Objective: Because the lipoprotein effects of statin and fibric acid derivativ es therapies differ, we studied the effects of these therapies in patients with hyperlipidemia on lipoproteins, vasomotor function, and pl...Objective: Because the lipoprotein effects of statin and fibric acid derivativ es therapies differ, we studied the effects of these therapies in patients with hyperlipidemia on lipoproteins, vasomotor function, and plaque stability. Method s: We administered simvastatin, 20 mg daily, to 27 patients with hypercholestero lemia and coronary artery disease, or fenofibrate, 200 mg daily, to 27 patients with pure hypertriglyceridemia during 8 weeks. Results: As expected, simvastatin significantly lowered total cholesterol and low density lipoprotein cholestero l (LDL C) more, and fenofibrate decreased triglyceride and increased high dens ity lipoprotein cholesterol(HDL C) more than either therapy. Simvastatin and fe nofibrate significantly improved the percent flow mediated dilator response to hyperemia by 183±41%and by 30±7%, respectively (each P< 0.001); however, sim vastatin significantly improved more (P< 0.001). Simvastatin and fenofibrate sig nificantly lowered plasma levels of tumor necrosis factor alpha (TNF α) by 13 ±4%and by 10±4%, respectively (P=0.009 and P=0.006, respectively) with a sim ilar degree(P=0.614). Simvastatin significantly reduced plasma levels of total M MP-9 and TIMP-1 more(P=0.005 and P=0.036, respectively), compared with fenofib rate showing no reduction. There were significant correlations between the degre e of changes in TNF-αand the degree of changes in MMP-9 activity (r=0.376, P= 0.053). Conclusions: Simvastatin and fenofibrate demonstrated antiatheroscleroti c effects via different mechanisms.展开更多
文摘Objective: Because the lipoprotein effects of statin and fibric acid derivativ es therapies differ, we studied the effects of these therapies in patients with hyperlipidemia on lipoproteins, vasomotor function, and plaque stability. Method s: We administered simvastatin, 20 mg daily, to 27 patients with hypercholestero lemia and coronary artery disease, or fenofibrate, 200 mg daily, to 27 patients with pure hypertriglyceridemia during 8 weeks. Results: As expected, simvastatin significantly lowered total cholesterol and low density lipoprotein cholestero l (LDL C) more, and fenofibrate decreased triglyceride and increased high dens ity lipoprotein cholesterol(HDL C) more than either therapy. Simvastatin and fe nofibrate significantly improved the percent flow mediated dilator response to hyperemia by 183±41%and by 30±7%, respectively (each P< 0.001); however, sim vastatin significantly improved more (P< 0.001). Simvastatin and fenofibrate sig nificantly lowered plasma levels of tumor necrosis factor alpha (TNF α) by 13 ±4%and by 10±4%, respectively (P=0.009 and P=0.006, respectively) with a sim ilar degree(P=0.614). Simvastatin significantly reduced plasma levels of total M MP-9 and TIMP-1 more(P=0.005 and P=0.036, respectively), compared with fenofib rate showing no reduction. There were significant correlations between the degre e of changes in TNF-αand the degree of changes in MMP-9 activity (r=0.376, P= 0.053). Conclusions: Simvastatin and fenofibrate demonstrated antiatheroscleroti c effects via different mechanisms.
