Microvascular Inflammatory Response in Cardiac Surgery

Abstract

Cardiac surgical procedures, with or without cardiopulmonary bypass, elicit a systemic inflammatory response in patients that induces the elaboration of multiple cytokines, chemokines, adhesion molecules, and destructive enzymes. This inflammatory reaction involves multiple interdependent and redundant cell types and humoral cascades, which allows for amplification and positive feedback at numerous steps. This systemic inflammatory response ultimately results in a broad spectrum of clinical manifestations, with multiple organ failure being the most severe form. Investigative efforts have focused on understanding the mechanism of this systemic inflammatory response syndrome in order to develop potential therapeutic targets to inhibit it, thereby possibly decreasing postoperative morbidity and mortality. Multiple therapeutic methods have been investigated, including pharmacologic inhibitors and modifications of surgical technique and the cardiopulmonary bypass circuit. Although studies have demonstrated that the use of these therapies in experimental and clinical settings has attenuated the systemic inflammatory response, they have failed to conclusively show clinical benefit from these therapies. These therapies may be too specific to minimize the deleterious effects of a systemic inflammatory response that results from the activation of multiple, interdependent, and redundant inflammatory cascades and cell types. Hence, further studies that investigate the molecular and cellular events underlying the systemic inflammatory response syndrome and the resultant effects of anti-inflammatory therapies are warranted to ultimately achieve improvements in clinical outcome after cardiac surgical procedures.