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To the Editor: In their study of very high-intensity statin therapy, Dr Nissen and colleagues¹ found that use of a high-dose statin may be able to reverse atherosclerosis. However, I am concerned about statements in the article such as "regression was achieved by reducing LDL-C" that imply that it was changes in low-density lipoprotein cholesterol (LDL-C) or high-density lipoprotein cholesterol (HDL-C) that were responsible for the observed plaque regressions.

This study showed only that giving rosuvastatin at 40 mg/d on average produced plaque regressions, large reductions in LDL-C levels, and modest increases in HDL-C levels; it did not show a causal link among these 3 findings. Whether it was the low LDL-C, the increase in HDL-C, some combination of these, or none of these but some other action of the drug (eg, pleiotropic effects) that was responsible cannot be inferred from the results reported. Table 4 in the article indicates . . . [Full Text of this Article]

Sid C. Port, PhD
sport@ucla.edu
University of California, Los Angeles

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