(Circulation. 1997;95:76-82.)
© 1997 American Heart Association, Inc.
Articles |
the Department of Internal Medicine III (O.T., H.M., Y.W., K.K., T.I.), Kurume University School of Medicine, Fukuoka, Japan, and the Department of Microbiology and Molecular Pathology, Faculty of Pharmaceutical Sciences, Teikyo University, Kanagawa, Japan (H.I.).
Background Although long-term lipid-lowering therapy improves endothelium-dependent vasodilatation in humans, it remains unknown whether the short-term removal of LDL per se ameliorates endothelial dysfunction.
Methods and Results To examine the effects of a single session of LDL apheresis on endothelial function in patients with hypercholesterolemia, we measured forearm blood flow (FBF) by strain-gauge plethysmography before and after single LDL apheresis while infusing acetylcholine (ACh; 4 to 24 µg/min) and sodium nitroprusside (SNP; 0.2 to 1.2 µg/min). The single session of LDL apheresis reduced total LDL (from 142.2±15.0 to 32.6±5.0 mg/mL, P<.0005) and oxidized LDL (from 111.6±22.8 to 30.0±5.4 ng/mL, P<.005). Although ACh and SNP increased FBF dose-dependently before and after LDL apheresis, the endothelium-dependent vasodilatation responses to ACh were significantly augmented (P<.01) after the single session of LDL apheresis without changes in the endothelium-independent vasodilatation responses to SNP. The plasma levels of total and oxidized LDL correlated with the degree of ACh-induced vasodilatation. Furthermore, the local production of nitrate/nitrite, metabolites of NO, during ACh infusion was significantly (P<.05) augmented by LDL apheresis, and there was a significant correlation between the degree of ACh-induced vasodilatation and the production in nitrate/nitrite (r=.99, P<.0005).
Conclusions We demonstrated that even a single session of LDL apheresis with the reduction of total LDL and oxidized LDL improved endothelial function. Our results suggest that total LDL and/or oxidized LDL may directly impair endothelial function in the human forearm vessel.
Key Words: acetylcholine arteriosclerosis blood flow endothelium-derived factors lipoproteins
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T. Neunteufl, K. Kostner, R. Katzenschlager, M. Zehetgruber, G. Maurer, and F. Weidinger Additional benefit of vitamin E supplementation to simvastatin therapy on vasoreactivity of the brachial artery of hypercholesterolemic men J. Am. Coll. Cardiol., September 1, 1998; 32(3): 711 - 716. [Abstract] [Full Text] [PDF] |
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R. W. Kalmansohn, D. L. Schiff, and R. B. Kalmansohn Present Status of HMG Reductase Inhibitors in Treatment of Dyslipidemia Angiology, September 1, 1998; 49(9): 801 - 805. [Abstract] [PDF] |
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R. A. Vogel and M. C. Corretti Estrogens, Progestins, and Heart Disease : Can Endothelial Function Divine the Benefit? Circulation, April 7, 1998; 97(13): 1223 - 1226. [Full Text] [PDF] |
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U. Laufs, V. La Fata, J. Plutzky, and J. K. Liao Upregulation of Endothelial Nitric Oxide Synthase by HMG CoA Reductase Inhibitors Circulation, March 31, 1998; 97(12): 1129 - 1135. [Abstract] [Full Text] [PDF] |
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S. Mii, A. Mori, H. Sakata, M. Nakayama, and H. Tsuruta LDL Apheresis for Arteriosclerosis Obliterans with Occluded Bypass Graft: Change in Prostacyclin and Effect on Ischemic Symptoms Angiology, March 1, 1998; 49(3): 175 - 180. [Abstract] [PDF] |
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L. Zhao and R. L. Tackett Oxidized Low-Density Lipoprotein Inhibits Acetylcholine-Induced Vasorelaxation and Increases 5-HT-Induced Vasoconstriction in Isolated Human Saphenous Vein J. Pharmacol. Exp. Ther., February 1, 1998; 284(2): 637 - 643. [Abstract] [Full Text] |
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E. Stroes, T. de Bruin, H. de Valk, W. Erkelens, J.-D. Banga, H. van Rijn, H. Koomans, and T. Rabelink NO activity in familial combined hyperlipidemia: potential role of cholesterol remnants Cardiovasc Res, December 1, 1997; 36(3): 445 - 452. [Abstract] [Full Text] [PDF] |
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N. Delanty and C. J. Vaughan Vascular Effects of Statins in Stroke Stroke, November 1, 1997; 28(11): 2315 - 2320. [Abstract] [Full Text] |
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A. P. Selwyn, S. Kinlay, P. Libby, and P. Ganz Atherogenic Lipids, Vascular Dysfunction, and Clinical Signs of Ischemic Heart Disease Circulation, January 7, 1997; 95(1): 5 - 7. [Full Text] |
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