Early initiation of low-dose atorvastatin treatment after an acute ST-elevated myocardial infarction, decreases inflammatory process and prevents endothelial injury and activation

• Published in: International journal of cardiology 2009-04, Vol.133 (2), p.266-268
• Main Authors: Stefanadi, Elli, Tousoulis, Dimitris, Antoniades, Charalambos, Katsi, Vasiliki, Bosinakou, Erini, Vavuranakis, Emmanuel, Triantafyllou, Georgia, Marinou, Kyriakoula, Tsioufis, Costas, Papageorgiou, Nikolaos, Latsios, George, Stefanadis, Christodoulos
• Format: Article
• Language: English
• Subjects: Atorvastatin Calcium; Biological and medical sciences; Biomarkers - blood; Cardiology. Vascular system; Cardiovascular; Coronary heart disease; Cytokines; Electrocardiography; Endothelium; Endothelium, Vascular - injuries; Female; Heart; Heptanoic Acids - therapeutic use; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Inflammation; Inflammation - blood; Inflammation - drug therapy; Interleukin-6 - blood; Male; Medical sciences; Middle Aged; Myocardial Infarction - blood; Myocardial Infarction - drug therapy; Myocardial Infarction - immunology; Myocarditis. Cardiomyopathies; Plasminogen Activator Inhibitor 1 - blood; Pyrroles - therapeutic use; ST-elevated myocardial infarction; Statins; Time Factors; Tissue Plasminogen Activator - blood; Vascular Cell Adhesion Molecule-1 - blood; von Willebrand Factor - analysis
• ISSN: 0167-5273; 1874-1754
• DOI: 10.1016/j.ijcard.2007.11.025

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 tPA were 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 < 0.05 vs baseline). Serum sVCAM-1 was increased in controls both at 1 and 6 weeks post-STEMI ( p < 0.05 vs baseline), an effect prevented by atorvastatin. Plasma vWF was increased 1 week post-STEMI in controls ( p < 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.