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Lp(a) predicts coronary artery disease regardless of family history in 4,512 Japanese patients (J Lipid Atheroscler 2025)

Original title: Association Between Lipoprotein (a) Levels and Coronary Artery Disease (CAD) Among Patients With or Without CAD Family History

J Lipid Atheroscler · · 7

Tada H, Kojima N, Yamagami K, Takeji Y, Sakata K, Usui S, Kawashiri MA, Takamura M

In 4,512 patients who underwent Lp(a) measurement at Kanazawa University Hospital between 2008 and 2016, both coronary artery disease (CAD) family history (odds ratio 1.32, 95% CI 1.12-1.52) and Lp(a) level (odds ratio 1.13, 95% CI 1.03-1.23 per 10 mg/dL) were independently associated with CAD, both P < 0.001. Among patients without CAD family history, Lp(a) at or above 30 mg/dL carried higher CAD risk than levels below 30 mg/dL (odds ratio 1.33, 95% CI 1.05-1.61). Among those with a family history, both lower and higher Lp(a) groups showed elevated CAD risk relative to the reference (odds ratio 1.24 and 1.68 respectively, both P < 0.001). Adding CAD family history and Lp(a) to conventional risk factors improved discrimination, raising the C-statistic from 0.744 to 0.791 (P < 0.05). Lp(a) predicted CAD development independent of family history status.

Read the paper (DOI)PubMed

Original abstract

Objective: Lipoprotein (a) (Lp[a]), which is a highly heritable trait, is associated with coronary artery disease (CAD). However, the insight into whether the association between Lp(a) and CAD differs according to the family history of CAD remains unclear.

Methods: We investigated clinical data of 4,512 participants who underwent serum Lp(a) level measurement at Kanazawa University Hospital between 2008 and 2016. The association between Lp(a) and CAD according to CAD family history was investigated through logistic regression analyses.

Results: CAD family history and Lp(a) levels were significantly associated with CAD development (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.12-1.52; p<0.001 and OR, 1.13; 95% CI, 1.03-1.23; p<0.001 per 10 mg/dL, respectively). In patients without CAD family history, those with Lp(a) levels ≥30 mg/dL had higher CAD risk than those with Lp(a) levels <30 mg/dL (reference) (OR, 1.33; 95% CI, 1.05-1.61; p<0.001). In patients with CAD family history, those who had Lp(a) levels <30 and ≥30 mg/dL were both highly at risk for CAD (OR, 1.24; 95% CI, 1.04-1.44; p<0.001 and OR, 1.68; 95% CI, 1.34-2.02; p<0.001, respectively). Adding CAD family history and Lp(a) information to other conventional risk factors enhanced CAD risk discrimination (C-statistics: 0.744 [0.704-0.784] to 0.768 [0.730-0.806], and 0.791 [0.751-0.831], respectively; p<0.05 for both).

Conclusion: Lp(a) level was associated with CAD development regardless of CAD family history status.

epidemiologygenetics

Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.