リポ蛋白(a)が動脈硬化の全過程に関与 50mg/dL以上でリスク上昇― 都市部地域住民を対象とした「吹田研究」の成果 ―

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2026-10-07 国立循環器病研究センター

国立循環器病研究センターは、都市部住民を対象とした「吹田研究」により、血中の**リポ蛋白(a)[Lp(a)]**が高いほど、頚動脈の動脈硬化が発生・進行し、最終的に血管狭窄へ至るリスクが高いことを日本で初めて明らかにした。循環器病の既往や頚動脈プラークのない3,272人を中央値11.5年間追跡した結果、Lp(a)が50 mg/dL以上の人では、15 mg/dL未満の人に比べ、新規プラーク発生リスクが約1.27倍、プラーク形成後に頚動脈狭窄へ進展するリスクが約2.3倍高かった。また、血管壁の肥厚速度も速かった。これらは従来の生活習慣病リスクとは独立した関連であり、Lp(a) 50 mg/dL以上が東アジア人における動脈硬化の重要な残余リスク指標となる可能性を示す。早期の高リスク者発見や新規治療薬の開発への応用が期待される。

リポ蛋白(a)が動脈硬化の全過程に関与 50mg/dL以上でリスク上昇― 都市部地域住民を対象とした「吹田研究」の成果 ―

<関連情報>

リポタンパク質(a)と頸動脈アテローム性動脈硬化症の連続性:プラーク形成から内腔狭窄まで:吹田研究 Lipoprotein(a) and the continuum of carotid atherosclerosis from plaque initiation to luminal stenosis: the Suita Study

Masayuki Teramoto, Yoshihiro Kokubo, Yuka Kato, Sakura Shinohara, Paramita Khairan, Yoko M Nakao, Jun Masui, Kanako Teramoto, Masatoshi Koga, Hiroharu Kataoka

European Journal of Preventive Cardiology  Published:07 October 2026
DOI:https://doi.org/10.1093/eurjpc/zwag443

Abstract

Aims
The aim of this study was to investigate the long-term association between lipoprotein(a) [Lp(a)] and the longitudinal continuum of carotid atherosclerosis, from initial plaque formation to progression to carotid stenosis, in a prospective study of a general Japanese population.

Methods and results
We studied 3272 participants in the Suita Study (mean age: 58.0 ± 11.5 years; 57.9% women) who were free of cardiovascular disease and carotid plaque at baseline (1995–2004). Follow-up carotid ultrasonography was performed biennially until June 2016. Incident carotid plaque was defined as a maximal intima–media thickness (IMT) ≥ 1.7 mm in the entire carotid artery. Progression from plaque to stenosis was defined as ≥50% stenosis in participants who developed plaques. We employed Cox proportional hazards models for incident plaques, linear mixed-effects models for annual IMT changes, and logistic regression for progression to stenosis. During a median follow-up of 11.5 years, 1432 participants developed carotid plaques. Compared with Lp(a) < 15 mg/dL, the multivariable-adjusted hazard ratio for incident plaque was 1.27 [95% confidence interval (CI), 1.01–1.61] for Lp(a) ≥ 50 mg/dL. Participants with Lp(a) ≥ 50 mg/dL had significantly accelerated annual progression of maximal IMT (β = 0.014 mm/year; 95% CI, 0.003–0.025) compared with those with Lp(a) < 15 mg/dL. Furthermore, high Lp(a) levels were associated with progression to ≥50% carotid stenosis (multivariable-adjusted odds ratio, 2.29; 95% CI, 1.15–4.57).

Conclusion
Elevated Lp(a) levels (≥ 50 mg/dL) were associated with the longitudinal continuum of carotid atherosclerosis, from plaque initiation to advanced stenosis. These findings suggest that high Lp(a) levels serve as a robust marker for long-term cardiovascular risk accumulation, highlighting the importance of screening and potential targeted interventions in individuals with Lp(a) ≥ 50 mg/dL.

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