Table 3.

Multivariate regression analyses showing the independent association between elevated Lp(a) and FH phenotype and the risk of premature CAD

	OR	95% CI	p Value
Model 1a
Male sex	1.37	0.78‐2.40	0.269
T2DM (Y vs N)	1.52	0.88‐2.67	0.134
HTN (Y vs N)	0.98	0.60‐1.61	0.943
Smoking status (ever vs never)	1.29	0.79‐2.11	0.307
Ln Cr	0.30	0.11‐0.78	0.014
Statin at admission (Y vs N)	0.44	0.25‐0.77	0.004
FH phenotype	3.02	1.33‐6.85	0.008
Elevated Lp(a)	1.88	1.09‐3.24	0.024
Model 2b
Male sex	1.38	0.79‐2.41	0.266
T2DM (Y vs N)	1.54	0.88‐2.69	0.131
HTN (Y vs N)	0.99	0.60‐1.63	0.961
Smoking status (ever vs never)	1.29	0.79‐2.11	0.305
Ln Cr	0.30	0.11‐0.79	0.015
Statin at admission (Y vs N)	0.44	0.25‐0.77	0.004
Elevated Lp(a) and FH phenotype composite	—	—	0.005
Elevated Lp(a) alone vs neither disorder	1.92	1.06‐3.46	0.031
FH phenotype alone vs neither disorder	3.17	1.16‐8.63	0.024
Elevated Lp(a) + FH phenotype vs neither disorder	5.27	1.47‐18.91	0.011

Abbreviations: CAD, coronary artery disease; CI, confidence interval; Cr, creatinine; FH, familial hypercholesterolemia; HTN, hypertension; Ln, logarithm; Lp(a), lipoprotein(a); N, no; OR, odds ratio; T2DM, type 2 diabetes mellitus; Y, yes.

^aModel 1 includes FH phenotype and elevated Lp(a) as separate variables. The significant association for both elevated Lp(a) and FH phenotype demonstrates their independent effects on the risk of developing premature CAD.

^bModel 2 investigates the interaction between elevated Lp(a) and FH phenotype. Patients with both elevated Lp(a) and phenotypic FH were at the highest risk of developing premature CAD.