Background: HMG-CoA reductase inhibitor, statins and ramipril prevented or retarded the progression of coronary heart disease in large-scaled, clinical studies. Endothelial function plays an important role in the pathogenesis of atherosclerosis. Because the mechanisms of the biological effects of statins and antiotensin converting enzyme inhibitor therapies differ, we studied the vascular responses to these therapies in hypercholesterolemic patients.
Methods: We administered simvastatin 20 mg and placebo or ramipril 10 mg daily during 2 months with washout 2 months to 32 hypercholesterolemic patients.
Results: Simvastatin alone or combined with ramipril significantly changed lipoproteins, and improved the percent flow-mediated dilator response (FMD) to hyperemia from 4.93±1.96 to 6.58±1.94 by 46±48% and from 4.66±1.66 to 6.78±1.95 by 59±66%, respectively (both P<0.001) and reduced plasma levels of nitrate from 88±44 to 75±32 uM by 0±52% and from 83±39 to 65±29 uM by 13±30%, respectively (P=0.183 and P=0.012, respectively), and plasma levels of malondialdehyde (MDA), a marker of free radical from 1.33±0.52 to 1.10±0.53 uM by 6±57% and from 1.34±0.60 to 1.01±0.41 uM by 13±47%, respectively (P=0.045 and P<0.001, respectively), compared with baseline measurements. However, simvastatin combined with ramipril changed to greater extent FMD and plasma levels of nitrate and MDA than simvastatin alone.
Conclusions; Compared with simvastatin alone, added ramipril to simvastatin showed additive effects on flow-mediated dilation and the plasma levels of nitrate and MDA in hypercholesterolemic patients.
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