Abstract
ObjectiveGrowth differentiation factor-15 (GDF-15) has been identified as a strong marker of cardiovascular disease; however, no data are available concerning the role of GDF-15 in the occurrence of organ dysfunction during coronary artery bypass grafting (CABG) associated with cardiopulmonary bypass (CPB).MethodsFive arterial blood samples were taken sequentially in 34 patients from anesthesia induction (IND) until 24 h after arrival at the intensive care unit (ICU). Plasma levels of GDF-15, follistatin-like 1 (FLST1), myeloperoxidases (MPO), hydroperoxides and plasma antioxidant status (PAS) were measured at each time-point. Markers of cardiac (cardiac-troponin I, cTnI) and renal dysfunction (neutrophil gelatinase-associated lipocalin, NGAL) and other classical biological factors and clinical data were measured.ResultsPlasma GDF-15 levels increased gradually during and after surgery, reaching nearly three times the IND levels in the ICU (3,075±284 ng/L vs. 1,061±90 ng/L, p<0.001). Plasma MPO levels increased dramatically during surgery, attaining their highest level after unclamping (UNCLAMP) (49±11 ng/mL vs. 1,679±153 ng/mL, p<0.001) while PAS significantly decreased between IND and UNCLAMP (p<0.05), confirming the high oxidative status induced by this surgical procedure. ICU levels of GDF-15 correlated positively with cTnI and NGAL (p = 0.006 and p = 0.036, respectively), and also with hemoglobin and estimated glomerular filtration rate (eGFR). Among all the post-operative biomarkers available, only eGFR, NGAL and GDF-15 measured at ICU arrival were significantly associated with the onset of acute kidney injury (AKI). Patients with a EuroSCORE >3 were shown to have higher GDF-15 levels.ConclusionsDuring cardiac surgery associated with CPB, GDF-15 levels increased substantially and were associated with markers of cardiac injury and renal dysfunction.
Highlights
During cardiopulmonary bypass (CPB), pro-inflammatory mediators activate leucocytes, vascular endothelial cells and platelets, producing a systemic inflammatory response that results in organ dysfunction, affecting the heart, brain, lungs and kidneys
We observed that radical production was significantly greater during and after the CPB procedure, and that circulating free-radical levels correlated with serum creatine kinase-MB (CK-MB)
The following criteria led to the exclusion of patients: surgical emergencies, aortic valve replacement, acute coronary syndromes (ACS) reported within 30 days before the surgery, left ventricular ejection fraction (LVEF),30%, chronic inflammatory pathologies, infectious or malignant diseases, chronic renal failure, transplant patients and patients treated with corticosteroids
Summary
During cardiopulmonary bypass (CPB), pro-inflammatory mediators activate leucocytes, vascular endothelial cells and platelets, producing a systemic inflammatory response that results in organ dysfunction, affecting the heart, brain, lungs and kidneys. The cellular response is mediated by the main effectors of the inflammatory response, including neutrophils, which degranulate and release cytotoxic molecules such as elastase, myeloperoxidase (MPO) and free radicals[1]. In a previous study carried out in our laboratory, we measured systemic and coronary sinus free-radical release during and following removal of the cross-clamp[3]. Various biological and hemodynamic markers are measured to estimate the pre-and postoperative risk of developing complications; no data exist to assess the role and impact of growth differentiation factor-15 (GDF-15) in the occurrence of organ dysfunction during coronary artery bypass grafting (CABG) associated with CPB
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