Rabbit Dilated Cardiomyopathy

  • Ralph S. Baric
  • Suzanne Edwards
  • J. David Small
Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 276)


Viruses have long been recognized as important etiologic agents of heart disease in man and experimental animals1. Epidemiologic evidence suggests that between 2–5% of a virus-infected population experiences some degree of cardiac involvement2. Virus infection may result in degeneration and necrosis of myocytes by direct cytotoxicity and cause myocarditis, or inflammation of the heart muscle3. Myocarditis may progress to arrhythmias, conduction disturbances, circulatory collapse and/or acute congestive (dilated) cardiomyopathy4. Clinically, dilated cardiomyopathy is diagnosed by an increase in the heart weight, heart weigh/body weight weight ratios, enlargement of the left and/or right ventricular cavities, thinning/hypertrophy of the ventricular walls, and low ejection fractions. In humans particularly ominous signs of dilated cardiomyopathy include the presence of pulmonary edema, pleural effusion, and congestion of the lungs and liver 4,5. The incidence of idiopathic dilated cardiomyopathy is estimated between 3–5 cases/100,000 population/year and accounts for about 30% of all heart disease related deaths in some areas of the world6. The mechanism(s) by which virus infection progresses to myocarditis and dilated cardiomyopathy is unclear.


Dilate Cardiomyopathy Ventricular Wall Ventricular Dilation Heart Weight Uninfected Control 
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  1. 1.
    Woodruff, J.F.(1980). Am. J. Path. 101:427–478.Google Scholar
  2. 2.
    Abelmann, W.H.(1973). Ann. Rev. Med. 24:145–152.PubMedCrossRefGoogle Scholar
  3. 3.
    Bolte, H.-D. eds. (1984). In: Viral Heart Disease, Springer-Verlag, New York, New York, pgs. 1–247.Google Scholar
  4. 4.
    Kishimoto, C. (1861) Cardiovascular Res. 20:665–671.Google Scholar
  5. 5.
    Hudson, E.B. (1972). In: Cardiomyopathy, G.E. Burch eds, Philadelphia Davis Co., p4.Google Scholar
  6. 6.
    Burch, G.E. and DePasquale, N.P. (1970). Circulation 42:A-47–53.Google Scholar
  7. 7.
    Woodruff, J.F. and Woodruff, J.J. (1974). J.Imm. 113:1726–1734.Google Scholar
  8. 8.
    Matsumori, A., and Kawai, C. (1826). Circulation 66:355–360.CrossRefGoogle Scholar
  9. 9.
    Matsumori,A., and Kawai, C. (1982). Circulation 64: 1230–1235.CrossRefGoogle Scholar
  10. 10.
    Reyes, M.P.1981) . J. Inf. Dis. 144:232–236.CrossRefGoogle Scholar
  11. 11.
    Small, J.D (1979) . Am. J. Path. 95:707.Google Scholar
  12. 12.
    Fennestad, R.L(1986). J. Gen. Virol. 67:993–1000.PubMedCrossRefGoogle Scholar
  13. 13.
    Matsumori, A. and Kawai, C. (1984). In: Viral Heart Disease, Bolte, H.-D ed, New York, NY pgs 35–56.CrossRefGoogle Scholar
  14. 14.
    Kishimoto, M.D.(1985). Circul. 71:1247.CrossRefGoogle Scholar
  15. 15.
    Matsumori, A. and Kawai, C.(1982). Circulation 66: 1349–1350.CrossRefGoogle Scholar
  16. 16.
    Wolf, D.K. (1981). In: Int. of Electropheretic pattern of proteins and isoenzymes. Masson Pub., New York, NY, pp56–60.Google Scholar
  17. 17.
    Lukehart, S.A. 1981). J. Imm. 127:1361.Google Scholar
  18. 18.
    Fennestad, R.L. (1983). Arch. of Virol. 76:179–187.CrossRefGoogle Scholar
  19. 19.
    Mackarthur, C.G.C.(1984). J. 5:1023–1035.Google Scholar
  20. 20.
    Matsumori, A. and Kawai, C.)1980) J. Path. 131:97–106.PubMedCrossRefGoogle Scholar
  21. 21.
    Uhl, H.S.M. (1952) Bull. John Hopkins Hosp. 91:197–209.PubMedGoogle Scholar
  22. 22.
    Fitchett, D.H.(1984).Google Scholar

Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • Ralph S. Baric
    • 1
  • Suzanne Edwards
    • 1
  • J. David Small
    • 2
  1. 1.Department of Parasitology and Laboratory PracticeUniversity of North Carolina at Chapel HillUSA
  2. 2.Glaxo CorporationsResearch Triangle ParkUSA

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