Copyright © 2004, European Society of Cardiology
Statins–is there no end to their usefulness?
School of Pharmacy, The Robert Gordon University, Aberdeen, Schoolhill, AB10 1FR, Scotland, UK
* Tel.: +44 1224 262450; fax: +44 1224 262555. Email address: c.wainwright@rgu.ac.uk
Received 22 November 2004; accepted 25 November 2004
| The first 10% of the full text of this article appears below. |
See also article by Birnbaum et al. [15] (pages 345–355) in this issue.
Ever since the data from the West of Scotland Coronary Prevention (WOSCOP) Study demonstrated an unequivocal beneficial effect in patients at risk from coronary events [1], statins have become a standard addition to the therapeutic management of this group of the population. As inhibitors of HMG-CoA reductase, the primary pharmacodynamic effect of the statins is to inhibit the synthesis of cholesterol by the liver, thereby increasing hepatic cholesterol uptake and reducing circulating lipid levels–or is it? While lipid lowering is more than likely to underpin the clinical observations of a deceleration of atherosclerotic lesion formation and induction of regression and stabilisation of plaques, evidence is growing that the pleiotropic effects of statins (i.e. their effects beyond lipid lowering) may also contribute to their beneficial effects in this setting and
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