Sudden infant death syndrome (SIDS) is multifactorial and may result from the interaction of a number of environmental, genetic, and developmental factors. We studied three major genes causing long QT syndrome in 42 Japanese SIDS victims and found five mutations, KCNQ1-K598R, KCNH2-T895M, SCN5A-F532C, SCN5A-G1084S, and SCN5A-F1705S, in four cases; one case had both KCNH2-T895M and SCN5A-G1084S. All mutations were novel except for SCN5A-F532C, which was previously detected in an arrhythmic patient. Heterologous expression study revealed significant changes in channel properties of KCNH2-T895M, SCN5A-G1084S, and SCN5A-F1705S, but did not in KCNQ1-K598R and SCN5A-F532C. Our data suggests that nearly 10% of SIDS victims in Japan have mutations of the cardiac ion channel genes similar to in other countries.

Cardiovascular complications associated with methamphetamine abuse have increasingly been reported. However, chronic cardiotoxicity of methamphetamine is not experimentally well documented. In this study, methamphetamine (1 mg/kg/day) was subcutaneously injected into 5-week-old male Wistar Kyoto rats (n = 30). Age- and sex-matched Wistar Kyoto rats served as controls (n = 30). After 14 and 56 days, hearts were examined by light and electron microscopy. Foci of myocytic degeneration and necrosis appeared in the sub-endocardial areas on day 14 of methamphetamine exposure. Myocytic degeneration and necrosis became more extensive on day 56. At this stage, myocytolysis, contraction bands, atrophied myocytes, and spotty fibrosis were patchily distributed throughout the myocardium in most of rats treated with methamphetamine. The accompanying ultrastructural features included marked degeneration of cardiac mitochondria with fractured and disrupted cristae, hypercontraction of myofibrils, and loss of myofilament. In contrast, cardiac myocyte lesions were not observed in control rats. These myocardial lesions in rats treated with methamphetamine for 56 days resemble the cardiomyopathy associated with methamphetamine abuse in humans.

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