BACKGROUND: Intimal hyperplasia is characterized by a proliferation of vascular smooth muscle cells in the intimal layer. Epigallocatechin-3-gallate (EGCG) is known to suppress smooth muscle cell proliferation. We propose that EGCG may have a protective effect against the development of intimal hyperplasia through the suppression of smooth muscle cell proliferation. MATERIAL AND METHOD: Human umbilical vein endothelial cells (HUVEC) and rat aortic smooth muscle cells (RASMC) were cultured with different concentrations of EGCG, and proliferation and migration speed were measured. In 20 dogs, the autologous jugular veins were interposed into the carotid arteries. For the study group (n=10), the graft was stored for 30 minutes in EGCG solution and 300 mM EGCG was applied to the perivascular space after grafting. After 6 weeks, the intimal and medial thickness was measured. RESULT: The proliferation of RASMC and HUVEC was suppressed with EGCG. The migration of RASMC was suppressed with EGCG, but that of HUVEC was not affected. In the in vivo study, the intimal thickness was thinner in EGCG group than in the control group (p<0.05), but the medial thickness did not show any difference. The intimal/medial thickness ratio was lower in the EGCG group (p<0.05). CONCLUSION: EGCG suppresses intimal hyperplasia after vascular grafting, and this may be mediated by prevention of migration and proliferation of vascular smooth muscle cells. The use of EGCG may offer new therapeutic modality to prevent intimal hyperplasia.
Animals ; Carotid Arteries ; Dogs ; Human Umbilical Vein Endothelial Cells ; Hyperplasia* ; Jugular Veins ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Rats ; Transplants ; Vascular Diseases ; Vascular Grafting*

BACKGROUND: Periprocedural treatment with high-dose statins is known to have cardioprotective and pleiotropic effects, such as anti-thrombotic and anti-inflammatory actions. We aimed to assess the efficacy of high-dose rosuvastatin loading in patients with stable angina undergoing off-pump coronary artery bypass grafting (OPCAB). MATERIALS AND METHODS: A total of 142 patients with stable angina who were scheduled to undergo surgical myocardial revascularization were randomized to receive either pre-treatment with 60-mg rosuvastatin (rosuvastatin group, n=71) or no pre-treatment (control group, n=71) before OPCAB. The primary endpoint was the 30-day incidence of major adverse cardiac events (MACEs). The secondary endpoint was the change in the degree of myocardial ischemia as evaluated with creatine kinase-myocardial band (CK-MB) and troponin T (TnT). RESULTS: There were no significant intergroup differences in preoperative risk factors or operative strategy. MACEs within 30 days after OPCAB occurred in one patient (1.4%) in the rosuvastatin group and four patients (5.6%) in the control group, respectively (p=0.37). Preoperative CK-MB and TnT were not different between the groups. After OPCAB, the mean maximum CK-MB was significantly higher in the control group (rosuvastatin group 10.7+/-9.75 ng/mL, control group 14.6+/-12.9 ng/mL, p=0.04). Furthermore, the mean levels of maximum TnT were significantly higher in the control group (rosuvastatin group 0.18+/-0.16 ng/mL, control group 0.39+/-0.70 ng/mL, p=0.02). CONCLUSION: Our findings suggest that high-dose rosuvastatin loading before OPCAB surgery did not result in a significant reduction of 30-day MACEs. However, high-dose rosuvastatin reduced myocardial ischemia after OPCAB.
Angina, Stable ; Coronary Artery Bypass ; Coronary Artery Bypass, Off-Pump ; Creatine ; Fluorobenzenes ; Humans ; Incidence ; Myocardial Ischemia ; Myocardial Revascularization ; Pyrimidines ; Risk Factors ; Sulfonamides ; Transplants ; Trinitrotoluene ; Troponin T ; Rosuvastatin Calcium