Mechanisms
Lp(a), not fibrinogen, independently predicts coronary plaque progression on serial imaging, a study of 60 left main coronary arteries (J Am Coll Cardiol 2006)
Original title: Relation between lipoprotein(a) and fibrinogen and serial intravascular ultrasound plaque progression in left main coronary arteries
This retrospective study analysed serial intravascular ultrasound (IVUS) of 60 left main coronary arteries, imaged a median 18 months apart, to test whether Lp(a) and fibrinogen relate to coronary plaque progression and cardiovascular events. Both Lp(a) (r=0.58, P<0.0001) and fibrinogen (r=0.48, P<0.0001) correlated positively with plaque area change; patients with plaque progression (n=41) had higher Lp(a) (30 vs 14 mg/dL, P<0.0012) and fibrinogen (295 vs 240 mg/dL, P=0.019) than those with regression (n=19). In multivariate analysis, log Lp(a) (regression coefficient 9.45, P=0.0008), but not fibrinogen, was independently associated with plaque progression, and log Lp(a) (odds ratio 10.20, 95% CI 2.36-44.13, P=0.0019) and fibrinogen (odds ratio 1.01, 95% CI 1.00-1.03, P=0.018) were both independently associated with adverse cardiovascular events among 19 affected patients. The findings show Lp(a), unlike fibrinogen, independently predicts coronary plaque progression and adds incremental value in predicting cardiovascular risk.
Original abstract
Objectives: Patients with elevated lipoprotein(a) [Lp(a)] and fibrinogen levels have an increased risk of coronary heart disease and adverse cardiovascular events. There is evidence that coronary plaque progression is linked to a higher risk for future cardiovascular events.
Background: There are no data demonstrating a relation between Lp(a), fibrinogen, and directly measured coronary plaque progression over time.
Methods: We performed a retrospective analysis of serial intravascular ultrasound (IVUS) studies of 60 left main stems (18 +/- 9 months apart) to evaluate plaque progression in relation to Lp(a) and fibrinogen levels and association with adverse cardiovascular events.
Results: There was a positive correlation between Lp(a) (r = 0.58; p < 0.0001), fibrinogen (r = 0.48; p < 0.0001), and changes in plaque-plus-media area. Patients with plaque progression (n = 41) had higher Lp(a) (30 +/- 26 mg/dl vs. 14 +/- 9 mg/dl; p < 0.0012) and fibrinogen (295 +/- 88 mg/dl vs. 240 +/- 72 mg/dl; p = 0.019) levels than patients with plaque regression (n = 19). Multivariate linear regression analysis showed Log Lp(a) (regression coefficient = 9.45; p = 0.0008) but not fibrinogen to be independently associated with plaque progression. A total of 19 patients suffered from adverse cardiovascular events; they had higher Lp(a) (44 +/- 30 mg/dl vs. 16 +/- 12 mg/dl; p < 0.0001) and fibrinogen (342 +/- 73 mg/dl vs. 248 +/- 76 mg/dl; p < 0.0001) levels. Multivariate logistic regression analysis showed Log Lp(a) (odds ratio 10.20, 95% confidence interval 2.36 to 44.13; p = 0.0019) and fibrinogen (odds ratio 1.01, 95% confidence interval 1.00 to 1.03; p = 0.018) were independently associated with adverse cardiovascular events.
Conclusions: Serial IVUS showed a positive correlation between Lp(a) and fibrinogen levels and plaque progression. Lp(a), but not fibrinogen, remains independently associated with plaque progression. In addition, the present data suggest a considerable incremental value of Lp(a) in predicting cardiovascular risk.
mechanismsrisk predictionthrombosis
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.