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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1707.)
© 2001 American Heart Association, Inc.

Editorial

Lp A-I and Niacin

New Views of an Antiatherogenic Duo

Lucian Saucan; Eliot A. Brinton

From the Carl T. Hayden VA Medical Center, Phoenix, Ariz.

Correspondence to Dr. Eliot Brinton, Phoenix VAMC, 650 East Indian School Rd, Phoenix, AZ 85012. E-mail Eliot.Brinton@med.va.gov

Increasing evidence from epidemiological, clinical, and basic mechanistic studies supports the importance of HDL in preventing or even reversing atherosclerosis. The well-known structural and compositional diversity of HDL subfractions seems to be an important, if still somewhat unclear, factor in the atheroprotective potential of a given HDL particle. Perhaps as important as the parameter of particle size is that of apolipoprotein content of HDL. HDL particles which lack apo A-II (Lp A-I) appear to associate with reduced atherosclerosis risk¹ and are reported to be better cholesterol acceptors in some^2,3 although not all studies⁴ as compared with HDL with apo A-II (Lp A-I/A-II).

See page 1783

Niacin generally is considered the most effective agent for raising HDL levels, typically increasing HDL-C by 30%.⁵ The mechanism of this effect has been shown, by in vivo human turnover studies, to be a decrease in its fractional catabolic rate^6,7 Interestingly, despite the clinical importance of both niacin and Lp A-I levels, the impact of the former on the latter has been little studied. One earlier intensive study of a small number of subjects showed that niacin selectively raised Lp A-I levels while Lp A-I/A-II declined somewhat,⁸ but this question appears not to have been further tested in almost two decades since. Gemfibrozil also is effective in raising HDL levels, although generally less than half as much as niacin.⁹ The major HDL-raising mechanism of gemfibrozil appears to be an increase in production of apo A-I, as demonstrated by Saku et al¹⁰ in vivo and by . . . [Full Text of this Article]