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.     

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.     

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.     

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.     

Right ventricular outflow tract fractional shortening: an echocardiographic index of right ventricular systolic function in dogs with pulmonary hypertension

Objectives

To create reference intervals for right ventricular outflow tract fractional shortening (RVOT-FS) in healthy dogs and examine diagnostic performance of this index in dogs with pulmonary hypertension (PH). In addition, we examine the impact of myxomatous mitral valve disease (MMVD) without PH on RVOT-FS.

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.     

Intramyocardial haematoma causing right ventricular outflow obstruction after brown snake (Pseudonaja species) envenomation in a dog

A 15-month-old, male neutered Staffordshire Bull Terrier cross was presented to its referring veterinarian collapsed and agonal. He was immediately intubated, manually ventilated, and treatment commenced for presumptive snake envenomation with two vials of Tiger/Multi-Brown Snake Antivenom (minimum 7000 units/vial). The dog was transferred to a referral hospital intubated. Additional diagnostics performed following arrival at the referral hospital included a urine snake venom detection kit test, which was positive for brown snake immunotype. Three additional vials of Tiger/Multi-Brown Snake Antivenom (minimum 7000 units/vial) were administered until the dog was extubated and able to stand. Venom-induced consumptive coagulopathy (VICC) was diagnosed based on prolonged clotting times and scleral haemorrhage. Paroxysms of right ventricular outflow tract (RVOT) origin ventricular arrhythmias were treated with lignocaine and sotalol. Four days after presentation, a new-grade IV/VI systolic heart murmur was auscultated, prompting an echocardiogram. An anechoic and compartmentalised mass measuring 43 mm × 19 mm was visualized within the right ventricular wall at the RVOT, immediately adjacent to the pulmonic valve. The mass was causing a RVOT obstruction. Its appearance was suggestive of an intramyocardial haematoma, most likely secondary to VICC. The dog remained cardiovascularly stable, and treatment consisted of supportive care. Recheck echocardiograms at 2 and 7 weeks after discharge revealed progressive improvement of the intramyocardial mass and resolution of the associated heart murmur. Although intramyocardial haematomas are rare, it should be considered as a differential in dogs that develop a newly diagnosed heart murmur and/or cardiac arrhythmia following brown snake envenomation.     

Echocardiographic assessment of right ventricular systolic function in Boxers with arrhythmogenic right ventricular cardiomyopathy

Objectives

To determine whether there are differences in measures of longitudinal right ventricular (RV) systolic function among Boxers with arrhythmogenic right ventricular cardiomyopathy (ARVC) compared with healthy control Boxer dogs. To explore relationships between markers of RV systolic function and age, body weight, gender, arrhythmia frequency, and markers of left ventricular (LV) systolic function in Boxer dogs.

Stenting of the right ventricular outflow tract in 2 dogs for palliation of dysplastic pulmonary valve stenosis and right-to-left intracardiac shunting defects

Two dogs with severe dysplastic pulmonary valve stenosis and right-to-left shunting defects (patent foramen ovale, perimembranous ventricular septal defect) underwent palliative stenting of the right ventricular outflow tract and pulmonary valve annulus using balloon expandable stents. One dog received 2 over-lapping bare metal stents placed 7 months apart; the other received a single covered stent. Both procedures were considered technically successful with a reduction in the transpulmonary valve pressure gradient from 202 to 90 mmHg in 1 dog and from 168 to 95 mmHg in the other. Clinical signs of exercise intolerance and syncope were temporarily resolved in both dogs. However, progressive right ventricular concentric hypertrophy, recurrent stenosis, and erythrocytosis were observed over the subsequent 6 months leading to poor long-term outcomes. Stenting of the right ventricular outflow tract is feasible in dogs with severe dysplastic pulmonary valve stenosis, though further study and optimization of the procedure is required.     

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.     

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.     

Tricuspid annular plane systolic excursion-to-aortic ratio provides a bodyweight-independent measure of right ventricular systolic function in dogs

Objectives

To evaluate whether tricuspid annular plane systolic excursion (TAPSE) can be normalized to aortic valve (Ao) measurements in dogs. To determine TAPSE:Ao reference intervals for healthy dogs and examine diagnostic performance of TAPSE:Ao in dogs with pulmonary hypertension (PH).

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.     

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.     

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.     

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.