Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 2000;101:e45

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wierzbicki, A. S.
Right arrow Articles by Furberg, C. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wierzbicki, A. S.
Right arrow Articles by Furberg, C. D.
Related Collections
Right arrow Risk Factors
Right arrow Coagulation and fibronolysis
Right arrow Lipid and lipoprotein metabolism

(Circulation. 2000;101:e45.)
© 2000 American Heart Association, Inc.


Circulation Electronic Pages

Natural Statins and Stroke

Anthony S. Wierzbicki

Senior Lecturer in Chemical Pathology

Martin A. Crook

Senior Lecturer in Chemical Pathology St. Thomas’ Hospital, London, UK

Dimitri P. Mikhailidis

Reader in Chemical Pathology

Anthony F. Winder

Professor of Chemical Pathology Royal Free Hospital, London, UK


*    Introduction
 
To the Editor:

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 non–peer-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 . . . [Full Text of this Article]

Curt D. Furberg, MD, PhD

Professor Wake Forest University, School of Medicine, Winston-Salem, NC