[Effect of rosuvastatin therapy and myocardial revascularization on angiogenesis in coronary artery disease patients].
We studied the influence of rosuvastatin therapy and myocardial revascularization on angiogenic growth factors in coronary artery disease (CAD) patients. Two main groups were examined: the first one consisted of patients passed through successful percutaneous coronary intervention (PCI), the second one consisted of patients on 3 months rosuvastatin therapy. Vascular endothelial growth factor (VEGF), VEGF receptor Flt-1 (sVEGF-Rl) and transforming growth factor-beta (TGF-bl) levels were measured in healthy volunteers and CAD patients before and 6 days after myocardial revascularization by PCI. VEGF and basic fibroblast growth factor (bFGF) levels were measured before and 3 month after rosuvastatin therapy, as well as total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDLC), C-reactive protein (CRP), interleukin 6 (IL-6) and endothelium dependent vasodilation. VEGF levels did not differ, but TGF - b levels were significantly lower in CAD patients compared to healthy subjects (11.0 +/- 4.9 pg/ml and 120.0 +/- 32.4 pg/ml, respectively, p < 0.000l). Myocardial revascularization caused changes in VEGF levels from 192.4 +/- 166.1 pg/ml to 264.7 +/- 226.6 pg/ml (p=0.0066) without significant influence on TGF and VEGF-R1 levels in 6 days. There were positive changes in lipid levels, lowering of CRP and IL-6 concentrations, improvement of endothelial function and decrease of VEGF levels from 382 +/- 249 pg/ml to 297 +/- 220 pg/ml (p=0.006) 3 month after start of rosuvastatin treatment (no changes in bFGF levels were observed). Chronic insufficient myocardial blood supply leads to decreasing of TGF - b levels. The elevation of VEGF after myocardial revascularization reflects transient ischemia and potentially may provoke hemodynamic instability, caused by atherosclerotic plaque neovascularization. Strengthening of statin therapy early after myocardial revascularization may allow to stabilize the atherosclerotic plaque condition, also by means of VEGF lowering.
Semenova
A E
AE
Cardiology Research Complex, ul Tretiya Cherepkovskaya 15a, Moscow, Russia.
Sergienko
I V
IV
Masenko
V P
VP
Gabrusenko
S A
SA
Kukharchuk
V V
VV
Belenkov
Iu N
IuN
D000924:Anticholesteremic Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D002784:Cholesterol / Q000378:metabolism; D005260:Female; D005464:Fluorobenzenes / Q000494:pharmacology* / Q000627:therapeutic use*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000150:complications* / Q000188:drug therapy*; D009204:Myocardial Revascularization / Q000379:methods*; D009389:Neovascularization, Pathologic / Q000188:drug therapy* / Q000209:etiology; D011743:Pyrimidines / Q000494:pharmacology* / Q000627:therapeutic use*; D040262:Receptors, Vascular Endothelial Growth Factor / Q000097:blood / Q000187:drug effects; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000494:pharmacology* / Q000627:therapeutic use*; D053773:Transforming Growth Factor beta1 / Q000097:blood / Q000187:drug effects; D014280:Triglycerides / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000097:blood / Q000187:drug effects
D000924:Anticholesteremic Agents; D005464:Fluorobenzenes; D011743:Pyrimidines; D013449:Sulfonamides; D053773:Transforming Growth Factor beta1; D014280:Triglycerides; D042461:Vascular Endothelial Growth Factor A; D000068718:Rosuvastatin Calcium; D002784:Cholesterol; D040262:Receptors, Vascular Endothelial Growth Factor