Inflammation & Prognosis in Decompensated Heart Failure

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Decompensated heart failure (DHF) is among the most common indications for hospitalization in the United States, and continues to increase in incidence with the increasing prevalence of heart failure and the aging of the population. Despite the substantial impact of this clinical syndrome, the ability to prospectively risk stratify patients DHF lags far behind that of other comparable cardiovascular disorders. Inflammation has been shown to play an important role in chronic heart failure, but its importance in DHF is unknown. The broad objectives of this proposal focus on defining optimal risk stratification strategies in DHF and on integrating measures of inflammation with traditional clinical data in order to predict future adverse events. Additionally, the project will seek to define the response of serologic markers of inflammation to current therapies and the relationship of that response to subsequent patient outcomes. These aims will be accomplished through a prospective cohort study of patients hospitalized with DHF. Successful completion of these aims will contribute to accurate risk stratification of patients with DHF and to the understanding of the role of inflammation in the transition from a compensated to decompensated clinical syndrome. This research will form the core of a 5-year career development plan for Dr. Michael Felker under the mentorship of Dr. Christopher O'Connor, a nationally recognized expert in patient oriented research in heart failure. They propose a career development plan that combines didactic training in research methodology, active collaboration with basic investigators, and ongoing clinical research experience within the unique research environment of the Duke Clinical Research Institute. In conjunction with carefully selected collaborators, this career development plan will foster Dr. Felker's development into an established independent clinical investigator with expertise in both complex clinical research methodology and the role of inflammation in the pathophysiology of heart failure.