Author + information
- Mark L. Smucker, MD, FACCa,b,
- Sanjiv Kaul, MD, FACC∗,a,b,1,
- Jerry A. Woodfield, DVMa,b,
- James C. Keith, DVM, PhDa,b,
- Scott A. Manning, BAa,b and
- Joseph A. Gascho, MD, FACCa,b
- ↵∗Address for reprints: Sanjiv Kaul, MD, Box 158, Division of Cardiology, University of Virginia School of Medicine, Charlottesville, Virginia 22908.
Currently there is no large animal model of dilated cardiomyopathy. The smaller animal models of cardiomyopathy, such as the Syrian hamster, cannot be studied with echocartography and cardiac catheterization, and the relevance of these models to human dilated cardiomyopathy is open to question. On the basis of some initial observations in Doberman pinschers, it was speculated that these dogs could have occult left ventricular dysfunction. Accordingly, studies were performed in 46 apparently healthy Doberman pinschers and in 41 mongrel dogs: two-dimensional echocardiography (30 dogs in each group), cardiac catheterization (16 Doberman pinschers and 12 mongrels) and coronary blood flow studies (13 Doberman pinschers and 6 mongrels). In the awake, unsedated dogs studied with echocardiography, left ventricular wall thickening was significantly less in the Dobermans than in the mongrels (28% versus 36%, p = 0.0003). In the anesthetized dogs undergoing cardiac catheterization, left ventricular ejection fraction was significantly lower in the Dobermans than in the mongrels (0.38 versus 0.63, p = 0.0001). Rest coronary blood flow and coronary blood flow reserve were similar in the two groups.
It is concluded that apparently healthy Doberman pinschers have occult left ventricular dysfunction. These dogs may serve as a large animal model of dilated cardiomyopathy and should not be used experimentally to study normal cardiac physiology.
↵1 Dr. Kaul is a recipient of a Clinical Investigator Award (K08-HL01833) and of a FIRST Award (R29-H138345) from the National Institutes of Health, Bethesda, Maryland.
☆ This study was presented in part at the Annual National Scientific Session of the American Federation for Clinical Research, May 1988, Washington, D.C. It was supported in part by a grant in aid from the American Heart Association (Virginia Affiliate). Glen Allen, Virginia and by the David A. Greiner Heart Valve Research Fund, Charlottesville, Virginia.