title: Age-related contribution of Lp(a) with coronary artery calcification in patients with acute coronary syndrome: a potential role of metabolic disorder in calcified plaque.
abstract: Lp(a) and coronary artery calcification (CAC) have recently been reported as predictors of plaque instability, but this is surrounded by much controversy. We investigated the influence of Lp(a) and CAC compared other acute coronary syndrome (ACS) risk factors. 698 patients diagnosed with at least minimal coronary artery obstructive disease from a coronary angiography were randomly selected using SPSS. Lp(a), other lipid profiles and past histories were checked, and CAC semi quantitatively graded on stored fluoroscopic images. The prevalence of CAC was significantly higher in the ACS than the non-ACS group (38.0% vs. 29.9%, p=0.026). The serum level of Lp(a) (26.89 +/- 30.64 vs. 20.85 +/- 21.63, p < 0.01) and prevalence of positive Lp(a) (> 35 mg/dl) was higher in the ACS group (24% vs. 15.7%, p < 0.01). The risk of ACS was higher in the patients with both CAC and elevated an Lp(a) than in those with only one (OR: 2.16, p=0.009, 95% CI; 1.213 - 3.843 vs. OR: 1.79, p < 0.001, 95% CI; 1.300 - 2.456). The risk of ACS was increased 1.451 times (p=0.040, 95% CI; 1.071- 2.071) in patients with CAC and 1.648 times (p=0.014, 95% CI; 1.107- 2.455) in patients with a Lp(a) > 35 mg/dl. In the younger patients (< 60 years), the Lp(a), but not the CAC, was an independent risk factor for ACS (OR=2.248, p=0.005, 95% CI; 1.281-3.943). In the older patients (> 60 years), CAC, but not the Lp(a), was an independent risk factor (OR=1.775, p=0.021, 95% CI; 1.090 - 2.890). Both the Lp(a) and CAC were risk factors for ACS, and they had a synergistic effect on its development. In the younger Lp(a), and the older CAC, was the more potent risk factor for ACS, respectively.
authors.affiliation: Department of Internal Medicine, Yonsei University College of Medicine, 146-92, Dogok-dong, Kangnam-gu, Seoul 135-270, Korea.
authors.forename: Sung Kee
authors.initials: SK
authors.lastname: Ryu
authors.forename: Bum Kee
authors.initials: BK
authors.lastname: Hong
authors.forename: Hyuck Moon
authors.initials: HM
authors.lastname: Kwon
authors.forename: Dong Soo
authors.initials: DS
authors.lastname: Kim
authors.forename: Wook Jin
authors.initials: WJ
authors.lastname: Chung
authors.forename: Byoung Eun
authors.initials: BE
authors.lastname: Park
authors.forename: Dong-Yeon
authors.initials: DY
authors.lastname: Kim
authors.forename: Yun-Hyeong
authors.initials: YH
authors.lastname: Cho
authors.forename: Se Jung
authors.initials: SJ
authors.lastname: Yoon
authors.forename: Young Won
authors.initials: YW
authors.lastname: Yoon
authors.forename: Seung-Yun
authors.initials: SY
authors.lastname: Cho
authors.forename: Hyun Seung
authors.initials: HS
authors.lastname: Kim
mesh_terms: D000208:Acute Disease; D000367:Age Factors; D000368:Aged; D000375:Aging / Q000097:blood*; D002114:Calcinosis / Q000097:blood / Q000150:complications*; D003324:Coronary Artery Disease / Q000097:blood / Q000209:etiology*; D003331:Coronary Vessels / Q000473:pathology*; D005260:Female; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008659:Metabolic Diseases / Q000150:complications; D008875:Middle Aged; D012307:Risk Factors; D013577:Syndrome
chemical_list: D017270:Lipoprotein(a)