Coenzyme A Reductase Inhibitors and Stroke

  1. John R. Crouse III, MD
  1. Wake Forest University School of Medicine; Winston Salem, NC 27157-1047

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    TO THE EDITOR:

    The article by Bucher and coworkers [1] confirms previous contributions that have identified an effect of statins to reduce stroke [2, 3]. However, it also raises several questions.

    First, the article reviewed only 8 of 15 published trials of statins that provide information on stroke [2, 3]. The criteria that led to the exclusion of these other available clinical trials would be of interest. This is important because 7 of the 8 statin trials reviewed by Bucher and coworkers are studies of the secondary prevention of cardiovascular disease. Our own work [2] and that of others [3] suggests that secondary prevention statin studies show a stronger effect of cholesterol reduction on stroke prevention than do stain studies that either include a mixture of persons with and without coronary disease or focus attention on primary prevention. In fact, for statins, there is a preponderance of trials of secondary (as opposed to primary) prevention. This may be one of the important differences between the new meta-analyses of statin trials and two previous negative meta-analyses of clinical trials that did not include 3-hydroxy-3-methylglutaryl coenzyme A (HMGcoA) reductase inhibitors. In the latter, a large proportion of the pharmacologic trials were trials of the primary prevention of coronary artery disease [4, 5].

    In addition, Bucher and colleagues conclude that “… in hyperlipidemic patients who have not previously had stroke, HMGcoA reductase inhibitors reduce the incidence of stroke.” It is not clear that patients who previously had stroke were, in fact, systematically excluded from the studies reviewed.

    Finally, we believe that it is now important to begin to better understand the mechanisms whereby cholesterol lowering reduces stroke. My colleagues and I have previously suggested three possibilities: plaque regression, improvement in endothelial stability, and reduction of coronary heart disease [2]. Does this most recent meta-analysis favor one of these mechanisms?

    John R. Crouse III, MD

    Wake Forest University School of Medicine; Winston Salem, NC 27157-1047

    The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:

    •Include no more than 300 words of text, three authors, and five references

    •Type with double-spacing

    •Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.

    Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.

    Annals welcomes electronically submitted letters.

    References

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