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Association Between Lipoprotein (a) Levels and Coronary Artery Disease (CAD) Among Patients With or Without CAD
Hayato Tada1, Nobuko Kojima1, Kan Yamagami1
1Department of Cardiovascular Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Insights
Lipoprotein (a) (Lp[a]) is linked to coronary artery disease (CAD) risk, irrespective of family history. Elevated Lp[a] levels increase CAD risk, particularly in individuals without a family history of the disease.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Biochemistry
Background:
- Lipoprotein (a) (Lp[a]) is a significant, heritable risk factor for coronary artery disease (CAD).
- The interplay between Lp[a] levels, family history of CAD, and an individual's risk for developing CAD requires further elucidation.
Purpose of the Study:
- To investigate the association between serum Lp[a] levels and coronary artery disease (CAD) risk.
- To determine if this association is modified by the presence or absence of a family history of CAD.
Main Methods:
- Analysis of clinical data from 4,512 participants who underwent Lp[a] level measurement.
- Logistic regression analyses were employed to assess the relationship between Lp[a], CAD family history, and CAD development.
Main Results:
- Both family history of CAD and Lp[a] levels were independently associated with increased CAD risk.
- Individuals with Lp[a] levels ≥30 mg/dL exhibited higher CAD risk, especially those without a family history.
- The combination of Lp[a] levels and family history improved CAD risk prediction compared to conventional risk factors alone.
Conclusions:
- Serum Lp[a] level is a significant predictor of CAD development.
- The association between Lp[a] and CAD risk persists regardless of an individual's family history of the disease.
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.
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