Emergency Medicine Cardiac Research and Education Group




ACTION Registry
ACTION Registry®–GWTG™ is a national, risk-adjusted, outcomes-based quality improvement program that helps participating facilities measure and improve care for high-risk ACS patients with STEMI and NSTEMI. The result of the collaboration between the two leading national coronary artery disease registries, the NCDR® ACTION Registry® and the American Heart Association (AHA) Get With The GuidelinesSM-CAD Registry, ACTION Registry–GWTG will be the largest, most comprehensive national cardiovascular patient database ever developed by the medical profession.

Combining the strengths of the two programs, ACTION Registry–GWTG will collect a comprehensive set of data elements that provide healthcare professionals and their facilities with the information they need to monitor and improve adherence to the most current, science-based ACC/AHA treatment guidelines. Participation will greatly facilitate quality improvement efforts, optimize clinical care, and improve clinical outcomes for acute coronary syndrome patients.

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Sustained release of a p38 inhibitor from non-inflammatory microspheres inhibits cardiac dysfunction



J Am Coll Cardiol 2008; 52: 1458–1465, 1466–1467 View citation

Objectives: The purpose of this study was to examine the patient-specific characteristics of the interleukin-1 receptor family member ST2 in patients with acute heart failure (HF).

Background: ST2 signaling is involved in the process of cardiac fibrosis and hypertrophy.

Methods: In all, 346 patients with acute HF had ST2 measured. Associations between ST2 and demographics, severity/type of HF, and other biomarkers were examined. Receiver-operator characteristic curves and multivariable Cox proportional hazards analyses evaluated the prognostic ability of ST2.

Results: The ST2 values correlated with the severity of HF (p < 0.001), left ventricular ejection fraction (r = –0.134; p = 0.014), creatinine clearance (r = –0.224; p < 0.001), B-type natriuretic peptide (r = 0.293; p < 0.001), amino terminal B-type natriuretic peptide (r = 0.413; p < 0.001), and C-reactive protein (r = 0.429; p < 0.001). ST2 was not associated with age, prior HF, or body mass index. The ST2 levels at presentation were higher among patients who died by 1 year. The area under the receiver-operator characteristic for death at 1 year was 0.71 (p < 0.001). In a multivariable Cox model containing established clinical and biochemical predictors (including natriuretic peptides), ST2 remained a predictor of mortality (hazard ratio: 2.04, 95% confidence interval: 1.30 to 3.24, p = 0.003), and was equally predictive in patients with HF and preserved or impaired systolic function. When both ST2 and natriuretic peptides were elevated, the highest rates of death were observed in cumulative hazard analysis (p < 0.001). In the presence of a low ST2 level, natriuretic peptides did not predict mortality.

Conclusions: Consistent with its proposed role in a myocardial-specific response to stretch, ST2 has strong clinical and biochemical correlates in patients with acute HF. Prognostically, ST2 is powerful in acute HF and is synergistic with natriuretic peptides for this use.





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