The influence of rosuvastatin therapy and percutaneous coronary intervention on angiogenic growth factors in coronary artery disease patients

Objective - The aim of our investigation was to assess the influence of rosuvastatin therapy and myocardial revascularization on angiogenic growth factors in coronary artery disease patients. Methods and results - Two main groups were examined: group one consisted of patients with successful percutaneous coronary intervention and group two consisted of patients 3 months on rosuvastatin therapy. Vascular endothelial growth factor (VEGF),VEGF receptor Flt-1 (sVEGF-R1) and transforming growth factor beta-1 (TGF-beta 1) levels were measured in healthy volunteers and CAD patients before and 6 days after myocardial revascularization. VEGF and basic fibroblast growth factor (bFGF) levels were measured before and 3 months after rosuvastatin therapy, as well as total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDLC), high-density lipoprotein cholesterol (HDLC), C-reactive protein (CRP), interleukin 6 (IL-6) and endothelium-dependent vasodilation. VEGF levels did not differ, but beta-TGF levels were significantly lower in CAD patients in comparison with healthy subjects, P < 0.0001. Myocardial revascularization caused changes of VEGF levels from 192.4 +/- 166.1 pg/ml to 264.7 +/- 226.6 pg/ml (P = 0.0066). There were positive changes in lipid levels, lowering of CRP and IL-6 concentrations, improving of endothelial function and decreasing of VEGF levels from 382 249 pg/ml to 297 +/- 220 pg/ml (P = 0.006) 3 months after rosuvastatin treatment. Conclusions - There is an elevation of VEGF levels early after myocardial revascularization that may reflect a transient ischaemia and potentially may provoke atherosclerotic plaque neovascularization. Rosuvastatin leads to a decrease of VEGF levels that can be a reflection of the influence on endogenous angiogenesis. There was no correlation between inflammatory factors and VEGF that gives a suggestion about an absence of direct CRP and IL-6 impact on VEGF decreasing during statin treatment.