Clinical Research Studies

All patients undergoing open heart surgery with the utilization of cardiopulmonary bypass (CPB) are at risk for developing varying degrees of vasoplegia. Although a precise definition is lacking, vasoplegia is a physiologic state characterized by hypotension (systolic blood pressure <90mmHg) with low systemic vascular resistance (SVR) <800 dynes, and adequate cardiac index (2.2). Patients demonstrating vasoplegia after CPB require escalating doses of vasoactive medications to maintain an adequate blood pressure, significantly increasing their risk for progressive organ failure and death. It is hypothesized that vasoplegia is related, at least in part, to an inflammatory cascade resulting from activation of cytokines during CPB. The timing and the identity of the cytokines/chemokines most prominently involved in this cascade as well as the immunologic consequences of vasoplegia have not been studied in detail. Moreover, whether a vasoplegia signature correlates with the vasoactive inotrope score (VIS), a standard scoring method used to describe the amount of vasoactive mediations required by a patient has not been performed. Discovery of such a signature evolving during CPB could lead to early interventions to decrease the chance for multiorgan failure. Using a panel of 48 cytokines measured from plasma in heart surgery patients placed on CPB, we will define changes in cytokine signatures during the bypass run compared to pre-CPB. Using a panel of 770 immune-oncologic genes measured from plasma in heart surgery patients placed on CPB we will define immune genes associated with the bypass run. We will correlate changes in CPB cytokine signatures with the development of vasoplegia and subsequent organ dysfunction of patients undergoing CPB for open heart surgery. We will correlate cytokine and immunotranscriptomic changes with the post-operative VIS as well as with the development of organ dysfunction and the risk of death.