Cellular inflammatory response and clinical outcome in cardiac surgery

Abstract

Purpose 

This review briefly summarizes recent advances in the understanding of the pathophysiology of the inflammatory response to cardiac surgery and its ties to clinical outcomes. Links between specific inflammatory mediators and vulnerable organs will be emphasized, along with genetic risk factors that render specific patients susceptible to these complications.

Recent findings 

Circulation of blood on the cardiopulmonary bypass circuit and the operative procedure itself provoke activation of circulating hematopoietic cells and vascular endothelial cells. These activated cells subsequently secrete mediators that amplify this inflammatory response and activated phagocytes undergo changes that facilitate their exit from the circulation into tissue, where they exacerbate organ complications of the procedure. Cardiac, renal and pulmonary dysfunction are among the most common complications of cardiac surgery and progress has been made in recent years demonstrating how the cellular inflammatory response is related to adverse outcomes in these organs. Accordingly, this review will focus on these three systems and the pathophysiology of their cardiac surgical complications.

Summary 

Advances in our understanding of the pathways by which inflammatory mediators contribute to host injury offers the promise of interventions that are tailored to specific risks and the possibility of preoperatively identifying those patients most likely to benefit.