Steroid-induced Reduction of Surgical Stress Study (STRESS)

The recruitment status of this study is unknown because the information has not been verified recently.
Verified January 2010 by VU University Medical Center.
Recruitment status was  Recruiting
Sponsor:
Information provided by:
VU University Medical Center
ClinicalTrials.gov Identifier:
NCT00807521
First received: December 11, 2008
Last updated: January 21, 2010
Last verified: January 2010

December 11, 2008
January 21, 2010
December 2008
December 2010   (final data collection date for primary outcome measure)
Expression of p38 in cultured cells and cardiac tissue [ Time Frame: One week ] [ Designated as safety issue: No ]
Same as current
Complete list of historical versions of study NCT00807521 on ClinicalTrials.gov Archive Site
Pro-apoptotic signaling, precursor peptides of ANP (proANP), vasopressin (Copeptin), proET-1 and Adrenomedullin (proADM). Age, gender, length, body weight, hematocrit, Hb, leukocytes, surgery time, clamp time, CPB time [ Time Frame: One week ] [ Designated as safety issue: No ]
Same as current
Not Provided
Not Provided
 
Steroid-induced Reduction of Surgical Stress Study
Reduction of the Cardiac Proapoptotic Stress Response by Dexamethasone in Patients Undergoing Coronary Artery Bypass Grafting Surgery

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.

Not Provided
Interventional
Not Provided
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Single Blind (Investigator)
Primary Purpose: Basic Science
  • Coronary Artery Stenosis
  • Coronary Artery Bypass Graft Surgery
  • Drug: Dexamethasone
    Single high dose bolus of dexamethasone before surgery
  • Drug: Placebo
    Placebo for dexamethasone
  • Active Comparator: 1
    High dose bolus of dexamethasone before surgery
    Intervention: Drug: Dexamethasone
  • Placebo Comparator: 2
    Placebo control
    Intervention: Drug: Placebo
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
96
June 2011
December 2010   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Patients undergoing coronary artery bypass surgery (CABG)
  • Age 18-75 years
  • Informed consent

Exclusion Criteria:

  • Re-operations and emergency operations
  • Patient with anemia (Hb < 5.0)
  • Emergency operation
  • Patients receiving blood transfusions < 3 months before operation
  • Insulin depended diabetes mellitus
  • Hepatic or renal failure
  • Pregnancy
  • Use of steroids
Both
18 Years to 75 Years
No
Contact: Dr. Christa Boer, PhD +31204443830 c.boer@vumc.nl
Contact: Jan R. de Jong, MD +31204444386 jr.dejong@vumc.nl
Netherlands
 
NCT00807521
08/214
No
Prof.dr. S.A. Loer, MD, MSc, VU University Medical Center Amsterdam
VU University Medical Center
Not Provided
Principal Investigator: Jan R. de Jong, MD VU University Medical Center Amsterdam
Study Chair: dr. Christa Boer, PhD VU University Medical Center Amsterdam
Principal Investigator: dr. Everaldo M. Redout, PhD VU University Medical Center Amsterdam
VU University Medical Center
January 2010

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP