Myocardial infarction as a complication of injury.

BACKGROUND: MI is a rare complication of trauma. We anticipate that the aging of the population and the concomitant rise in geriatric trauma will result in an increase in acute illnesses of the elderly (such as MI) complicating recovery from injury. The purpose of this article is to define the presentation of MI in the immediate postinjury period. STUDY DESIGN: Medical records of all trauma patients in whom MI developed during their hospitalizations at a single Level I trauma center, the Barnes Hospital/Washington University Medical Center, between 1990 and 1999 were screened through the trauma registry. Nineteen patients with possible postinjury MI were identified. Of these, five had bona fide cases of postinjury MI, five had ambiguity about whether MI preceded or followed trauma, one had an MI resulting in trauma, and eight were excluded because they did not meet strict diagnostic criteria for MI. RESULTS: The five patients with posttraumatic MI were older than the general trauma population with ages ranging from 51 to 81 years (mean +/- SD = 72 +/- 14 years). Each had preexisting medical illnesses, some of which are recognized to predispose to coronary artery disease. There were no identifiable precipitants other than the recent injury. Importantly, only one of the five patients had chest pain as a presenting symptom and each of the five cases was complicated by acute congestive heart failure. CONCLUSIONS: MI remains a rare but important complication of injury and may increase owing to the changing demographics of trauma victims. Methods for thorough history-gathering to identify preexisting conditions, for early hemodynamic monitoring and anticoagulation for MI in the setting of trauma, and for identifying preexisting conditions should be defined. The presentation of MI in the setting of injury is atypical and complications are frequent.

A novel L23-related gene 40 kb downstream of the imprinted H19 gene is biallelically expressed in mid-fetal and adult human tissues.

The closely linked IGF2 and H19 genes on human chromosome 11p15.5 are monoallelically expressed as a result of genomic imprinting and show altered expression in Wilms' tumors (WTs). To map regional imprinting we have sought to isolate additional human genes close to IGF2/H19 and to characterize their allelic expression patterns. Here we report a novel gene, provisionally named L23MRP [L23 (mitochondrial)-related protein], which is oriented 'tail-to-tail' with H19 and is transcribed to within 40 kb of the last H19 exon. L23MRP is expressed biallelically in many mid-fetal and adult human tissues. This gene is also expressed at normal levels in WTs which have lost expression of H19 either via loss of the maternal chromosome 11p15.5 or via an epigenetic pathway involving site-specific DNA hypermethylation. These data indicate that, at least in post-embryonic stages, L23MRP is functionally insulated from the IGF2/H19 imprinted domain.

Epigenetic lesions at the H19 locus in Wilms' tumour patients.

To test the potential role of H19 as a tumour suppressor gene we have examined its expression and DNA methylation in Wilms' tumours (WTs). In most WTs (18/25), H19 RNA was reduced at least 20-fold from fetal kidney levels. Of the expression-negative tumours ten retained 11p15.5 heterozygosity: in nine of these, H19 DNA was biallelically hypermethylated and in two cases hypermethylation locally restricted to H19 sequences was also present in the non-neoplastic kidney parenchyma. IGF2 mRNA was expressed in most but not all WTs and expression patterns were consistent with IGF2/H19 enhancer competition without obligate inverse coupling. These observations implicate genetic and epigenetic inactivation of H19 in Wilms' tumorigenesis.