From the University of Glasgow and Glasgow Royal Infirmary, Scotland, UK.
Correspondence to Professor Chris J. Packard, FRCPath, DSc, Department of Pathological Biochemistry, Glasgow Royal Infirmary University NHS Trust, Fourth Floor, Queen Elizabeth Building, Glasgow G31 2ER, UK. E-mail chrispackard{at}compuserve.com
Background—The West of Scotland
Coronary Prevention Study was a primary prevention trial that
demonstrated the effectiveness of pravastatin (40 mg/d) in
reducing morbidity and mortality from coronary heart disease
(CHD) in moderately hypercholesterolemic men. The
present analysis examines the extent to which differences
in LDL and other plasma lipids both at baseline and on treatment
influenced CHD risk reduction.
Methods and Results—Relationships between baseline lipid
concentrations and incidence of all cardiovascular
events and between on-treatment lipid concentrations and risk reduction
in patients taking pravastatin were examined by use of Cox
regression models and by division of the cohort into quintiles.
Variation in plasma lipids at baseline did not influence the relative
risk reduction generated by pravastatin therapy. Fall in
LDL level in the pravastatin-treated group did not
correlate with CHD risk reduction in multivariate
regression. Furthermore, maximum benefit of an
Conclusions—We conclude that the treatment effect of 40 mg/d of
pravastatin is proportionally the same regardless of
baseline lipid phenotype. There is no CHD risk reduction unless
LDL levels are reduced, but a fall in the range of 24% is sufficient
to produce the full benefit in patients taking this dose of
pravastatin. LDL reduction alone does not appear to account
entirely for the benefits of pravastatin therapy.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Influence of Pravastatin and Plasma Lipids on Clinical Events in the West of Scotland Coronary Prevention Study (WOSCOPS)
45% risk reduction
was observed in the middle quintile of LDL reduction (mean 24% fall);
further mean decrements in LDL (up to 39%) were not associated with a
greater decrease in CHD risk. Comparison of event rates between
placebo- and pravastatin-treated subjects with the same LDL
cholesterol level provided evidence for an apparent
treatment effect that was independent of LDL.
Key Words: cholesterol • coronary disease • risk factors
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C.G. Isles and J.R. Paterson Identifying patients at risk for coronary heart disease: implications from trials of lipid-lowering drug therapy QJM, September 1, 2000; 93(9): 567 - 574. [Abstract] [Full Text] [PDF]
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A. L. Avins and J. M. Neuhaus Do Triglycerides Provide Meaningful Information About Heart Disease Risk? Arch Intern Med, July 10, 2000; 160(13): 1937 - 1944. [Abstract] [Full Text] [PDF]
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C. R. Meier, R. G. Schlienger, M. E. Kraenzlin, B. Schlegel, and H. Jick HMG-CoA Reductase Inhibitors and the Risk of Fractures JAMA, June 28, 2000; 283(24): 3205 - 3210. [Abstract] [Full Text] [PDF]
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D.S. GRIMES, E. HINDLE, and T. DYER Respiratory infection and coronary heart disease: progression of a paradigm QJM, June 1, 2000; 93(6): 375 - 383. [Abstract] [Full Text] [PDF]
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E. EDMUNDS and G.Y.H. LIP Cardiovascular risk in women: the cardiologist's perspective QJM, March 1, 2000; 93(3): 135 - 145. [Full Text] [PDF]
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F. H. de Man, A. W. E. Weverling-Rijnsburger, A. van der Laarse, A. H. M. Smelt, J. W. Jukema, and G. J. Blauw Not Acute but Chronic Hypertriglyceridemia Is Associated With Impaired Endothelium-Dependent Vasodilation : Reversal After Lipid-Lowering Therapy by Atorvastatin Arterioscler Thromb Vasc Biol, March 1, 2000; 20(3): 744 - 750. [Abstract] [Full Text] [PDF]
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A. M. Gotto Jr, E. Whitney, E. A. Stein, D. R. Shapiro, M. Clearfield, S. Weis, J. Y. Jou, A. Langendorfer, P. A. Beere, D. J. Watson, et al. Relation Between Baseline and On-Treatment Lipid Parameters and First Acute Major Coronary Events in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS) Circulation, February 8, 2000; 101(5): 477 - 484. [Abstract] [Full Text] [PDF]
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C. J. Vaughan, A. M. Gotto Jr., and C. T. Basson The evolving role of statins in the management of atherosclerosis J. Am. Coll. Cardiol., January 1, 2000; 35(1): 1 - 10. [Abstract] [Full Text] [PDF]
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A. Corsini Reviews: Fluvastatin: Effects Beyond Cholesterol Lowering Journal of Cardiovascular Pharmacology and Therapeutics, January 1, 2000; 5(3): 161 - 175. [Abstract] [PDF]
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F. A. McAlister, A. Laupacis, G. A. Wells, D. L. Sackett, and for the Evidence-Based Medicine Working Group Users' Guides to the Medical Literature: XIX. Applying Clinical Trial Results; B. Guidelines for Determining Whether a Drug Is Exerting (More Than) a Class Effect JAMA, October 13, 1999; 282(14): 1371 - 1377. [Full Text] [PDF]
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R. H. Knopp Drug Treatment of Lipid Disorders N. Engl. J. Med., August 12, 1999; 341(7): 498 - 511. [Full Text] [PDF]
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P. O. Lim, K. M. Yee, C.J. Packard, J. Shepherd, P. W. Macfarlane, S. M. Cobbe, I. Ford, and C. G. Isles Overlap Analysis of the West of Scotland Coronary Prevention Study (WOSCOPS) • Response Circulation, August 10, 1999; 100 (6): 685 - 688. [Full Text] [PDF]
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 U. Laufs, D. Marra, K. Node, and J. K. Liao 3-Hydroxy-3-methylglutaryl-CoA Reductase Inhibitors Attenuate Vascular Smooth Muscle Proliferation by Preventing Rho GTPase-induced Down-regulation of p27Kip1 J. Biol. Chem., July 30, 1999; 274(31): 21926 - 21931. [Abstract] [Full Text] [PDF]
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P. M. Ridker, N. Rifai, M. A. Pfeffer, F. Sacks, and E. Braunwald Long-Term Effects of Pravastatin on Plasma Concentration of C-reactive Protein Circulation, July 20, 1999; 100(3): 230 - 235. [Abstract] [Full Text] [PDF]
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A. Zambon, J. E. Hokanson, B. G. Brown, and J. D. Brunzell Evidence for a New Pathophysiological Mechanism for Coronary Artery Disease Regression : Hepatic Lipase–Mediated Changes in LDL Density Circulation, April 20, 1999; 99(15): 1959 - 1964. [Abstract] [Full Text] [PDF]
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K. A. Eagle Estimation of Risk Reduction Circulation, April 13, 1999; 99 (14): 1922 - 1926. [Full Text] [PDF]
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G. Dangas, J. J. Badimon, D. A. Smith, A. H. Unger, D. Levine, J. H. Shao, P. Meraj, C. Fier, J. T. Fallon, and J. A. Ambrose Pravastatin therapy in hyperlipidemia: effects on thrombus formation and the systemic hemostatic profile J. Am. Coll. Cardiol., April 1, 1999; 33(5): 1294 - 1304. [Abstract] [Full Text] [PDF]
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A. M. Gotto Jr and S. M. Grundy Lowering LDL Cholesterol : Questions From Recent Meta-Analyses and Subset Analyses of Clinical Trial DataIssues From the Interdisciplinary Council on Reducing the Risk for Coronary Heart Disease, Ninth Council Meeting Circulation, March 2, 1999; 99 (8): e1 - e7. [Abstract] [Full Text] [PDF]
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A. D Hingorani and P. Vallance A simple computer program for guiding management of cardiovascular risk factors and prescribing BMJ, January 9, 1999; 318(7176): 101 - 105. [Abstract] [Full Text]
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W. H. Kaesemeyer, R. B. Caldwell, J. Huang, and R. W. Caldwell Pravastatin sodium activates endothelial nitric oxide synthase independent of its cholesterol-lowering actions J. Am. Coll. Cardiol., January 1, 1999; 33(1): 234 - 241. [Abstract] [Full Text] [PDF]
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G. Assmann, H. Schulte, P. Cullen, C. J. Packard, J. Shepherd, S. M. Cobbe, P. W. Macfarlane, A. R. Lorimer, J. H. McKillop, I. Ford, et al. Pravastatin and Coronary Heart Disease • Response Circulation, December 22, 1998; 98 (25): 2932 - 2935. [Full Text] [PDF]
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S. Fazio, M. F. Linton, and S. M. Grundy On the Relationship Between Cholesterol Lowering and Coronary Disease Event Rate • Response Circulation, December 8, 1998; 98(23): 2645 - 2646. [Full Text] [PDF]
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T. A. Jacobson, J. R. Schein, A. Williamson, and C. M. Ballantyne Maximizing the Cost-effectiveness of Lipid-Lowering Therapy Arch Intern Med, October 12, 1998; 158(18): 1977 - 1989. [Abstract] [Full Text] [PDF]
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U. Laufs and J. K. Liao Post-transcriptional Regulation of Endothelial Nitric Oxide Synthase mRNA Stability by Rho GTPase J. Biol. Chem., September 11, 1998; 273(37): 24266 - 24271. [Abstract] [Full Text] [PDF]
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