Ultrastructural alterations in nutritional cardiomyopathy of selenium-vitamin E deficient swine. I. Fiber lesions.

Cardiomyopathy was produced in 38 weanling swine by feeding a semisynthetic diet deficient in selenium and vitamin E for 13 to 59 days. Pigs were killed for morphologic studies of the cardiac lesions at sequential times after development of the deficiency disease. Gross examination disclosed hydropericardium and scattered pale streaks and patches of necrosis in the myocardium, especially the left ventricle. Histopathologically, the lesions were scattered throughout the heart but were most severe in the atria. Ultrastructurally, the damaged fibers had many features of myofibrillar degeneration with hypercontraction bands, myofibrillar lysis, and mitochondrial swelling, disruption, and mineralization. Numerous macrophages appeared to have passed through focal disruptions in the external laminae of the muscle cells and engulfed sarcoplasmic and nuclear debris. Stromal collapse and mild fibrosis persisted as residual lesions in scattered areas of myocardium in pigs with long term deficiency. Although vascular lesions were present in the hearts of selenium and vitamin E deficient pigs, it was concluded that the fiber alterations developed independently of the vascular changes. The pathogenesis of this cardiomyopathy induced by nutritional deficiency is thought to be related to lack of protection by the selenoenzyme, glutathione peroxidase, and the antioxidant, vitamin E, from lipoperoxidative damage.