Lipoprotein(a) is associated differentially with carotid stenosis, occlusion, and total plaque area
Jonathan H Klein1, Robert A Hegele, Daniel G Hackam
1Schulich School of Medicine and Dentistry, University of Western Ontario, London, Canada.
Insights
Elevated Lipoprotein(a) [Lp(a)] levels independently predict carotid artery stenosis and occlusion, suggesting a link to thrombosis rather than plaque buildup. This finding highlights Lp(a) as a key factor in cardiovascular risk.
Area of Science:
- Cardiovascular Medicine
- Atherosclerosis Research
- Lipidology
Background:
- Lipoprotein(a) [Lp(a)] is implicated as a risk factor for myocardial infarction and stroke.
- Lp(a) is associated with thrombosis and impaired fibrinolysis.
- Atherosclerosis manifests in distinct phenotypes like carotid stenosis, occlusion, and plaque area.
Purpose of the Study:
- To investigate the relationship between Lp(a) levels and specific phenotypes of carotid atherosclerosis.
- To determine if Lp(a) differentially affects carotid stenosis, occlusion, and plaque area.
- To explore the role of thrombosis and fibrinolysis in Lp(a)]-associated cardiovascular risk.
Main Methods:
- Multivariable linear and logistic regression analyses were employed.
- The study included 876 consecutive patients from an atherosclerosis prevention clinic.
- Data on Lp(a) levels and carotid atherosclerosis phenotypes were analyzed.
Main Results:
- Lp(a) was a significant independent predictor of carotid stenosis (P<0.0001).
- Lp(a) also significantly predicted carotid artery occlusion (P=0.001).
- Lp(a) was not a significant predictor of carotid plaque area (P=0.13).
- Patients with carotid occlusion had higher Lp(a) levels (0.27+/-0.25 g/L vs. 0.17+/-0.18 g/L).
Conclusions:
- Lp(a) is a significant independent predictor of carotid stenosis and occlusion.
- The findings support the hypothesis that Lp(a)]'s cardiovascular risk is linked to thrombosis and impaired fibrinolysis, not plaque progression.
- Stenosis and occlusion may result from plaque rupture and thrombosis, a mechanism potentially applicable to other arterial beds.
Background:
Lipoprotein(a) [Lp(a)] is a putative risk factor for myocardial infarction and stroke and is related to thrombosis and impaired fibrinolysis. We studied relationships of Lp(a) with carotid stenosis, occlusion, and total plaque area, distinct phenotypes of atherosclerosis that may be differentially affected by cardiovascular risk factors.
Methods And Results:
Multivariable linear regression analysis was used to study relationships of Lp(a) to phenotypes of carotid atherosclerosis among 876 consecutive patients from an atherosclerosis prevention clinic with complete data for all variables used in the model. Occlusion of an internal carotid artery was present in 22 (2.5%) patients (one with bilateral occlusions). Risk factors predicted carotid plaque area, stenosis, and occlusion differently. Lp(a) was a significant independent predictor of baseline stenosis (P<0.0001) but not of plaque area (P=0.13); in logistic regression, Lp(a) significantly predicted occlusion (P=0.001). Patients with occlusion had significantly higher levels of Lp(a): 0.27+/-0.25 g/L versus 0.17+/-0.18 g/L without occlusion; P=0.007.
Conclusions:
Lp(a) was a significant independent predictor of carotid stenosis and occlusion, but not of carotid plaque area, supporting the hypothesis that the effect of Lp(a) on atherogenesis and cardiovascular risk is largely related to thrombosis and impaired fibrinolysis. Stenosis and occlusion may not be attributable to plaque progression, but to plaque rupture and thrombosis; this relationship may also apply to other arterial beds.
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