Consider The Evidence: Med/Peds Journal Roundup

March 20, 2006

Plaque-busting with statins

Filed under: Cardiology, JAMA, statins — medblog @ 11:14 pm

JAMA 3/13 – Nissen et al. produce the latest, and largest of several trials documenting the effect of statin therapy on atherosclerotic plaques. The earlier studies suggested that intensive therapy with statins led to the decrease in atheroma volume. The authors of this study contend that their measurement parameters (taken via IVUS) were more rigorous than the past studies, allowing them to make a much more definitive conclusion on the issue.

A dramatic result of the study was the reduction median LDL-C levels by over 50% to approx 60mg/dl.“The achieved LDL-C levels were the lowest values ever observed in a statin atherosclerosis progression trial.” The mean change in atheroma volume in the most diseased 10-mm subsegment was –6.1 mm3. Change in total atheroma volume showed a 6.8% median reduction; with a mean reduction of –14.7 mm3. They conclude that, “When viewed in this context, the results of the current study demonstrate that there exists no apparent threshold LDL-C level beyond which the benefits of statin therapy are no longer evident. If regression of disease is the desired outcome, then lower LDL-C is better.”

Put them in the water…..

Steven E. Nissen; Stephen J. Nicholls; Ilke Sipahi; Peter Libby; Joel S. Raichlen; Christie M. Ballantyne; Jean Davignon; Raymond Erbel; Jean Charles Fruchart; Jean-Claude Tardif; Paul Schoenhagen; Tim Crowe; Valerie Cain; Kathy Wolski; Marlene Goormastic; E. Murat Tuzcu; for the ASTEROID Investigators
Effect of Very High-Intensity Statin Therapy on Regression of Coronary Atherosclerosis: The ASTEROID Trial
JAMA 2006 0: 295.13.jpc60002



  1. Studies focusing on lowering LDL are no benefit to anyone. Its just a surrogate marker that pharma industry likes to use. To see all the evidence of statins for endpoints that matter you should check out

    Comment by Steve — August 21, 2006 @ 6:11 pm

  2. I think the true focus of the study is reversal of atherosclerotic plaque burden, not LDL lowering. However, it is difficult to provide a standard measurement of treatment intensity among different statins that does not include LDL levels. In this study the LDL lowering functions more as proxy measurement of the independent variable (statin treatment intensity) and the atheroma volume as the dependent variable. Although, I guess plaque volume is still a surrogate marker for cardiovascular outcomes, but isnt it still important as a study of the mechanism of treament?

    Comment by medblog — August 21, 2006 @ 8:59 pm

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