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Published on: October 12, 2017
Association of lipoprotein(a), oxidized phospholipids and apolipoprotein B100 in acute ischemic stroke cohort
Yihao Li1, Emmie Then1, Salwa Rahman2
1Department of Medicine, Division of Preventive Medicine and Nutrition, Columbia University Vagelos College of Physicians and Surgeons, 630 West 168th Street, P & S 8-503, New York, NY 10032, USA.
Insights
High lipoprotein(a) [Lp(a)] levels and specific Lp(a) biomarkers are linked to atherosclerotic stroke. These findings highlight Lp(a) as a key factor in stroke development, particularly extracranial atherosclerotic disease (ECAD).
Area of Science:
- Cardiovascular Science
- Neurology
- Biomarkers
Background:
- Atherosclerosis in major arteries is a leading cause of stroke.
- Elevated lipoprotein(a) [Lp(a)] levels are implicated in atherosclerotic stroke, particularly intracranial disease.
- The specific role of Lp(a) in different ischemic stroke subtypes requires further clarification.
Purpose of the Study:
- To investigate the association between Lp(a)-related biomarkers and ischemic stroke subtypes.
- To clarify the role of Lp(a) in the pathogenesis of atherosclerotic stroke.
Main Methods:
- Analysis of plasma samples from 244 acute ischemic stroke patients.
- Measurement of Lp(a) concentrations, apolipoprotein B100 (APOB), and oxidized phospholipids (OxPL) using ELISA.
- Determination of APO(a) isoform size via gel electrophoresis and stroke subtype classification.
Main Results:
- High Lp(a) concentrations, percentage of APOB in Lp(a), and OxPL-APO(a) were significantly associated with atherosclerotic stroke.
- These biomarkers were also significantly associated with extracranial atherosclerotic stroke (ECAD).
Conclusions:
- Lp(a) concentration, APOB percentage within Lp(a), and OxPL-APO(a) are positively linked to acute atherosclerotic ischemic stroke.
- These findings underscore the role of Lp(a) and its modifications in the development of atherosclerotic stroke, especially ECAD.
Aims:
Atherosclerosis, affecting the aorta, cervical, or intracranial arteries, is a common cause of stroke. Previous studies have shown a strong link between high Lp(a) levels and atherosclerotic stroke due to intracranial atherosclerotic disease, implicating Lp(a) in disease development and progression. The precise role of Lp(a) in stroke subtypes remains unclear, although smaller isoform sizes and oxidized phospholipids on Lp(a) are associated with the disease presence. To clarify Lp(a)'s connection with ischemic stroke subtypes, we evaluated various plasma biomarkers previously linked to Lp(a) and disease.
Methods:
We used stored plasma samples and data from 244 participants enrolled in an acute ischemic stroke registry at Columbia University Medical Center in New York. Plasma Lp(a) concentrations, apolipoprotein B100 (APOB), and oxidized phospholipids were measured via enzyme-linked immunosorbent assay. APO(a) isoform size was measured via gel electrophoresis. Stroke subtypes were classified based on etiologies using clinical and imaging data. Adjusted multivariate logistic regression models were built to assess associations between Lp(a)-related biomarkers and stroke subtype.
Results:
In participants with acute ischemic stroke, high Lp(a) concentrations, percentage of APOB in Lp(a), and OxPL-APO(a) concentrations were significantly associated with the presence of atherosclerotic stroke compared to those with non-atherosclerotic strokes [OR = 1.30 (p = 5.7e - 3), 1.29 (p = 6.9e - 3), 1.27 (p = 1.7e - 2), respectively]. In participants with atherosclerotic stroke, these changes were significantly associated with extracranial atherosclerotic stroke (ECAD), with an OR = 0.69, p = 4e - 2.
Conclusion:
In addition to Lp(a) concentrations, the percentage of APOB in Lp(a), and OxPL-APO(a) concentrations are positively associated with acute atherosclerotic ischemic stroke, specifically ECAD.
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