Early initiation of low-dose atorvastatin treatment after an acute ST-elevated myocardial infarction, decreases inflammatory process and prevents endothelial injury and activation Elli Stefanadi, Dimitris Tousoulis ⁎ , Charalambos Antoniades, Vasiliki Katsi, Erini Bosinakou, Emmanuel Vavuranakis, Georgia Triantafyllou, Kyriakoula Marinou, Costas Tsioufis, Nikolaos Papageorgiou, George Latsios, Christodoulos Stefanadis 1st Cardiology Department, University of Athens, Medical School, Greece Received 31 August 2007; accepted 17 November 2007 Available online 9 January 2008 ⁎ Corresponding author. Athens University Medical School, 1st Cardiol- ogy Department, Vasilissis Sofias 114, 115 28, Ampelokipi, Athens-Greece. E-mail address: drtousoulis@hotmail.com (D. Tousoulis). Abstract Background: High-dose statin treatment improves clinical outcome of ST-elevated myocardial infarction (STEMI). However, the effect of low-dose atorvastatin treatment on inflammatory and pro-thrombotic molecules during the post-STEMI period is unclear. We investigated the effect of low-dose atorvastatin treatment on the kinetics of cytokine IL-6, vascular cell adhesion molecule (sVCAM-1) and endothelium-derived markers of thrombosis/ fibrinolysis such as von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA), post STEMI. Methods: Twenty-four normocholesterolemic patients with STEMI were randomised to receive atorvastatin 10mg/day or no statin treatment for 6 weeks after the event. Blood samples were obtained by their admission to the hospital as well as at weeks 1 and 6. Circulating levels of IL-6, sVCAM-1, vWF, PAI-1 and tPAwere determined by ELISA. Results: Atorvastatin induced a decrease of IL-6 at 1 week, an effect which reached significance compared to baseline at 6 weeks post STEMI (p b 0.05 vs baseline). Serum sVCAM-1 was increased in controls both at 1 and 6 weeks post-STEMI (p b 0.05 vs baseline), an effect prevented by atorvastatin. Plasma vWF was increased 1 week post-STEMI in controls (p b 0.05 vs baseline) and returned to baseline at 6 weeks, an effect prevented by atorvastatin. Plasma PAI-1, tPA and the PAI-1/tPA ratio remained unchanged in both groups. Conclusion: Early initiation of low-dose atorvastatin treatment decreases the expression of IL-6 and sVCAM-1 and the release of vWF in patients with STEMI. Therefore, low-dose atorvastatin, modulates inflammatory response and decreases endothelial injury and activation in patients with recent STEMI. © 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: ST-elevated myocardial infarction; Statins; Cytokines; Endothelium; Inflammation Inflammation is a key feature in the development of unstable atheromatic plaque and subsequently acute coronary events [1]. Evidence suggest that statins beyond their lipid- lowering effects exert anti-inflammatory, antioxidant, and antithrombotic properties [2]. However, the effect of low-dose of atorvastatin on inflammatory and thrombotic process during the acute phase of STelevation myocardial infarction (STEMI) is unknown. In the present study we examined the impact of early initiation of low-dose atorvastatin treatment on the variations of inflammatory markers (such as interleukin 6 (IL- 6) and vascular cells adhesion molecule (VCAM-1)) and in molecules implicated in the thrombosis/fibrinolysis system (such as von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA)) during the first 6 weeks post STEMI. Twenty-four patients with STEMI were included in the study. All the patients had been in a stable clinical state for at least 3 months before study entry. Exclusion criteria included left ventricular hypertrophy, heart failure, overt atherosclerotic peripheral vascular disease, acute and chronic inflammatory diseases involving organs other than the heart (e.g. liver diseases), the use of anti-inflammatory agents and the presence of any other cardiac disease, abnormal fasting cholesterol levels N 200 mg/dl or use of lipid-lowering agents during the past 6 months. All patients were thrombolised (none received primary PTCA), and they all received the standard treatment by their admission to the hospital, according to the guidelines. Baseline blood samples were obtained 6 h after patient's admission to the hospital, after thrombolysis. Patients were allocated into two groups immediately after their admission, and received atorvastatin 10 mg/day (n =12) or no statin (control group, n =12) for 6 weeks (Table 1). Venous blood samples were obtained at the beginning of the study before atorvastatin was started, and 266 Letters to the Editor