BackgroundExercise treadmill testing (ETT) has been standard for evaluating outpatients at risk for cardiovascular events. Few studies have demonstrated its prognostic usefulness in emergency department chest pain units or have used the Duke score [(exercise duration in minutes) − (5 × ST-segment deviation in millimeters) − (4 × treadmill angina index)] to grade its performance.Aims Our objective was to assess the usefulness of this score in a chest pain unit to predict cardiovascular events.MethodsFrom November 2000 to October 2001, we retrospectively studied consecutive patients in the chest pain unit. Those undergoing ETT were stratified into “low” (Duke score ≥ 5) and “moderate/high” risk groups (< 5). Cardiovascular events defined as death, myocardial infarction > 24 h after presentation, revascularization, acute congestive heart failure, stroke or arrhythmia were identified within 1 year after presentation. Differences in risk of having a cardiovascular event among low-risk and moderate/high-risk groups are presented.ResultsDuring the study period, 1,048 patients entered the chest pain unit; 800 met inclusion criteria. Of these, 599 received ETT and 201 had contraindications or a positive finding in the chest pain unit protocol before ETT. Cardiovascular event rates were 0.7% (3/454), 15.2% (22/145) and 14.9% (30/201) after 1 month of follow-up for low-risk, moderate/high-risk and no-ETT groups, respectively.ConclusionsAccording to the Duke score, the low-risk group developed minimal cardiovascular events compared with the moderate/high-risk group. The Duke score appears effective for risk stratification of chest pain patients in chest pain units.

Nonobese diabetic mice are a well-known model for human insulin-dependent diabetes mellitus. These mice develop autoimmune-mediated inflammation of the pancreatic islets, followed by destruction of the insulin-producing β cells and development of diabetes. Nonobese diabetic mice also have salivary gland inflammation, and serve as a model for human Sjogren’s syndrome. T cells are a prominent component of the inflammatory infiltrate in these sites, and T cell recruitment from the blood is thought to be essential for the initiation and maintenance of pathologic tissue damage. A unique mAb to murine CD43, L11, has recently been shown to block the migration of T cells from blood into organized lymphoid tissues. Here we demonstrate that L11 significantly inhibits T cell migration from blood into inflamed islets and salivary glands. Treatment of nonobese diabetic mice with L11 from 1 to 4 or 8 to 12 wk of age led to significant protection against the development of diabetes. Moreover, protection was long-lived, with decreased incidence of diabetes even months after cessation of Ab administration. When treatment was started at 1 wk of age, L11 inhibited the development of inflammation in pancreatic islets and salivary glands. L11 treatment had no long-term effect on numbers or phenotypes of peripheral lymphocytes. These data indicate that anti-CD43 Abs that block T cell migration may be useful agents for the prevention or treatment of autoimmune diseases including insulin-dependent diabetes mellitus and Sjogren’s syndrome.

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