(Circulation. 2000;101:e45.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
Senior Lecturer in Chemical Pathology
Senior Lecturer in Chemical Pathology St. Thomas Hospital, London, UK
Reader in Chemical Pathology
Professor of Chemical Pathology Royal Free Hospital, London, UK
| Introduction |
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The comprehensive review by Furberg1 of natural statins and stroke raises a number of issues. Stroke was a secondary end point in these studies in patients with cardiovascular disease (CVD). Primary end-point trials in stroke are awaited. Surrogate markers can be valuable guides to the introduction of better therapies before large-scale trials are completed. LDL may be the best surrogate marker of prognosis in CVD. In stroke, the primary role of LDL is less clear, but the subgroup analyses and the association of LDL reduction with mechanisms of plaque stabilization imply the need for effective therapy. The new target of LDL <100 mg/dL (<2.5 mmol/L) may be difficult to achieve with some natural statins. The extent to which comparative trials between statins are necessary to demonstrate a class effect is debatable, as they seem to share many ancillary actions.2
The effects of statins on fibrinogen are controversial. Epidemiological
evidence suggests fibrinogen is an independent risk factor, but it is
unnecessary as an additional predictor in models of CVD risk. No
clinical trials have demonstrated that a reduction in fibrinogen alone
will reduce events or the converse. In contrast to the
nonpeer-reviewed communication cited with its claimed 50% increase
in fibrinogen,1 we have published observational data of
19% to 23% median increases in fibrinogen with atorvastatin in 89
patients with familial hyperlipidemias3
and a subset of 21 patients at high risk of CVD.4 We have
extended these observations to 201 patients with familial
hyperlipidemias and have found a
Professor Wake Forest University, School of Medicine, Winston-Salem, NC
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