Citations

Background— Sirolimus-eluting stents (SESs) reduce angiographic restenosis in patients with focal, native coronary artery stenoses. This study evaluated the usefulness of SESs in complex native-vessel lesions at high risk for restenosis. Methods and Results— Angiographic follow-up at 240 days was obtained in 701 patients with long (15- to 25-mm) lesions in small-diameter (2.5- to 3.5-mm) native vessels who were randomly assigned to treatment with SESs or bare-metal stents (BMSs) in the SIRIUS trial. Quantitative angiographic measurements of minimal lumen diameter and percent diameter stenosis were obtained within the treated segment, within the stent, and within its 5-mm proximal and distal edges. Patients treated with SESs had lower rates of binary (>50% diameter stenosis) angiographic restenosis within the segment (8.9% versus 36.3% with the BMS; P <0.001) and within the stent (3.2% versus 35.4% with the BMS; P <0.001). SESs were associated with significantly less late lumen loss within the treated segment, within the stent, and within its 5-mm proximal and distal edges (all P <0.001). The reduction of restenosis with the SES was consistent in patients at risk for restenosis, including those with small vessels, long lesions, and diabetes mellitus. The frequency of late aneurysms was similar in the 2 groups. Conclusions— Compared with BMSs, SESs reduced angiographic late lumen loss within the stent and its adjacent 5-mm margins in patients with complex native-vessel lesions.

AbstractTherapeutic endoscopy (TE) has provided a new means for treating peptic ulcer disease, prompting a reevaluation of surgery's role. The aim of this study was to determine if surgical therapy of bleeding duodenal ulcers has changed since the advent of TE. This retrospective review involved consecutive time periods during which TE was (1985–1990) and was not (1980–1984) widely available. Exclusion criteria were prior gastric surgery, nonpeptic conditions, and untreated ulcers. Inclusion standards were met by 252 patients (180 men, 72 women) whose mean age was 67 years. Patients were grouped by the initial therapeutic intervention. Groups were similar in age, medical condition (mean APACHE II score 16), and morbidity. Seventy‐five patients had surgery alone during 1980–1984 and 38 during 1985–1990. TE was initially performed on 134 patients during 1985–1990. Bleeding (n=30) and perforation (n=1) prompted emergent operation in 23% of cases following TE. Thus 69 (38+31) patients underwent surgery between 1985 and 1990. Preprocedure transfusions averaged 4.1 units in the endoscopic group and 8.2 units in the operative groups (p<0.0001). Disagreement existed between the endoscopic and surgical descriptions of ulcer location in 53% of cases. Emergent surgery was required in 45% of hemodynamically unstable patients versus 14% of stable patients who initially underwent TE (p<0.0001). Sixty‐one percent of incompletely visualized TE‐treated lesions required operation, and 18% of well visualized ulcers underwent operation (p<0.0001). Hospital mortality was similar (8% versus 16%) in the endoscopic and operated groups (p=0.7). Mean follow‐up was 540 days. The number of operations performed for bleeding duodenal ulcer did not change significantly during the TE era, and a significant subset (23%) of endoscopically treated patients required surgical therapy. TE failure was portended by hemodynamic instability or incomplete endoscopic visualization.

Expression of B7-H1, a costimulating glycoprotein in the B7 family, is normally restricted to macrophage-lineage cells, providing a potential costimulatory signal source for regulation of T cell activation. In contrast, aberrant expression of B7-H1 by tumor cells has been implicated in impairment of T cell function and survival, resulting in defective host antitumoral immunity. The relationship between tumor-associated B7-H1 and clinical cancer progression is unknown. Herein, we report B7-H1 expression by both renal cell carcinoma (RCC) tumors of the kidney and RCC tumor-infiltrating lymphocytes. In addition, our analysis of 196 clinical specimens reveals that patients harboring high intratumoral expression levels of B7-H1, contributed by tumor cells alone, lymphocytes alone, or tumor and/or lymphocytes combined, exhibit aggressive tumors and are at markedly increased risk of death from RCC. In fact, patients with high tumor and/or lymphocyte B7-H1 levels are 4.5 times more likely to die from their cancer than patients exhibiting low levels of B7-H1 expression (risk ratio 4.53; 95% confidence interval 1.94–10.56; P < 0.001.) Thus, our study suggests a previously undescribed mechanism whereby RCC may impair host immunity to foster tumor progression. B7-H1 may prove useful as a prognostic variable for RCC patients both pre- and posttreatment. In addition, B7-H1 may represent a promising target to facilitate more favorable responses in patients who require immunotherapy for treatment of advanced RCC.