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Biomedical subjects

B J Gavaghan

Publications and source records attributed to B J Gavaghan.

6 recordsLinked to original sources
PubMed2001

Eisenmenger's complex in a Holstein-Friesian cow.

A 4.5-year-old, Holstein-Friesian cow presented with a 1-month history of severe exercise intolerance. Rectal examination and transrectal ultrasonography revealed a large mass in the left retroperitoneum. The heart rate was 70 to 80/min. Premature ventricular complexes and ventricular bigeminy were present on an electrocardiogram. Erythrocytosis was present and blood gas analysis revealed marked hypoxaemia. An echocardiogram demonstrated a large ventricular septal defect, a partially dextroposed aorta, and concentric hypertrophy of the right ventricular free wall. Colour flow Doppler echocardiography and a contrast echocardiographic study demonstrated a right-to-left shunt through the ventricular septal defect. Eisenmenger's complex was diagnosed. The patient was euthanased. Necropsy confirmed the gross cardiac lesions identified by echocardiography and an abscess in the apex of the left ventricle. Severe pulmonary arterial lesions were present, consistent with a marked increased in pulmonary vascular resistance. Actinomyces pyogenes was cultured from abscesses of the retroperitoneum and the ventricular apex.

Abdominal Abscess↗
PubMed1999

Persistent atrial standstill in a cat.

A domestic shorthaired cat was presented with a 1-month history of cardiomegaly and recurrent chylothorax. The heart rate was 130 beats/min and no P waves were present on a surface electrocardiogram. Thoracic radiographs and an echocardiogram demonstrated severe biatrial dilatation, pleural effusion and restrictive pleural disease. Permanent atrial standstill was suspected. Pleurocentesis was performed and therapy was started with enalapril, frusemide and aspirin. Intracardiac electrograms revealed no atrial activity, and atrial pacing failed to elicit atrial or ventricular depolarisations. The patient was euthanased. Necropsy showed severe atrial wall thinning with marked cardiocyte loss. Persistent atrial standstill is a rare disease in the cat. Clinical signs may have been due to loss of atrial function, ventricular diastolic dysfunction, bradycardia, neurohormonal activation and reduced atrial natriuretic peptide plasma concentrations.

Animals↗
PubMed1999

Quantification of left ventricular diastolic wall motion by Doppler tissue imaging in healthy cats and cats with cardiomyopathy.

OBJECTIVE: To assess Doppler tissue imaging (DTI) for evaluating left ventricular diastolic wall motion in healthy cats and cats with cardiomyopathy. ANIMALS: 20 healthy cats, 9 cats with hypertrophic cardiomyopathy (HCM), and 9 cats with unclassified cardiomyopathy (UCM). PROCEDURE: A pulsed wave DTI sample gate was positioned at a subendocardial region of the left ventricular free wall in the short axis view and at the lateral mitral annulus in the apical 4-chamber view. Indices of diastolic wall motion were measured, including peak diastolic velocity (PDV), mean rate of acceleration and deceleration of the maximal diastolic waveform (MDWaccel and MDWdecel, respectively), and isovolumetric relaxation time (IVRT). RESULTS: The PDV of cats with HCM and 6 of 9 cats with UCM was significantly decreased, compared with that of healthy cats. In the 3 cats with UCM that had a PDV that was not different from healthy cats, MDWaccel and MDWdecel were greater, and IVRT was shorter than those of healthy cats. The IVRT in cats with HCM was longer than that of other cats. CONCLUSIONS AND CLINICAL RELEVANCE: Indices of diastolic function in cats with HCM, and in many cats with UCM, differed from those of healthy cats and were similar to those reported in humans with HCM and restrictive cardiomyopathy, respectively. However, the hemodynamic abnormality was not the same for all cats with UCM; some cats with an enlarged left atrium and a normal left ventricle (ie, UCM) had abnormal left ventricular wall motion consistent with restrictive cardiomyopathy while others did not.

Animals↗
PubMed1997

Dilated cardiomyopathy in an American cocker spaniel with taurine deficiency.

An American Cocker Spaniel with low plasma taurine concentration (< 2 nmol/mL) was presented with dyspnoea associated with pulmonary oedema and a left ventricular shortening fraction of 9%. Emergency therapy with furosemide, dobutamine, nitroglycerine and oxygen supplementation led to a good response. Chronic therapy was started with enalapril, furosemide, digoxin and taurine. Improvement in all echocardiographic indices were noted over a 22 week follow-up, most notably an increase in left ventricular shortening fraction to 20%, a decrease of E-point septal separation from 14 mm to 7 mm and marked left ventricular remodelling. This degree of improvement in myocardial function may represent a direct link between dilated cardiomyopathy in the American Cocker Spaniel and plasma taurine deficiency. Alternatively, this response may reflect a breed-related cardiomyopathy with a natural history and therapeutic response not commonly seen in the more common large breed cardiomyopathy presentations.

Animals↗