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ApoA-1 Milano and Regression of AtherosclerosisApoA-1 Milano and Regression of Atherosclerosis

JAMA. 2004;291(11):1319-1320. doi:10.1001/jama.291.11.1319-a
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AUTHOR INFORMATION

Letters Section Editor: Stephen J. Lurie, MD, PhD, Senior Editor.

APOA-1 MILANO AND REGRESSION OF ATHEROSCLEROSIS

To the Editor: Dr Nissen and colleagues1 reported that 5 weeks of treatment with intravenous recombinant ApoA-I Milano–phospholipid complexes (ETC-216) resulted in an average of 4.2% reduction in the volume of coronary atheroma. We disagree, however, with their speculation that this benefit is related to dimerization of high-density lipoprotein (HDL) and improved reverse cholesterol transport. In fact, the HDL pattern of individuals with the ApoA-I Milano variant has been shown to consist primarily of the smaller HDL-3 particles with a nearly total absence of the larger HDL-2 particles.2 Consequently, the infusion of ApoA-I Milano is likely to generate HDL-3 rather than HDL-2 particles. The misconception regarding the term dimerization may originate from the finding that ApoA-I Milano is indeed capable of giving rise to ApoA-I dimers while the size of the resultant HDL particles on lipidation remains small.1

It is also of interest that individuals with another cardioprotective isoform, ApoA-I Paris, also show an HDL pattern that consists primarily of HDL-3 particles.3 A recent epidemiologic study4 found that HDL-3, but not HDL-2, was associated with a reduced risk of progression of coronary artery disease (CAD). Furthermore, the ability of HDL-3 particles to prevent and/or release oxidative damage to LDL offers a potentially important mechanism of cardioprotection while HDL-2 particles show little activity in this regard.5 Both ApoA-I Milano and ApoA-I Paris also have been reported to exhibit more potent antioxidant activity than wild type ApoA-I.6 Taken together, the emerging evidence suggests small HDL particles are antiatherogenic, and this concept appears to be supported by the findings of Nissen et al.

References
Nissen SE, Tsunoda T, Tuzcu EM.  et al.  Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial.  JAMA.2003;290:2292-2300.
PubMed
Franceschini G, Calabresi L, Tosi C.  et al.  Apolipoprotein A-I Milano: disulfide-linked dimers increase high density lipoprotein stability and hinder particle interconversion in carrier plasma.  J Biol Chem.1990;265:12 224-12 231.
PubMed
Bruckert E, von Eckardstein A, Funke H.  et al.  The replacement of arginine by cysteine at residue 151 in apolipoprotein A-I produces a phenotype similar to that of apolipoprotein A-I Milano.  Atherosclerosis.1997;128:121-128.
PubMed
Yu S, Yarnell JW, Sweetnam P.  et al.  High density lipoprotein subfractions and the risk of coronary heart disease: 9-years follow-up in the Caerphilly Study.  Atherosclerosis.2003;166:331-338.
PubMed
Kontush A, Chantepie S, Chapman MJ.  et al.  Small, dense HDL particles exert potent protection of atherogenic LDL against oxidative stress.  Arterioscler Thromb Vasc Biol.2003;23:1881-1888.
PubMed
Bielicki JK, Oda MN. Apolipoprotein A-I Milano and apolipoprotein A-I Paris exhibit an antioxidant activity distinct from that of wild-type apolipoprotein A-I.  Biochemistry.2002;41:2089-2096.
PubMed

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Nissen SE, Tsunoda T, Tuzcu EM.  et al.  Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial.  JAMA.2003;290:2292-2300.
PubMed
Franceschini G, Calabresi L, Tosi C.  et al.  Apolipoprotein A-I Milano: disulfide-linked dimers increase high density lipoprotein stability and hinder particle interconversion in carrier plasma.  J Biol Chem.1990;265:12 224-12 231.
PubMed
Bruckert E, von Eckardstein A, Funke H.  et al.  The replacement of arginine by cysteine at residue 151 in apolipoprotein A-I produces a phenotype similar to that of apolipoprotein A-I Milano.  Atherosclerosis.1997;128:121-128.
PubMed
Yu S, Yarnell JW, Sweetnam P.  et al.  High density lipoprotein subfractions and the risk of coronary heart disease: 9-years follow-up in the Caerphilly Study.  Atherosclerosis.2003;166:331-338.
PubMed
Kontush A, Chantepie S, Chapman MJ.  et al.  Small, dense HDL particles exert potent protection of atherogenic LDL against oxidative stress.  Arterioscler Thromb Vasc Biol.2003;23:1881-1888.
PubMed
Bielicki JK, Oda MN. Apolipoprotein A-I Milano and apolipoprotein A-I Paris exhibit an antioxidant activity distinct from that of wild-type apolipoprotein A-I.  Biochemistry.2002;41:2089-2096.
PubMed
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