Steroid-induced Reduction of Surgical Stress Study
Status:
Withdrawn
Trial end date:
2011-06-01
Target enrollment:
Participant gender:
Summary
The stress response as induced by myocardial cellular damage during cardiac surgery may lead
to myocardial stunning and apoptosis, and could therefore impair postoperative patient
recovery. Surgical trauma typically induces the liberation of cytokines. Some of these
cytokines are strongly associated with the initiation of intracellular proapoptotic pathways
through activation of tyrosine kinases and integrins. The latter are known for their
deteriorating effects on cardiac function and are strongly involved in cardiac remodeling.
Dexamethasone is typically administered prior to cardiac surgery in order to especially
reduce the release of proinflammatory cytokines. It has however never been investigated
whether this additionally reduces proapoptotic signaling in the human heart, thereby
eliminating risk factors for the induction of cardiac dysfunction. In the present study, the
investigators therefore aim to investigate whether dexamethasone inhibits proapoptotic
pathways in patients undergoing cardiac surgery. Furthermore, the investigators would like to
elucidate whether this proposed effect of dexamethasone is related to the reduction of the
stress response in the heart or indirectly by suppression of cytokine release. For this
purpose the investigators will obtain cardiac biopsies and plasma from patients, who are
randomly assigned to placebo or dexamethasone treatment and undergo on and off-pump coronary
artery bypass grafting (CABG) surgery.