Key result
Elevated Lipoprotein(a) was independently associated with left main coronary plaque progression and an increased risk of adverse cardiovascular events (OR 10.20; 95% CI 2.36-44.13; P=0.0019).
Why the study?
There are no data demonstrating a relation between Lp(a), fibrinogen, and directly measured coronary plaque progression over time.
Do elevated Lipoprotein(a) and fibrinogen levels predict plaque progression and adverse cardiovascular events in patients undergoing serial IVUS of left main coronary arteries?
Observational (n=60)
Do elevated Lipoprotein(a) and fibrinogen levels predict plaque progression and adverse cardiovascular events in patients undergoing serial IVUS of left main coronary arteries?
Elevated Lipoprotein(a) is independently associated with both coronary plaque progression and adverse cardiovascular events, highlighting its incremental value in predicting cardiovascular risk.
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.
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Hartmann et al. (2006) conducted an observational in Coronary plaque progression (n=60). Elevated Lipoprotein(a) and fibrinogen levels vs. Lower Lipoprotein(a) and fibrinogen levels was evaluated on Adverse cardiovascular events (OR 10.20, 95% CI 2.36-44.13, p=0.0019). Elevated Lipoprotein(a) was independently associated with left main coronary plaque progression and an increased risk of adverse cardiovascular events (OR 10.20; 95% CI 2.36-44.13; P=0.0019).
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