Targeted versus standard feedback: results from a randomized quality improvement trial.

BACKGROUND: Quality improvement is central to improving the care of patients with cardiovascular disease; however, the optimum type of data feedback to support such efforts is unknown. METHODS: Over 26 months, 149 eligible Acute Coronary Treatment and Intervention Outcomes Network Registry-Get With The Guidelines hospitals were randomized to receive either standard (n = 76 control) or targeted (n = 73 intervention) performance feedback reports for acute myocardial infarction patient care. Each report summarized performance on identified metrics (providing hospitals with detailed data on their 3 lowest-performing quality metrics, relative to their peers). Intervention sites received 5 targeted feedback reports. Overall composite performance was compared between cohorts at end of study and as a change from baseline. RESULTS: Intervention (n = 60) and control (n = 64) hospitals that completed the study had similar baseline performance (median score 83.7% vs 84.2%). Over 26 months of follow-up, the change in overall composite score across hospitals was neutral (median 0.1% [interquartile range {IQR} -2.4% to 3.3%]). There was no difference in observed improvement in either the intervention (median -0.2% [IQR-2.6% to 3.3%]) or control (median 0.1% [IQR -2.2% to 3.4%]) hospitals. CONCLUSIONS: We were unable to demonstrate that targeted performance feedback reports lead to more rapid care improvements than standard reports. Future directions should explore the relationship between hospital self-selection of targeted metrics and the identification and promulgation of less common metrics--particularly those that reflect processes of care.

Pattern of liver enzyme elevations in acute ST-elevation myocardial infarction.

OBJECTIVES: Liver enzyme elevations occur with ST-segment elevation myocardial infarction (STEMI); however, their significance in the modern era is not well-defined. The incidence of liver enzyme elevations in STEMI, temporal trends, correlations with creatine kinase-MB (CK-MB), and associations with clinical outcomes were evaluated. METHODS: The Complement Inhibition in Myocardial Infarction Treated with Angioplasty and Complement Inhibition in Myocardial Infarction Treated with Thrombolytics trials evaluated 1903 patients with STEMI. A core lab analyzed liver enzymes at baseline, days 1, 6, and 14, and CK-MB measured sequentially over 72 h. The GUSTO model for 30-day mortality was used to predict clinical endpoints. RESULTS: A total of 1783 patients were included in the analysis. Aspartate transaminase (AST) was elevated above the upper limit of normal in 85.6% and alanine transaminase (ALT) was elevated in 48.2% of patients at baseline or day 1. CK-MB area under the curve correlated with maximum AST (r=0.727) and maximum ALT (r=0.456). Both AST and ALT elevations were independent predictors of worse outcomes in multivariable adjusted analysis, even after adjustment for CK-MB. Hazard ratios and 95% confidence intervals of AST elevation were 1.12 (1.05-1.19) for all-cause mortality, and 1.08 (1.02-1.13) for the composite endpoint of death, congestive heart failure, shock, or stroke. Hazard ratios and 95% confidence intervals of ALT elevation were 1.15 (1.04-1.27) for mortality and 1.47 (1.10-1.98) for the composite endpoint. CONCLUSION: AST and ALT elevations are common in STEMI. Both markers are correlated with CK-MB area under the curve, but independently associated with worse mortality and clinical outcomes.

Paradoxical effects of interleukin-18 on the severity of acute graft-versus-host disease mediated by CD4+ and CD8+ T-cell subsets after experimental allogeneic bone marrow transplantation.

Administration of exogenous interleukin-18 (IL-18) regulates experimental acute graft-versus-host disease (GVHD) in a Fas-dependent manner when donor CD4(+) T cells are required for mortality after experimental allogeneic bone marrow transplantation (BMT). However, CD4(+) and CD8(+) T cells can induce acute GVHD after clinical allogeneic BMT, and the role of IL-18 in CD8(+)-mediated acute GVHD is unknown. We, therefore, determined the role of IL-18 in GVHD mediated by CD4(+) or CD8(+) T cells across major histocompatibility complex (MHC) class II- and class I-disparate allogeneic BMT, respectively. Administering IL-18 significantly increased survival in CD4(+)-mediated GVHD but reduced survival in CD8(+)-mediated GVHD. This increase in deaths was associated with significantly greater clinical, biochemical, and histopathologic parameters of GVHD damage and was independent of Fas expression on donor T cells. Administering IL-18 significantly enhanced allospecific cytotoxic function and expansion of CD8(+) cells. Endogenous IL-18 was critical to GVHD mediated by CD8(+) donor T cells because IL-18 receptor-deficient donors caused significantly less GVHD but exacerbated CD4(+)-mediated, GVHD-related death. Furthermore, administering anti-IL-18 monoclonal antibody significantly reduced CD8(+)-mediated, GVHD-related death. Together these findings demonstrate that IL-18 has paradoxical effects on CD4(+) and CD8(+) cell-mediated GVHD.