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.

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.

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.

Evaluation of N-terminal prohormone of brain natriuretic peptide and cardiac troponin-I levels in cats with systolic anterior motion of the mitral valve in the absence of left ventricular hypertrophy.

OBJECTIVES: To identify the prevalence of systolic anterior motion of the mitral valve (SAM) in apparently healthy cats in the absence of left ventricular hypertrophy (LVH) and examine the relationship between specific cardiac biomarker concentrations and echocardiographic parameters in these individuals. ANIMALS: eighty client-owned cats. MATERIALS AND METHODS: retrospective study; inclusion criteria were the presence of SAM on conscious echocardiography and concurrent measurement of plasma N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and serum cardiac troponin-I (cTnI). Cats were excluded if they had LVH, left atrial enlargement or systemic disease. The percentages of cats with NT-proBNP and cTnI concentrations above the normal reference range were calculated. The correlation between each biomarker concentration and left ventricular myocardial wall thickness, left atrial size and maximum left ventricular outflow tract velocity was evaluated. RESULTS: Thirty-four of 80 patients with SAM showed no evidence of cardiac remodelling (LVH or left atrial enlargement). Of these patients, 30 of 34 had elevated NT-proBNP, and cTnI was elevated in 13 of 27 (48.1%) cats where this biomarker was measured in association with the NT-proBNP assay. A positive correlation was observed between concentration of plasma NT-proBNP and maximum left ventricular outflow tract velocity (rs = 0.67, p<0.0001). No significant correlations were found between the concentration of biomarkers and the remaining echocardiographic parameters. CONCLUSIONS: SAM is frequently observed in cats even in the absence of cardiac remodelling, and these individuals often demonstrate elevated plasma NT-proBNP and serum cTnI concentrations. Plasma NT-proBNP elevation is correlated with the severity of the left ventricular outflow obstruction caused by SAM.

Left ventricular outflow tract pressure gradient changes after carvedilol-disopyramide cotherapy in a cat with hypertrophic obstructive cardiomyopathy.

Disopyramide reduces the left ventricular outflow tract (LVOT) pressure gradient and improves symptoms in humans with hypertrophic obstructive cardiomyopathy (HOCM). However, the efficacy of disopyramide in cats has not been reported. We treated a cat with HOCM with carvedilol and disopyramide cotherapy and monitored the changes in LVOT flow velocity and N-terminal pro B-type natriuretic peptide (NT-proBNP) concentration. A 10-month-old neutered male Norwegian Forest cat was referred with a moderate systolic cardiac murmur. Echocardiography revealed thickening of the left ventricular wall, systolic anterior motion of the mitral valve leaflets, and turbulent aortic flow in the LVOT at systole. The LVOT flow velocity was 5.6 m/s. The plasma NT-proBNP concentration exceeded 1,500 pmol/L. The cat was diagnosed with HOCM and the ß-blocker carvedilol was started and gradually increased to 0.30 mg/kg, bid. After 57 days, the LVOT flow velocity (4.8 m/s) and plasma NT-proBNP concentration (870 pmol/L) had decreased but remained elevated. Therefore, disopyramide was added at 5.4 mg/kg po bid and increased to 10.9 mg/kg po bid after 22 days. After 141 days of carvedilol and disopyramide treatment, the systolic anterior motion of the mitral valve leaflets had disappeared and the LVOT flow velocity and plasma NT-proBNP concentration had decreased to 0.7 m/s and 499 pmol/L, respectively. No adverse effect has been observed during the follow-up. Disopyramide might relieve feline LVOT obstruction after only partial response to a beta-blocker. Further large-scale studies are required to investigate the efficacy and safety of disopyramide use in cats with moderate to severe HOCM.

Obstructive right ventricular outflow tract myxosarcoma in an adult dog.

An 8-year-old female spayed German Shepherd cross was presented for acute onset of respiratory distress. Four days before presentation, the owner noticed a reduced appetite and reluctance to move. Clinical examination identified muffled lung sounds and a left base, diamond-shaped systolic murmur graded 4/6. Echocardiography identified pleural and pericardial effusion, ascites and a myxoid mass (39 mm/18.9 mm) obstructing the right ventricular outflow tract and interfering with the pulmonary valve function. Given the poor prognosis, the dog was euthanatised, and a postmortem examination was performed. Grossly, a mass with a heterogeneous appearance was identified below the pulmonary valve leaflets. Based on histopathological and immunohistochemical findings, a diagnosis of intracardiac myxosarcoma affecting the subvalvular region of the pulmonary artery was made. To the author's knowledge, this is the first report of right ventricle out flow tract myxosarcoma in the canine species.

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.

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.

Congestive heart failure caused by transvenous pacemaker lead prolapse and associated right ventricular outflow tract obstruction in a dog.

A 16-year-old dog was presented for cough as well as increased respiratory rate and effort three years after implantation of a single-lead transvenous artificial pacemaker system. Thoracic radiographs and echocardiography disclosed prolapse of the pacemaker lead into the main pulmonary artery, causing severe pulmonary insufficiency and right-sided volume overload. Repositioning of the pacemaker lead led to improvement of pulmonary insufficiency and resolution of the dog's clinical signs and cavitary effusions. This case describes a late complication of pacemaker implantation that may be avoided by appropriate use of the manufacturer-provided anchoring sleeve and avoidance of excessive lead redundancy.

Mitral valve dysplasia characterized by isolated cleft of the anterior leaflet resulting in fixed left ventricular outflow tract obstruction.

A 7-month-old, sexually intact male English toy spaniel weighing 4 kg was referred for evaluation of a subclinical cardiac murmur. Echocardiography disclosed fixed left ventricular outflow tract obstruction that was caused by attachment of a cleft anterior mitral valve leaflet to the interventricular septum. Neither atrial nor ventricular septal defects were detected. Fixed obstruction of the left ventricular outflow tract by a malformed mitral valve is rare in human beings and has not been previously reported in the dog.

[Mitral valve dysplasia in a cat causing reversible left ventricular hypertrophy and dynamic outflow tract obstruction]. / Mitraalklepdysplasie als oorzaak voor een reversibele hypertrofie en dynamische uitstroombaanobstructie van de linker ventrikel bij een kat.

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.

Cause of heart murmurs in 57 apparently healthy cats.

Heart murmurs are caused by turbulent blood flow or by vibration of cardiac structures. Turbulent blood flow may originate from structural heart disease or from physiological phenomena. The aims of this study were to establish the cause of heart murmurs in apparently healthy adult cats and to determine whether a heart murmur is a reliable indicator of heart disease. In this retrospective study, we reviewed the medical records of cats in which a heart murmur was detected during physical examination by one of the authors in the period January 2008 to December 2009. Cats younger than 6 months and those with systemic disease were excluded. Timing, grade, and point of maximum intensity of the murmur were determined by one observer (MD) before 2D-, M-mode and Doppler echocardiography. Fifty-seven cats (median age 76 months, range 6-194) were included, 30 neutered females and 27 neutered males. All murmurs were systolic and varied in intensity from 2/6 to 5/6. The point of maximum intensity was the left or right parasternal region in 34/57 (61%) of murmurs. Murmurs were caused by dynamic left ventricular outflow tract obstruction in 25/57 (44%) cats, dynamic right ventricular outflow tract obstruction in 9/57 (16%) cats, and combined dynamic left and right outflow tract obstruction in 11/57 (19%) cats. In 5 (9%) cats the cause of the murmur could not be identified. Heart disease was present in 50 (88%) cats, namely, left ventricular hypertrophy in 44 (77%) and congenital defects in 6 (11%) cats. In conclusion, most heart murmurs in apparently healthy cats are detected in the left or right parasternal region and are caused by dynamic left and right ventricular outflow tract obstruction. Because most cats (88%) with a heart murmur had heart disease in this study, if a heart murmur is detected in an apparently healthy cat, echocardiography is recommended to determine the cause of the heart murmur and the presence of heart disease.

External splinting for treatment of pectus excavatum in a dog with right ventricular outflow obstruction.

Right ventricular outflow tract obstruction was diagnosed by Doppler echocardiography in a young dog with a cardiac murmur, severe dyspnea, and a prominent sternal depression. Thoracic radiography confirmed a diagnosis of pectus excavatum involving the caudal third of the sternum. The right ventricular outflow obstruction was attributed to cardiac compression from the dorsally deviated sternum. External surgical splinting of the sternabrae, demonstrated by video in this report, was used to treat the pectus excavatum. Radiographic and Doppler echocardiographic examination 3 weeks and 4 months post-splinting documented resolution of both pectus excavatum and right ventricular outflow obstruction.

Echocardiographic assessment of left ventricular geometry and the mitral valve apparatus in cats with hypertrophic cardiomyopathy.

OBJECTIVES: This retrospective study addressed the general hypothesis that abnormalities of the mitral valve apparatus are common in cats with idiopathic hypertrophic cardiomyopathy (HCM) and contribute to dynamic obstruction of the left ventricular outflow tract (LVOT). ANIMALS, MATERIALS AND METHODS: 106 cats (28 controls and 78 with HCM) had transthoracic two-dimensional and Doppler echocardiography performed with quantification of 33 variables. Three groups of cats (control [Group-1], HCM without obstruction [Group-2], and HCM with obstruction [Group-3]) were identified and compared by analysis of variance, chi(2) analysis, and correlation analysis. RESULTS: Cats in Group-3 had more LV and papillary muscle hypertrophy, increased length of the anterior mitral valve leaflet, and a higher prevalence of false tendons in the LVOT compared to cats in Group-2 (P < or = 0.05). The length of the anterior mitral valve leaflet was correlated to the severity of dynamic obstruction (P < or = 0.05) and the magnitude of LV hypertrophy (P < or = 0.001). Systolic anterior motion of chordae tendineae (CAM) was observed in 16% of control cats and >50% of cats with HCM (P < or = 0.05). CONCLUSIONS: Abnormalities of the mitral valve are common in cats with HCM suggesting a possible role in the pathogenesis of dynamic outflow tract obstruction.

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 beta-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.

Systolic anterior motion of the mitral valve associated with right ventricular systolic hypertension in 9 dogs.

OBJECTIVES: To describe the zoographic and echocardiographic characteristics of canine patients in which systolic anterior motion of the mitral valve (SAM) was identified in association with right ventricular systolic hypertension (RVSH). ANIMALS, MATERIALS AND METHODS: Medical records and digitally recorded echocardiographic examinations were reviewed for RVSH and two-dimensional (2DE) or M-mode echocardiographic evidence of SAM. RESULTS: SAM was identified in association with RSVH in 9 patients; 5 had pulmonic stenosis, 2 had tetralogy of Fallot and 2, pulmonary hypertension. Relative to body weight, the end-diastolic and end-systolic left ventricular dimensions were subnormal in all patients. Hyperdynamic left ventricular systolic performance was identified in 8 of 9 patients. In 5 of the 9 patients, SAM was mild or moderate in degree. Left ventricular outflow tract (LVOT) obstruction and mitral valve regurgitation were documented by Doppler studies in only 3 of the 4 patients with marked SAM. However, late systolic acceleration within the LVOT was recorded in 2 additional patients for whom peak velocities were normal. CONCLUSIONS: In the cases described here, the presence of SAM is likely explained by alterations in left ventricular geometry and function associated with diminished pulmonary venous return together with sympathetic activation resulting from subnormal stroke volume. Although the hemodynamic consequences were apparently minor, the association of SAM with right-sided heart disease might be of interest to those engaged in the practice of veterinary echocardiography.

Clinical and echocardiographic features of primary infundibular stenosis with intact ventricular septum in dogs.

BACKGROUND: Primary infundibular stenosis is a rare congenital defect in which the right ventricle is divided into a proximal "high-pressure" chamber and a distal "low-pressure" chamber. The condition can be misdiagnosed as ventricular septal defect or valvular pulmonic stenosis and the disease severity underestimated. The purpose of this study was to provide a detailed clinical and echocardiographic description of this anomaly in a series of dogs. HYPOTHESIS: Several anatomic forms of infundibular stenosis exist. High resolution two-dimensional echocardiography could differentiate 3 gross anatomic substrates. Knowledge of the anatomy of the obstructing lesion could influence options for corrective interventions. ANIMALS: Thirteen dogs examined at the Ontario Veterinary College teaching hospital from 1994 to 2005 with an ultrasound diagnosis of subpulmonic stenasis. METHODS: A retrospective review was made of case records from 1994 to 2005. RESULTS: Thirteen dogs were identified as having primary infundibular stenosis, with apparent increased prevalence in Golden Retrievers (8/13, 62%) and Siberian Huskies (3/13, 23%). Three types of infundibular lesions were identified by ultrasound in 11/13 dogs: a fibrous diaphragm (6), fibromuscular (4), and muscular obstruction (1). Two dogs with a fibrous diaphragm underwent direct surgical dilation without the use of cardiopulmonary bypass or inflow occlusion, resulting in substantial reduction of the severity of stenosis. CONCLUSION AND CLINICAL IMPORTANCE: Accurate determination of the severity of the stenosis and the anatomy of the obstructing lesion are important in devising a treatment strategy. Recognition of the fibrous diaphragm by echocardiography identifies a subset of dogs potentially amenable to surgical dilation without the need for cardiopulmonary bypass.

Auscultation and echocardiographic findings in Bull Terriers with and without polycystic kidney disease.

OBJECTIVE: To investigate a possible association between Bull Terrier polycystic kidney disease (BTPKD) and cardiac disease, to determine the prevalence of mitral valve disease (MVD) and left ventricular outflow tract obstruction (LVOTO) in the Australian Bull Terrier population, and to compare auscultation and echocardiography in detection of cardiac disease in Bull Terriers. DESIGN: Ninety-nine Bull Terriers, ranging in age from 8 weeks to 13 years and 11 months were auscultated and examined using renal ultrasonography; 86 were also examined using echocardiography. The prevalence and severity of heart defects in dogs with BTPKD was compared with that in dogs without BTPKD. RESULTS: Nineteen of these 99 dogs were diagnosed with BTPKD. Forty-two percent of Bull Terriers with BTPKD and 28% of those without BTPKD had murmurs characteristic of mitral regurgitation or LVOTO. How recently an animal was descended from an ancestor with BTPKD was associated with presence (P = 0.008) and loudness of a murmur (P = 0.009). Overall, echocardiography detected MVD in 39% of Bull Terriers, with increased prevalence in older animals (P = 0.003). Mitral stenosis was found in eight cases. Fifty-three percent of dogs in this study had evidence of LVOTO, with obstruction consisting of a complex of lesions including dynamic or fixed subvalvular LVOTO, significantly narrowed left ventricular outflow tract or valvular aortic stenosis. Dogs with BTPKD, or those descended from dogs with BTPKD, were more likely to have MVD (P = 0.006), and while LVOTO was not more common in these dogs, if they did have LVOTO, they were more likely to have severe obstruction than dogs with no ancestors with BTPKD (analysed in three ways P = 0.028 to 0.001). In this study, 46% of Bull Terriers without a murmur or arrhythmia had cardiac disease detected on echocardiographic examination. CONCLUSION: Cardiac disease, especially MVD and LVOTO, was common in Bull Terriers in this study, and those with BTPKD had an increased risk of cardiac abnormalities. Auscultation did not detect a significant number of Bull Terriers with cardiac disease.