Fenofibrate,a peroxisome proliferator-activated receptor alpha activator,suppresses experimental autoimmune myocarditis by stimulating the interleukin-10 pathway in rats

Experimental autoimmune myocarditis (EAM) in rats is an animal model of human giant cell myocarditis and postmyocarditis dilated cardiomyopathy. As the heart consumes large amounts of energy, heart diseases such as myocarditis and dilated cardiomyopathy are associated with abnormal fatty acid metabolism. Peroxisome proliferator-activated receptor alpha (PPARalpha) is a regulator of the oxidative degradation of fatty acids. To investigate the role of PPARalpha in EAM, fenofibrate (a PPARalpha activator) was administered to rats with EAM for 4 weeks. Reductions in the ratios of both ventricular weight to body weight and the area of inflammatory lesions to the total area of heart sections were observed in fenofibrate-treated rats when compared with controls. Fenofibrate ameliorated changes in serum albumin and sialic acid, which are markers of inflammation. Cardiac expression of interleukin-10 (IL-10) mRNA was more pronounced in the fenofibrate group than in the control group (1.3 +/- 0.2 vs 0.7 +/- 0.1; p < 0.01), and the area of intact myocardium correlated with the IL-10 mRNA level (p = 0.0297, r = 0.620). We suggest that PPARalpha activators may prevent the progression of myocarditis through increased expression of the gene encoding the anti-inflammatory cytokine IL-10, although the mechanisms involved remain to be determined.     

Reversible T‐Wave Inversions and Neurogenic Myocardial Stunning in a Patient with Recurrent Stress‐Induced Cardiomyopathy

A 72‐year‐old female was diagnosed as a stress‐induced cardiomyopathy from apical ballooning pattern of left ventricular dysfunction without coronary artery stenosis after the mental stress. ECG showed the transient T‐wave inversions after the ST‐segment elevations. By the mental stress after 1 year, she showed a transient dysfunction with similar ECG changes again. T‐wave inversions recovered earlier, and cardiac sympathetic dysfunction showed a lighter response corresponding to the less severe dysfunction than those after the first onset. Wellens’ ECG pattern was associated with the degree of neurogenic myocardial stunning with sympathetic hyperinnervation caused by mental stress.