CALCIFIC arterial disease of infants with myocardial infarcts is uncommon, but at least 50 cases have been reported in the medical literature.1 , 2 The etiology has remained a complete mystery. It has been suggested that the arterial changes result from a basic defect in calcium metabolism.1 , 2 However, no such defect has been demonstrated, and the general distribution of the lesions is not that of diseases known to result from abnormalities of calcium metabolism. Another possibility is that the disease results from a defect in the formation of elastic tissue and that the calcium deposition is a secondary feature.1 2 3 The nature of . . .
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Thomas et al. (1956) studied this question.
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