Valtimotautia sairastavista potilasta jopa neljäsosalla on suurentunut triglyseridipitoisuus
tehokkaasta lipidilääkityksestä huolimatta «Lawler PR, Kotrri G, Koh M, ym. Real-world risk of...»16. Statiinihoidon aikana LDL-kolesterolin tavoitepitoisuuden saavuttaneilla tyypin
2 diabetesta sairastavilla aterian jälkeinen triglyseridipitoisuuden suurentuminen
liittyi aterogeenisten apoB-48-hiukkasten viisi kertaa hitaampaan poistumiseen verrattuna
henkilöihin, joilla ei ollut diabetesta «Taskinen MR, Matikainen N, Björnson E, ym. Contrib...»17. Hypertriglyseridemian odotetaan edelleen lisääntyvän obesiteetin, metabolisen oireyhtymän
ja tyypin 2 diabeteksen esiintyvyyden lisääntymisen myötä.
Tutkimuksen perusteella tehokkaan statiinihoidon aikana todettu plasman triglyseriditaso
≥ 4 mmol/l suurentaa valtimotaudin riskiä 52 % verrattuna joukkoon, jolla triglyseridipitoisuus
on < 1 mmol/l «Lawler PR, Kotrri G, Koh M, ym. Real-world risk of...»16.
Keskeinen aterogeenisyyden mekanismi näillä triglyseridirikkailla lipoproteiineilla
on sama kuin LDL-partikkeleilla, eli ne siirtyvät endoteelin läpi verisuonen intimaan,
retentoituvat hepariinisulfaatti-glykoproteiinien välityksellä ja saavat aikaan vaahtosolujen
muodostumisen kautta ateroomaplakin muodostumisen «Tabas I, Williams KJ, Borén J. Subendothelial lipo...»11.
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