Dietary taurine deficiency and dilated cardiomyopathy in the fox

Taurine deficiency has been implicated as a potential cause of dilated cardiomyopathy. However, the relationship between taurine and myocardial function is presently unclear. The purpose of this study was to determine whether dilated cardiomyopathy in the fox is associated with dietary taurine deficiency. A total of 68 foxes from farms with a history of death caused by dilated cardiomyopathy and 14 foxes from a farm with no history of dilated cardiomyopathy were studied. Dilated cardiomyopathy was diagnosed by echocardiography in 48% of the foxes from one farm with a positive history and in none of the foxes from the control farm. Foxes less than 9 months of age were more commonly affected than older foxes (p = 0.03). Plasma taurine concentrations were significantly less (p < 0.01) in foxes that had dilated cardiomyopathy (26.8 ± 16.4 nmol/ml) than in the control foxes (99.3 ± 60.2 nmol/ml). A significantly higher (p < 0.01) incidence of dilated cardiomyopathy was present in foxes with a history of a sibling or offspring that died of dilated cardiomyopathy than in foxes without a family history of cardiac death. In one fox with dilated cardiomyopathy that was tested, the myocardial taurine concentration was lower (1.7 μmol/gm wet weight) than that of control foxes (7.3 ± 1.6 μmol/gm wet weight). Hepatic cysteinesulfinic acid decarboxylase activity was significantly less (p < 0.001) in foxes with dilated cardiomyopathy (0.97 ± 0.2 nmol/mm · mg protein) than in control foxes (2.11 ± 0.07 nmol CO2/mm · mg protein). In a trial with one fox in congestive heart failure, dilated cardiomyopathy was reversed with taurine treatment (plasma taurine increased from 3.4 nmol/ml to 120 nmol/ml). It was concluded that dilated cardiomyopathy is associated with dietary taurine deficiency and that the disease is more likely to occur in young foxes with low hepatic cysteinesulfinic acid decarboxylase activity.