Lipoprotein(a) is Independently Associated with Polyvascular Disease Burden
Abstract
AIMS: Lipoprotein(a) [Lp(a)] is an established, genetically determined risk factor for atherosclerotic cardiovascular disease. However, its association with the polyvascular disease burden remains unclear. This study investigated the relationship between the Lp(a) concentration and polyvascular disease burden. METHODS: We retrospectively analyzed data from 1,799 patients who underwent Lp(a) measurements between 2012 and 2025. The polyvascular disease burden was assessed using a polyvascular score based on the presence of coronary artery disease, cerebrovascular disease, lower-extremity artery disease, aneurysmal aortic disease, and calcific aortic valve disease. Patients were categorized according to the number of affected disease domains (scores 0, 1, 2, 3, and ≥ 4). A multivariable ordinal logistic regression analysis was performed to identify the factors associated with an increasing polyvascular disease burden. RESULTS: Patients with polyvascular disease (polyvascular score ≥1) had significantly higher Lp(a) concentrations than those without clinically overt vascular disease (57.9 [24.0-118.3] vs. 42.9 [20.2-76.8] nmol/L, P＜0.001). The Lp(a) concentrations increased progressively with increasing polyvascular scores, and the prevalence of elevated Lp(a) (≥ 125 nmol/L) increased stepwise across the score categories (both P＜0.001). In a multivariable ordinal logistic regression analysis adjusted for age, sex, hypertension, smoking history, family history of ischemic heart disease, eGFR, and LDL-C, higher Lp(a) levels remained independently associated with an increased polyvascular disease burden (OR 1.07 per 10 nmol/L increase, 95% CI 1.05-1.10; P＜0.001). CONCLUSIONS: Higher Lp(a) concentrations were independently associated with an increased polyvascular disease burden, suggesting that Lp(a) may reflect the extent of cardiovascular disease involvement across multiple disease domains.
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BibTeX
@article{yamada2026lipoproteina,
title = {{Lipoprotein(a) is Independently Associated with Polyvascular Disease Burden}},
author = {Ryotaro Yamada and Teruyoshi Kume and Hiroshi Okamoto and Yumi Matsutani and Kanako Ichiki and Yuya Murakami and Kaede Iteya and Yuuki Yamada and Masahiro Yamashita and Satoshi Koto and Kyo Kamisaka and Yoshitaka Sasahira and Tomoko Tamada and Terumasa Koyama and Koichiro Imai and Yoji Neishi and Shiro Uemura},
journal = {Journal of Atherosclerosis and Thrombosis},
year = {2026},
month = oct,
doi = {10.5551/jat.66432},
url = {https://www.jstage.jst.go.jp/article/jat/advpub/0/advpub_66432/_article},
note = {CC BY-NC-SA},
}
RIS
TY - JOUR
TI - Lipoprotein(a) is Independently Associated with Polyvascular Disease Burden
AU - Ryotaro Yamada
AU - Teruyoshi Kume
AU - Hiroshi Okamoto
AU - Yumi Matsutani
AU - Kanako Ichiki
AU - Yuya Murakami
AU - Kaede Iteya
AU - Yuuki Yamada
AU - Masahiro Yamashita
AU - Satoshi Koto
AU - Kyo Kamisaka
AU - Yoshitaka Sasahira
AU - Tomoko Tamada
AU - Terumasa Koyama
AU - Koichiro Imai
AU - Yoji Neishi
AU - Shiro Uemura
PY - 2026
DA - 2026/10/07
JO - Journal of Atherosclerosis and Thrombosis
DO - 10.5551/jat.66432
UR - https://www.jstage.jst.go.jp/article/jat/advpub/0/advpub_66432/_article
AB - AIMS: Lipoprotein(a) [Lp(a)] is an established, genetically determined risk factor for atherosclerotic cardiovascular disease. However, its association with the polyvascular disease burden remains unclear. This study investigated the relationship between the Lp(a) concentration and polyvascular disease burden. METHODS: We retrospectively analyzed data from 1,799 patients who underwent Lp(a) measurements between 2012 and 2025. The polyvascular disease burden was assessed using a polyvascular score based on the presence of coronary artery disease, cerebrovascular disease, lower-extremity artery disease, aneurysmal aortic disease, and calcific aortic valve disease. Patients were categorized according to the number of affected disease domains (scores 0, 1, 2, 3, and ≥ 4). A multivariable ordinal logistic regression analysis was performed to identify the factors associated with an increasing polyvascular disease burden. RESULTS: Patients with polyvascular disease (polyvascular score ≥1) had significantly higher Lp(a) concentrations than those without clinically overt vascular disease (57.9 [24.0-118.3] vs. 42.9 [20.2-76.8] nmol/L, P＜0.001). The Lp(a) concentrations increased progressively with increasing polyvascular scores, and the prevalence of elevated Lp(a) (≥ 125 nmol/L) increased stepwise across the score categories (both P＜0.001). In a multivariable ordinal logistic regression analysis adjusted for age, sex, hypertension, smoking history, family history of ischemic heart disease, eGFR, and LDL-C, higher Lp(a) levels remained independently associated with an increased polyvascular disease burden (OR 1.07 per 10 nmol/L increase, 95% CI 1.05-1.10; P＜0.001). CONCLUSIONS: Higher Lp(a) concentrations were independently associated with an increased polyvascular disease burden, suggesting that Lp(a) may reflect the extent of cardiovascular disease involvement across multiple disease domains.
SN - 1880-3873
SN - 1340-3478
ER -