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Vincent M. G. Maher, MD, MRCPI; B. Greg Brown, MD, PhD
University of Washington School of Medicine Seattle

JAMA. 1997;277(3):209.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—The article by Dr Bostom and colleagues¹ reaffirms the importance of an elevated lipoprotein(a) [Lp(a)] level as a cardiac risk factor. We have postulated previously, based on our analysis of published works,² that a pathological interaction exists between increased Lp(a) levels and elevated low-density lipoprotein (LDL) cholesterol levels, which is confirmed by our own experience.³ Furthermore, by lowering LDL cholesterol levels alone, the adverse effects of the interaction of these 2 particles is greatly diminished.³

Bostom and colleagues did not observe such an interaction. The most likely explanation is that LDL cholesterol levels in their study were low (mean, 3.5 mmol/L [135 mg/dL]) relative to the mean LDL cholesterol levels in most studies previously published.² We observed that, in the presence of such low LDL cholesterol levels, increased Lp(a) levels had only a small or negligible impact on disease outcome.² In . . . [Full Text PDF of this Article]

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