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.

Visit How To Join to request additional information or to download an enrollment package. Or, visit the ACTION website for more information.



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



Nature Materials 2008; Advance Online Publication View citation

Cardiac dysfunction following acute myocardial infarction is a major cause of death in the world and there is a compelling need for new therapeutic strategies. In this report we demonstrate that a direct cardiac injection of drug-loaded microparticles, formulated from the polymer poly(cyclohexane-1,4-diylacetone dimethylene ketal) (PCADK), improves cardiac function following myocardial infarction. Drug-delivery vehicles have great potential to improve the treatment of cardiac dysfunction by sustaining high concentrations of therapeutics within the damaged myocardium. PCADK is unique among currently used polymers in drug delivery in that its hydrolysis generates neutral degradation products. We show here that PCADK causes minimal tissue inflammatory response, thus enabling PCADK for the treatment of inflammatory diseases, such as cardiac dysfunction. PCADK holds great promise for treating myocardial infarction and other inflammatory diseases given its neutral, biocompatible degradation products and its ability to deliver a wide range of therapeutics.





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