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.

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.

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.

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.