Can remnant cholesterol (triglyceride-rich lipoproteins) reclassify estimated risk of atherosclerotic cardiovascular disease?

Takahito Doi, Børge G. Nordestgaard, Anne Langsted*

*Corresponding author af dette arbejde

Publikation: Bidrag til tidsskriftReviewForskningpeer review

9 Citationer (Scopus)
7 Downloads (Pure)

Abstract

Purpose of review
To summarize recent studies analyzing reclassification of estimated risk of myocardial infarction (MI) and ischemic heart disease (IHD) by inclusion of remnant cholesterol (= cholesterol content in triglyceride-rich lipoproteins) in primary and secondary prevention settings.

Recent findings
For individuals in a primary prevention setting with remnant cholesterol levels at least 95th percentile (≥1.6 mmol/l, 61 mg/dl), 23% of MI and 21% of IHD events developed later were reclassified correctly from below to above 5% for 10-year occurrence when remnant cholesterol levels were added to models based on conventional risk factors, whereas no events were reclassified incorrectly. Overall improved reclassification of MI was also observed for remnant cholesterol levels as low as at least 50th percentile (≥0.6 mmol/l, 25 mg/dl); however, the addition of remnant cholesterol over the entire concentration range yielded insignificant improvements of NRI for MI but slightly improved reclassification of NRI for IHD. In a secondary prevention setting, addition of remnant cholesterol over the entire concentration range to a conventional risk model improved reclassification.

Summary
Elevated remnant cholesterol levels considerably improves reclassification of individuals who later develop MI and IHD, in primary as well as in secondary prevention settings.
OriginalsprogEngelsk
TidsskriftCurrent Opinion in Endocrinology, Diabetes and Obesity
Vol/bind30
Udgave nummer2
Sider (fra-til)128-135
Antal sider8
ISSN1752-296X
DOI
StatusUdgivet - 2023

Bibliografisk note

Funding Information:
This work was partly supported by the Capital Region of Denmark to B.G.N. (the Global Excellence Programme), to A.L. (Research Fund, grant number: A7160), and to T.D. (Research Fund, grant number: A7165 and A7272); the Department of Clinical Biochemistry, Herlev and Gentofte Hospital, Copenhagen University Hospital, Denmark; by Scandinavia-Japan Sasakawa Foundation to T.D. (Research Fund, grant number: GA22-JPN-0019); and Japan Society for the Promotion of Science to T.D. (JSPS Overseas Research Fellowship).

Publisher Copyright:
© 2023 Lippincott Williams and Wilkins. All rights reserved.

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