Background: Elevated plasma (Lp(a)) levels may represent an independent risk factor for atherothrombotic complications but the relation between Lp(a) levels and the extent of coronary artery disease (CHD) has been discussed controversially. Little is known about potential atherothrombogenic mechanisms of Lp(a).
Design: Case-control study.
Methods: We assessed the relationship between plasma Lp(a) and angiographically defined CHD, evaluating the severity of coronary atherosclerosis by three different scores. A total of 312 patients with stable angina aged 40-68 years with at least one coronary stenosis > 50% were studied. A group of 479 voluntary blood donors matched for age and sex served as controls. A complete lipid profile and a large number of markers of coagulation, fibrinolysis and inflammation were measured.
Results: Plasma levels of Lp(a) were significantly higher in patients (14.8 mg/dl; 5.4-47.1 mg/dl; median/interquartile range) than in controls (9.7 mg/dl; 3.5-25.3) (P<0.0001). In a logistic regression model, the fully adjusted Odds Ratio for CHD was 3.3 (95% confidence interval (CI) 1.8-5.6, P<0.0001) for patients in the upper quartile of the Lp(a) distribution compared to the bottom quartile. There was no appreciable association between Lp(a) and apolipoproteins, markers of haemostasis, fibrinolysis and inflammation and the severity of CHD.
Conclusions: These results indicate that elevated plasma Lp(a) levels may be an independent risk factor for CHD but unrelated to the severity and extension of CHD. Furthermore, there is no good evidence that the presumed link between Lp(a) and CHD is mediated by increased levels of markers of inflammation, or interference with markers of fibrinolysis or coagulation.