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Biomedical subjects

C W Lombard

Publications and source records attributed to C W Lombard.

28 records · Page 2Linked to original sources
PubMed1983

Ventricular septal defects in the horse.

Clinical, echocardiographic, and right-side cardiac catheterization data were collected in 6 horses with ventricular septal defects. The defects were confirmed by necropsy in 5 horses. On echocardiography, the cardiac dimensions were normal in 3 horses and enlarged in 2 others. A step-up in partial oxygen pressure between right atrium and right ventricle suggested a left-to-right shunt in 3 of the 4 horses catheterized. In 1 foal, a small defect without PO2 step-up was documented by angiocardiography. The oxymetry and pressure data were compared with previous cases from the reviewed literature, and the importance of pressure measurements to rule out concomitant defects was emphasized.

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PubMedDate not supplied

Recommendations for standards in transthoracic two-dimensional echocardiography in the dog and cat. Echocardiography Committee of the Specialty of Cardiology, American College of Veterinary Internal Medicine.

Recommendations are presented for standardized imaging planes and display conventions for two-dimensional echocardiography in the dog and cat. Three transducer locations ("windows") provide access to consistent imaging planes: the right parasternal location, the left caudal (apical) parasternal location, and the left cranial parasternal location. Recommendations for image display orientations are very similar to those for comparable human cardiac images, with the heart base or cranial aspect of the heart displayed to the examiner's right on the video display. From the right parasternal location, standard views include a long-axis four-chamber view and a long-axis left ventricular outflow view, and short-axis views at the levels of the left ventricular apex, papillary muscles, chordae tendineae, mitral valve, aortic valve, and pulmonary arteries. From the left caudal (apical) location, standard views include long-axis two-chamber and four-chamber views. From the left cranial parasternal location, standard views include a long-axis view of the left ventricular outflow tract and ascending aorta (with variations to image the right atrium and tricuspid valve, and the pulmonary valve and pulmonary artery), and a short-axis view of the aortic root encircled by the right heart. These images are presented by means of idealized line drawings. Adoption of these standards should facilitate consistent performance, recording, teaching, and communicating results of studies obtained by two-dimensional echocardiography.

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PubMedDate not supplied

Cardiomyopathy in dystrophin-deficient hypertrophic feline muscular dystrophy.

A colony of cats affected with hypertrophic feline muscular dystrophy was used to study the occurrence of cardiomyopathy associated with dystrophin deficiency. Affected male and female cats, obligate carrier females, and unaffected healthy littermates were followed from 12 weeks of age into adulthood. Thoracic radiography, 2-D echocardiography, and 2-D-derived M-mode echocardiography were performed at 3-month intervals until 12 months of age and regularly thereafter. From 9 months of age, all affected cats had larger hearts than normal and carrier animals. Left ventricular wall thickness in systole and in diastole and interventricular septal thickness in systole were greater in affected cats 12 months and older when compared with normal or heterozygous animals (P < .05). The myocardium of affected cats was diffusely hypoechoic and thickened. Multiple hyperechoic foci were in the myocardium and papillary musculature. Shortening fraction was normal in all cats. Changes seen in carrier females included enlargement and hyperechogenicity of the papillary musculature after the age of 2 years. Gross and light microscopic examination revealed left ventricular wall thickening with multiple foci of mineralization in 2 of 5 hearts from dystrophin-deficient cats. Although approximately 10% of the normal dystrophin amount was present in the skeletal muscle, dystrophin could not be detected in the myocardium. Early onset concentric myocardial hypertrophy was present in all adult cats. Lesions were mainly localized in the myocardium of the left ventricular free wall and interventricular septum, papillary musculature, and the endocardium. Clinical signs of heart failure developed only infrequently in cats with hypertrophic feline muscular dystrophy.

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