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The proposed set of ICD-10 codes encompasses the codes used in different countries for most SUDI cases. Use of these codes will allow for better international comparisons and tracking of trends over time.

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Well-designed, hypothesis-driven prospective cohort studies are warranted to improve our understanding of the mechanisms underlying the relationship between bed sharing, its benefits, and its harms.

Although evidence shows that victims of sudden infant death syndrome (SIDS) suffer repetitive episodes of hypoxemia, only subtle abnormalities have been found in their brains by light microscopy. The aim of the present study was to determine whether apoptosis, a form of cell death that can be triggered by hypoxemia and that leaves no scarring detectable by light microscopy, would be present in hypoxia-sensitive brain regions of SIDS victims. We looked for the presence of apoptosis with an in situ end-labeling method that detects DNA fragmentation. We studied 29 SIDS victims who were age-matched to nine control cases. We found significant neuronal apoptosis in 79% of the SIDS cases: 55% of the cases positive in the hippocampus and 96% positive in the brainstem. Whereas the distribution of apoptosis in the hippocampus was in hypoxia-sensitive subregions, the distribution in the brainstem was mostly in dorsal nuclei, including those involved with sensation in the face and position of the head (nucleus of the spinal trigeminal tract and vestibular nuclei). The control cases showed no significant apoptosis in the hippocampus and a mild degree in the brainstem in three cases. Our results indicate the occurrence of an acute insult at least several hours before death, an insult from which the infants had apparently recuperated. This suggests that SIDS victims suffered repeated apoptosis resulting in significant neuronal damage and, thus, functional loss in key brain regions. The involvement of specific nuclei in the brainstem may be linked to the fact that prone sleeping is a significant risk factor for SIDS. Enhanced neuronal death by apoptosis may thus have major implications for understanding the sequence of events leading to SIDS.

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Background-Management of severe ischemic mitral regurgitation remains difficult with disappointing early and intermediate-term surgical results of valve repair. Methods and Results-Forty-four patients with severe (4ϩ) Carpentier type IIIb ischemic mitral regurgitation underwent mitral valve repair, with or without surgical revascularization, by posterior leaflet extension with a patch of bovine pericardium and a remodeling annuloplasty. Serial echocardiography was performed preoperatively, intraoperatively, and postoperatively to assess mitral valve competence. The postoperative functional status of patients was assessed. The average Parsonnet score was 38Ϯ13. Thirty-day mortality was 11%, and late mortality was 14%. Mean follow-up was 38 months. The actuarial freedom from moderate or severe recurrent mitral regurgitation was 90% at 2 years, whereas 90% of patients were in New York Heart Association class I at 2 years. Conclusion-Posterior