Abstract
Objectives: Cardiac surgery with cardiopulmonary bypass provokes systemic inflammatory response, which may cause organ dysfunction. Studies have suggested that pre-operative statin therapy can reduce morbidity and mortality associated with cardiac surgery; the mechanism for this remains unclear. We hypothesise that underlying mechanism of action for these effects of statins is through inhibition of neutrophil transendothelial migration. Methods: We recruited 151 patients undergoing cardiac surgery. Of these 41 patients were on no-statin; 48 patients on low-dose (10 - 30 mg) and 62 patients were on high-dose statin (40 - 80 mg). Ex vivo neutrophil migration was performed on pre-operative blood samples of 90 patients. Of these 90 patients we used 36 patients to assess the levels of TNF-α and sICAM-1. Clinical parameters of total 151 patients were assessed to analyse outcome. Results: Ex vivo neutrophil migration was decreased in high-dose statin group when compared to neutrophils isolated from no-statin or low-dose statin groups (p < 0.001). Serum TNF-α levels were lower in the high-dose statin group (p = 0.002) and sICAM-1 levels were decreased in both low (p = 0.02) and high-dose statin (p = 0.01) groups. Conclusion: Our study demonstrates that high-dose statins reduce ex-vivo transendothelial neutrophil migration, TNF-α and sICAM-1 serum levels suggesting that statins may help in decreasing the post-cardiac surgery morbidity.
Highlights
Cardiac surgery with extracorporeal circulation is associated with neutrophil activation, inflammation and oedema, which may lead to organ dysfunction [1]
Our study demonstrates that high-dose statins reduce ex-vivo transendothelial neutrophil migration, TNF-α and sICAM-1 serum levels suggesting that statins may help in decreasing the post-cardiac surgery morbidity
We have previously demonstrated that statins inhibit neutrophil migration in vitro by specific inhibition of Rho activity [5]
Summary
Cardiac surgery with extracorporeal circulation is associated with neutrophil activation, inflammation and oedema, which may lead to organ dysfunction [1]. Multiple factors are involved in initiating SIRS, which include exposure of blood to non-physiologic surfaces, surgical trauma, ischemia-reperfusion injury, changes to body temperature and release of endotoxins. All these factors are well established to induce complex inflammatory responses including complement activation, release of cytokines, leukocyte activation and production of various substances like oxygen free radicals, arachidonic acid metabolites, platelet activating factors and endothelins [3]. These inflammatory cascades can lead to the development of post operative complications like renal dysfunction, respiratory failure, neurological dysfunction or
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