LVOT obstruction and left ventricular concentric hypertrophy had almost completely resolved. Dynamic LVOT obstruction is a rare condition of young dogs of different breeds. The precise aetiology of the condition remains uncertain. Whether resolution of the outflow obstruction in these four cases was a consequence of treatment or due to changes in ventricular architecture brought about by ageing cannot be established.     

Left ventricular outflow tract to left atrial fistula associated with endocarditis in a dog

A one-year-old, intact male, 28-kg, mixed-breed dog developed neurological episodes consistent with emboli. An acquired III/VI holosystolic heart murmur was ausculted in the mitral area, and valvular endocarditis with pulmonic and aortic insufficiency were noted at echocardiographic examination. An abnormal communication (i.e., fistula) between the left ventricular outflow tract (LVOT) and the left atrium adjacent to the mitral valve annulus was noted with Doppler imaging and confirmed with angiography. Infective valvular endocarditis was confirmed based on two of three blood cultures being positive for Staphylococcus intermedius. In humans, a sequela to infective endocarditis of the aortic or mitral valve, or both, is rupture of the mitral-aortic intervalvular fibrosa, resulting in a communication between the LVOT and the left atrium. This is the first report of this sequela in the dog.     

Echocardiographic features of accessory mitral valve tissue presenting left ventricular outflow tract obstruction in a dog

In a 3-year-old Samoyed, aortic bulging was found on radiography during a general check-up. On echocardiography, turbulent flow was found in left ventricular outflow tract (LVOT) with high velocity (6.1 m/s). A linear structure was attached to the interventricular septum and connected to the chordae tendineae reaching the papillary muscle. A part of the structure moved during cardiac cycle, similar to mitral motion. This dog was diagnosed with LVOT obstruction caused by accessory mitral valve tissue (AMVT). This is the first report of AMVT in veterinary medicine. AMVT should be considered as a possible cause of LVOT obstruction in dogs.     

Echocardiographic assessment of the left ventricular outflow tract in the Boxer

BACKGROUND: Soft, variable ejection murmurs are common in Boxers and are associated with increased left ventricular outflow tract (LVOT) ejection velocities. Whether these murmurs are physiologic or indicate mild aortic stenosis is controversial. Ejection velocity is impacted by LVOT area and ventricular stroke volume (SV), suggesting that these variables are pertinent to murmur development. HYPOTHESIS: Boxers with ejection murmurs have a smaller LVOT and equivalent SV indices, compared with values in dogs without murmurs. ANIMALS: Three age- and weight-matched groups of dogs--15 Boxers with soft ejection murmurs (group I); 15 Boxers without murmurs (group II); and 15 nonBoxer dogs without murmurs (group III)--were studied. METHODS: All dogs underwent 2-dimensional and Doppler echocardiographic examinations. The LVOT size at multiple levels; LVOT ejection velocity, stroke distance, and SV index; and right ventricular SV index were determined and compared by analysis of variance. RESULTS: Indexed LVOT areas in Boxer groups were not different, but were significantly smaller than those of non-Boxer dogs. Ejection velocities and stroke distances were significantly different across all groups, with group I having the highest and group III having the lowest values. Doppler SV indices (ml/m2) for group-I versus group-II Boxers were 70 +/- 16(SD) versus 62 +/- 12 for the LVOT (P = .27) and 58 +/- 12 versus 48 +/- 9 for the right ventricle (P = .14). CONCLUSIONS AND CLINICAL IMPORTANCE: These data suggest that a relatively smaller LVOT in Boxers predisposes them to increased ejection velocity and development of murmurs. The contribution of SV to the genesis of these often labile murmurs requires additional study.     

Extracardiac intrapericardial myxosarcoma causing right ventricular outflow tract obstruction in a dog

A 13-year-old male castrated pomeranian cross was referred for evaluation of episodes of collapse and a suspected cardiac mass. The presence of a mass at the base of the heart within the pericardial space was confirmed by echocardiography. Additional diagnostics included computed tomography, ultrasound-guided fine-needle aspirate, and thoracic radiographs. The mass was surgically debulked and diagnosed as myxosarcoma via histopathology. This case report describes the diagnostic imaging, laboratory findings, and short-term positive clinical outcome of a dog with a myxosarcoma in a previously undescribed location.     

Dynamic left ventricular outflow tract obstruction secondary to hypovolemia in a German Shepard dog with splenic hemangiosarcoma

Dynamic left ventricular outflow tract obstruction (DLVOTO) is a common condition in cats and humans. In this case report, a dog is described with DLVOTO secondary to severe intra-abdominal hemorrhage caused by a hemangiosarcoma. The dog was a 9-year-old, 35.7-kg, spayed female German Shepard dog that presented with a history of tachypnea and collapse. A Levine II/VI systolic murmur was present at the heart base. Abdominal ultrasonography revealed a splenic mass and a large amount of ascites. Echocardiography showed a reduced left ventricular diameter and an increased aortic velocity caused by systolic anterior motion (SAM) of the mitral valve apparatus. The heart murmur and the SAM were resolved after treatment including a splenectomy and a blood transfusion.     

Balloon dilation of right ventricular outflow tract in a dog with tetralogy of Fallot.

Balloon dilation was performed on a dog with tetralogy of Fallot. Immediately following balloon dilation, the peak systolic pressure gradient across the pulmonic valve declined from 97 to 63 mmHg. Doppler echocardiography following balloon dilation revealed increased pulmonary blood flow. Clinical symptoms obviously improved and the dog's improved condition was maintained for 4 months. There were no serious complications in performing the procedure. It was concluded that balloon dilation was a safe and effective treatment for a dog case with tetralogy of Fallot. Long-term follow-up studies will be required to identify the exact indications of balloon dilation for tetralogy of Fallot.     

Left ventricular outflow tract obstruction caused by a congenital accessory mitral valve leaflet and treated by open-heart surgery in a young dog

A 3-month-old Shetland sheepdog presented with a loud ejection murmur and exercise intolerance. Echocardiography revealed an accessory mitral valve leaflet, characterised by a valve-like structure separate from the mitral valve seen in the subaortic region of the ventricular septum. The left ventricular outflow tract was partially obstructed with a pressure gradient of 12 mmHg. Accessory mitral valve leaflet resection and mitral valvuloplasty were performed during open-heart surgery. Histology performed on the membrane-like structures were indicative of fibrous connective tissues. Postoperative echocardiography confirmed removal of the valve-like structure with resolution of the left ventricular outflow tract obstruction. The pressure gradient was decreased to 4.6 mmHg. The dog was in good condition and no further treatment was required 5 months after surgery. Both cardiac troponin I and NT-proBNP were markedly decreased. In this dog, surgical resection combined with mitral valve plasty resolved the left ventricular outflow tract obstruction and the clinical signs.     

Dynamic right ventricular outflow tract (infundibular) stenosis and pectus excavatum in a dog

This is the first published report of a dog with dynamic right ventricular outflow tract (infundibular) stenosis, right ventricular hypertrophy, and pectus excavatum. A juvenile dog presented with a grade V/VI left base systolic heart murmur, tachycardia, and pectus excavatum. Diagnosis of the aforementioned conditions was based on radiography, electrocardiography, and echocardiography. At 9 1/2 wk of age the heart murmur was no longer audible and the right ventricular stenosis and hypertrophy had dissipated and regressed, respectively. Resolution may be associated with growth of the dog. A good prognosis is foreseen.     

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.     

A prospective study of systolic ejection murmurs and left ventricular outflow tract in boxers

Objectives : To investigate the prevalence and progression of murmurs and the development of the left ventricular outflow tract (LVOT) and flow velocities in the great arteries in boxer puppies through adolescence until three years of age. Methods : Nineteen boxer puppies with or without a low‐intensity murmur, but without evidence of congenital heart disease, were studied prospectively. Examinations were carried out at 7 weeks, 3, 4, 6, 9, 12 and 36 months of age by cardiac auscultation and Doppler echocardiography. Results : Presence and intensity of heart murmurs varied in the same dog and between dogs, but flow velocities did not change. Estimated effective orifice diameter (EOD) and indexed EOD was significantly narrower than measured subvalvular and valvular diameters. Clinical Significance : The variability in presence and intensity of low‐intensity ejection murmurs is high during growth in boxers.     

Doppler echocardiographic effects of medetomidine on dynamic left ventricular outflow tract obstruction in cats

OBJECTIVE: To evaluate the effects of medetomidine on dynamic left ventricular outflow tract (LVOT) obstruction in cats with left ventricular hypertrophy. DESIGN: Clinical trial. ANIMALS: 6 domestic shorthair cats with echocardiographic evidence of dynamic LVOT obstruction. PROCEDURE: Cats were restrained in lateral recumbency, and baseline M-mode and Doppler echocardiographic examinations were performed. An ECG was recorded continuously, and blood pressure was measured indirectly with Doppler instrumentation. Medetomidine (20 microg/kg 19.1 microg/lb]) was then administered i.m., and examinations were repeated 15 minutes later. RESULTS: Significant decreases in heart rate, LVOT velocity, and the LVOT pressure gradient were documented following medetomidine administration. After adjusting for the effects of heart rate by ANCOVA, there were no significant differences in any other systolic or diastolic indices of left ventricular function. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that administration of medetomidine to cats with dynamic LVOT obstruction may result in elimination of outflow tract obstruction; medetomidine may be a suitable sedative and analgesic agent in this subpopulation of cats.     

Primary cardiac tumor presenting as left ventricular outflow tract obstruction and complex arrhythmia

An adult female mixed breed dog presented for recurrent collapsing episodes over several weeks. Holter evaluation revealed periods of sinus arrest and echocardiography identified a soft tissue mass with subsequent severe dynamic obstruction of the left ventricular outflow tract. The patient was euthanized five days after presentation for severe dyspnea. Necropsy revealed an irregular mass circumferentially lining the left ventricular outflow tract as well as multiple myocardial metastases. The final diagnosis was an undifferentiated pleomorphic endocardial sarcoma.     

Canine dynamic left ventricular outflow tract obstruction: assessment of myocardial function and clinical outcome

Objective : The aims of this study were (i) to evaluate echocardiographic findings and myocardial function including pulsed wave tissue Doppler imaging in dogs with naturally occurring dynamic left ventricular outflow tract obstruction and (ii) to investigate the clinical outcome and response to therapy in these dogs. Methods : Two cases were retrospectively reviewed and three cases were prospectively evaluated including clinical findings, diagnostic test results (including standard Doppler echocardiography and pulsed wave tissue Doppler imaging), response to treatment and outcome. The two retrospective cases received no treatment. Other cases were treated with a β‐blocker. Results : All dogs had a variable intensity left apical systolic murmur. Concentric left ventricular hypertrophy, systolic anterior motion of the mitral valve and scimitar‐shaped left ventricular outflow tract Doppler flow profile were present in all cases. Pulsed wave tissue Doppler imaging interrogation of the interventricular septum revealed E′/A′ reversal in all but one patient. Regression of left ventricular hypertrophy and total resolution of the dynamic left ventricular outflow tract obstruction were observed in all cases. Clinical Significance : Young dogs are affected with a possible terrier breed predisposition. Dynamic left ventricular outflow tract obstruction may be distinguished from canine hypertrophic cardiomyopathy as progressive resolution of echocardiographic abnormalities was documented. Pulsed wave tissue Doppler imaging abnormalities provide further evidence for significant diastolic dysfunction associated with the hypertrophy.     

Advanced imaging findings in a cat with left ventricular apical aneurysm

An eight-year-old, male neutered, domestic shorthair cat presented with severe anemia. Two-dimensional echocardiography identified severe left ventricular apical dilation with wall thinning and akinesia. The basal portion of the left ventricle showed equivocal hypertrophy and subjective hyperkinesis. Speckle tracking echocardiography showed marked abnormalities in all deformation planes (longitudinal, circumferential, radial strain) and twist. Three-dimensional Bull's eye plot reconstruction was also performed. Post-mortem evaluation showed a pale and paper-thin left ventricular apex and histopathology confirmed full-thickness cardiomyocytes loss with fibrous replacement. Left ventricular acquired apical aneurysms are the result of chronic damage of the myocardium and are associated with many disease conditions in people, including coronary artery disease and cardiomyopathy. The exact pathophysiological mechanism could not be determined with certainty in the cat of the present report, but advanced echocardiographic evaluation added some fine details into the characterization of this infrequently reported abnormality.     

Primary left ventricular hemangiosarcoma diagnosed by endomyocardial biopsy in a dog

An 8-year-old spayed Golden Retriever was examined because of recent onset of congestive heart failure complicated by ventricular arrhythmias. Echocardiography revealed a thickened, hypokinetic region of the left ventricular free wall. Fluoroscopically guided transarterial endomyocardial biopsy of the hypokinetic region of the left ventricle revealed infiltration of the endocradium by neoplastic cells consistent with hemangiosarcoma. The dog's clinical condition deteriorated 7 weeks later, and necropsy confirmed the diagnosis and primary site of origin of the tumor. This report describes the clinical use of an endomyocardial biopsy technique to diagnose an infiltrating myocardial tumor that was associated with signs mimicking canine dilated cardiomyopathy.