aterosklerozАтеросклерозAteroscleroz2078-256X2949-3633НИИТПМ-филиал ИЦиГ СО РАНateroskleroz-641Research ArticleОБЗОРЫREVIEWSАпопротеид (а) изоформы, связь с количественным уровнем липопротеида (а), аспекты многоступенчатой атерогенности и другие корреляции АПО (а)Apoprotein (a) isoforms: a link with quantitative levels of lipoprotein(a), aspects of multi-stage atherogenicity and other apo (a) correlationsТихоновА. В.TikhonovA. V.

Александр Виленович Тихонов, д-р мед. наук, ведущий научный сотрудник

СО РАМН

ФГБУ «НИИ терапии»

лаборатория клинических биохимических и гормональных исследований терапевтических заболеваний

630089

ул Бориса Богаткова, 175/1

Новосибирск

SB RAMS

Establishment of the Russian Academy of Medical Sciences Research Institute of Therapy

630089

st. Boris Bogatkov, 175/1

Novosibirsk

alex-tikh@mail.ruШабалинА. В.ShabalinA. V.

Алексей Васильевич Шабалин, д-р мед. наук, проф., член-кор.

СО РАМН

ФГБУ «НИИ терапии»

630089

ул Бориса Богаткова, 175/1

Новосибирск

SB RAMS

Establishment of the Russian Academy of Medical Sciences Research Institute of Therapy

630089

st. Boris Bogatkov, 175/1

Novosibirsk

РагиноЮ. И.RaginoYu. I.

Юлия Игоревна Рагино, д-р мед. наук, проф., зав. лабораторией

СО РАМН

ФГБУ «НИИ терапии»

лаборатория клинических биохимических и гормональных исследований терапевтических заболеваний

630089

ул Бориса Богаткова, 175/1

Новосибирск

SB RAMS

Establishment of the Russian Academy of Medical Sciences Research Institute of Therapy

630089

st. Boris Bogatkov, 175/1

Novosibirsk

ragino@mail.ruНикитинЮ. П.NikitinYu. P.

Юрий Петрович Никитин, д-р мед. наук, проф., академик, зав. лабораторией 

СО РАМН

ФГБУ «НИИ терапии»

лаборатория этиопатогенеза и клиники внутренних заболеваний

630089

ул Бориса Богаткова, 175/1

Новосибирск

SB RAMS

Establishment of the Russian Academy of Medical Sciences Research Institute of Therapy

630089

st. Boris Bogatkov, 175/1

Novosibirsk

yuri-nikitin@ngs.ruРАМНРоссияRAMSRussian Federation201203042022814353Copyright © Тихонов А.В., Шабалин А.В., Рагино Ю.И., Никитин Ю.П., 20222022Тихонов А.В., Шабалин А.В., Рагино Ю.И., Никитин Ю.П.Tikhonov A.V., Shabalin A.V., Ragino Y.I., Nikitin Y.P.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://ateroskleroz.elpub.ru/jour/article/view/641

   Большая часть современных исследований демонстрирует, что количественный уровень Лп (a) и особенно его низкомолекулярные фенотипы апо (а) являются независимыми факторами риска коронарного атеросклероза и прямо коррелируют с наличием, прогрессированием и степенью выраженности ишемической болезни сердца.

   В ряде исследований при сопоставлении количественного уровня Лп (a) и низкомолекулярных изоформ апо (а) у больных, перенесших инсульты или транзиторные ишемические атаки, учитывали наличие, тяжесть атеросклероза магистральных артерий головы с риском инсультов, а также цереброваскулярных осложнений атеросклероза. Было отмечено, что эти показатели менее информативны для диагностики, прогноза, тяжести течения данных заболеваний, чем при коронарном атеросклерозе и ишемической болезни сердца. С другой стороны, в ретроспективных исследованиях у больных с перенесенным ишемическим инсультом количественный уровень Лп (a) и его низкомолекулярных изоформ апо (а) были достоверно выше, чем в группе практически здоровых (стандартизированное отношение шансов составило 1,37 и 1,74, соответственно). Некоторое противоречие результатов, полученных в этих исследованиях и исследовании Physicians Health Study при изучении риска развития инсультов (как в целом, так и ишемических), объясняется, возможно, изменением концентрации уровня Лп (a) уже после развития инсульта, а также различной значимостью уровня Лп (a) и фенотипов апо (а) в разных популяциях.   Единого мнения о необходимости какой-либо коррекции высокого уровня Лп (a) не существует, хотя при наличии высокого уровня Лп (a) одним из реальных подходов является воздействие на установленные факторы риска ИБС, в первую очередь агрессивное снижение концентрации ХС ЛПНП, что может быть полезным и целесообразным у больных ИБС. Достаточно эффективных способов с применением диеты и / или медикаментозного воздействия на уровень Лп (a) и / или низкомолекулярных фенотипов апо (а) в настоящее время не существует, за исключением применения больших доз никотиновой кислоты и неомицина, а также эстрогенсодержащих препаратов. Однако назначение этих лекарственных средств в рекомендуемых дозах сопряжено с большим количеством побочных эффектов. Все вышесказанное является аргументом в пользу необходимости определения фенотипа / генотипа апо (а) и уровня концентрации Лп (a).

   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.

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The authors declare that there are no conflicts of interest present.