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
BackgroundThe 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 ResultsRelationships 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
ConclusionsWe 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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