Abstract
Cardiac thrombosis, especially atrial thrombosis, accounts for more deaths in the world than any other disease, and major conditions in which thrombosis plays a principal role include several cardiovascular diseases, such as atrial fibrillation, myocardial infarction and stroke. Results from the induction of chemical thrombosis in rodents are useful to identify substances in our environment that may contribute to cardiac thrombosis. We evaluated atrial thrombosis induced by chemical exposures in rodents, compared it to similarly induced lesions reported in the literature, from the results of more than 500 chemicals in National Toxicology Program (NTP) database, and summarized a putative pathogenesis. The incidences of atrial thrombosis were increased in high-dosed groups in the NTP rodent studies of 13 compounds: 2-butoxyethanol, C.I. Direct Blue 15, bis(2-chloroethoxy)methane, diazoaminobenzene, diethanolamine, 3,3'-dimethyl-benzidine dihydrochloride, hexachloroethane, isobutene, methyleugenol, oxazepam, C.I. Pigment Red 23, C.I. Acid Red 114, and 4,4'-thiobis(6-t-butyl-m-cresol). The left atrium was the main localization in spontaneous and chemically induced thrombosis. The literature survey suggested that chemical-induced atrial thrombosis might be closely related to myocardial injury, endothelial injury, circulatory stasis and/or hypercoagulability. Impaired atrial mechanical activity, such as atrial fibrillation, could cause stasis of blood within the left atrial appendage, contributing to left atrial thrombosis.
