Effects of preoperative statin therapy on cytokines after cardiac surgery
O J Liakopoulos1, H Dörge, J D Schmitto
1Department of Thoracic and Cardiovascular Surgery, University of Göttingen, Göttingen, Germany. oliver@liakopoulos.de
Insights
Preoperative statin therapy reduces IL-6 and increases IL-10 after cardiac surgery. However, it does not affect myocardial NF-kappaB inhibitor IkappaB-alpha phosphorylation, indicating a partial anti-inflammatory effect.
Area of Science:
- Cardiology
- Immunology
- Pharmacology
Background:
- Statins possess anti-inflammatory properties beyond lipid reduction.
- Cardiac surgery triggers systemic inflammatory responses.
- Investigating statins' impact on perioperative inflammation is crucial.
Purpose of the Study:
- To evaluate the effect of preoperative statin therapy on systemic inflammatory markers.
- To assess the impact of statins on myocardial NF-kappaB inhibitor IkappaB-alpha.
- To analyze changes in pro- and anti-inflammatory cytokines after cardiac surgery.
Main Methods:
- Thirty-six patients undergoing coronary artery bypass grafting were divided into statin and control groups.
- Plasma cytokine levels (TNF-alpha, IL-6, IL-8, IL-10) were measured pre- and post-cardiopulmonary bypass (CPB).
- Myocardial IkappaB-alpha phosphorylation was assessed via atrial biopsies before and after CPB.
Main Results:
- Statin group showed lower IL-6 release at 4 and 10 hours post-CPB.
- Anti-inflammatory IL-10 was higher in the statin group at 1 hour post-CPB.
- Statin therapy did not alter TNF-alpha, IL-8, or myocardial IkappaB-alpha phosphorylation post-CPB.
Conclusions:
- Preoperative statins attenuate IL-6 and upregulate IL-10 after cardiac surgery.
- Statin therapy demonstrates a partial anti-inflammatory effect in this context.
- Myocardial NF-kappaB signaling remains unaffected by preoperative statin use.
Introduction:
In addition to their lipid-lowering action, it has been demonstrated that statins can exert direct anti-inflammatory effects. We investigated the effect of preoperative statin therapy on systemic inflammatory markers and myocardial NF-kappaB inhibitor IkappaB-alpha after cardiac surgery.
Methods:
Thirty-six patients undergoing elective coronary artery bypass grafting with cardiopulmonary bypass (CPB) with cardioplegia were divided into two groups (statin group, n = 18; control group, n = 18). Plasma concentrations of pro-inflammatory cytokines (tumor necrosis factor alpha [TNFalpha], interleukin [IL]-6, IL-8) and anti-inflammatory IL-10 were measured before and 1, 4, 10, and 24 hours (h) after CPB. Phosphorylated IkappaB-alpha/total IkappaB-alpha ratio was assessed before and after CPB in right atrial biopsies.
Results:
Baseline and operative data did not differ between groups. Statin therapy was associated with lower preoperative low-density lipoprotein levels compared to control (73+/-6 vs. 92+/-6 mg/dL; P=0.03). Release of IL-6 was attenuated in the statin group at 4 h (2270+/-599 vs. 5120+/-656 pg/ml; P<0.01) and 10 h (1295+/-445 vs. 3116+/-487 pg/ml; P<0.05) compared to the control group. IL-10 increased after surgery in both groups (P<0.05), but was higher in the statin group at 1 h (66+/-15 vs. 26+/-16 pg/mL; P<0.01). Phosphorylated IkappaB-alpha/total IkappaB-alpha ratio before CPB did not differ between groups, but was elevated after CPB in both groups (P<0.05), indicating enhanced degradation of IkappaB-alpha. Statin therapy had no effect on TNFalpha and IL-8.
Conclusions:
Preoperative statin therapy attenuates the release of pro-inflammatory IL-6 and up-regulates anti-inflammatory IL-10 after cardiac surgery with cardioplegia, but fails to inhibit phosphorylation of myocardial IkappaB-alpha.
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