Association of lipoprotein(a), oxidized phospholipids and apolipoprotein B100 in acute ischemic stroke cohort

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.