Publishing House SB RAS:

Publishing House SB RAS:

Address of the Publishing House SB RAS:
Morskoy pr. 2, 630090 Novosibirsk, Russia

Advanced Search

The journal "Ateroskleroz"

2012 year, number 1

Apoprotein(a) isoforms: a link with quantitative levels of lipoprotein(a), aspects of multi-stage atherogenicity and other apo(a) correlations

A.V. Tikhonov, A.V. Shabalin, YU.I. Ragino, YU.P. Nikitin
Keywords: atherosclerosis, genetics, lipid metabolism, lipoprotein(a), apo(a) isoforms, structure
Pages: 43-54


Most of the recent studies demonstrate that the quantitative level of Lp(a) and especially its low-molecular apo(a) phenotypes are independent risk factors of coronary atherosclerosis and correlate directly with the appearance, progress, and severity of manifestation of ischemic heart disease (IHD).
Several studies investigated the quantitative levels of Lp(a) and low-molecular apo(a) phenotypes in patients with stroke or transient ischemic attacks taking into account the presence and severity of atherosclerosis of the main arteries of the head with high risk of stroke and cerebrovascular complications of atherosclerosis. These indices appeared to be less informative for diagnostics, prognosis, and the severity of clinical course of these disorders than for the coronary atherosclerosis and IHD. On the other hand, in the retrospective studies of patients with stroke, quantitative Lp(a) levels and its low-molecular apo(a) isoforms were significantly higher than in the control group of healthy individuals (standardized odds ratio was 1.37 and 1.74, respectively). The contradiction between the results obtained in the mentioned studies and the Physicians Health Study about the risk of the development of ischemic and other types of stroke may be explained by post-stroke augmentation of Lp(a) level and by the different significance of Lp(a) level and apo(a) phenotypes in different populations.
There is no common opinion about necessity to correct high levels of Lp(a). But in case of augmented Lp(a) level, one of the actual strategy to influence the established risk factors of IHD is aggressive decreasing the concentration of cholesterol of low-density lipoproteins first of all that seems to be useful and reasonable in IHD patients. There are no highly effective methods of diet and/or drug management to correct the levels of Lp(a) and/or low-molecular phenotypes of apo(a), except for using high doses of nicotine acid, neomycin and estrogen-containing drugs. However, recommended doses of these drugs are associated with a lot of side effects. All these arguments evidence the necessity for determining the apo(a) phenotype/genotype and Lp(a) concentration levels.