Doxorubicin (DX)-treated mice represent an animal model for studying n
ew drugs for heart disease. Coincidentally, in the collection of damag
ed myocardial tissue, thrombosis was detected in the atrium. The incid
ence reached 75% in mice given 4 mg/kg DX iv 10 times. They were white
thrombi consisting of the fibrin, platelets, and neutrophils. Cardiac
muscle damage was more prominent in the atria than in the ventricles.
Light microscopically, vacuolization and degeneration of atrial myocy
tes and interstitial inflammatory cell infiltration were observed. Ele
ctron microscopy revealed dilatation of the sarcoplasmic reticulum and
an increase in number of normal and/or degenerate mitochondria. Infla
mmation extended from the cardiac muscle to the endocardium. The cause
of atrial thrombosis in DX-treated mice is unknown but may relate to
endocardial damage and changes of blood flow in the atrium secondary t
o cardiac muscle damage. DX-treated mice could serve as an experimenta
l animal model for the evaluation of efficacy and toxicity of antithro
mbotic or antiplatelet drugs.