To explore the role of apolipoprotein A (apoA), apolipoprotein B (apoB), and lipoprotein(a) (lpa) in the formation of intracranial atherosclerosis (ICAS) and development of ischemic stroke (IS). 

Although numerous studies have linked LDL and HDL cholesterol levels to ICAS and IS, previous research has not fully examined other lipids that are not routinely measured in clinical care, such as apoA, apoB, and lpa. 

This is a secondary analysis of stroke-free patients in Atherosclerosis Risk in Communities who had lipid measurements in 1987-89 and vessel wall MRI in 2011-13. The primary outcomes were ≥50% ICAS of a major intracranial artery on MRI and incident IS from 1987-2014. We compared lipid levels with Student’s t-test and further divided lipid levels into quartiles and report: 1) comparison of the highest to lowest quartile for logistic regression fit to ≥ 50% ICAS and 2) Cox regression fit to IS, both adjusted for patient age, sex, race, cigarette smoking, history of hypertension, statin use, and diabetes.

We included 1,536 patients, of which 152 (9.9%) had ≥50% ICAS and 56 (3.7%) had IS. The levels of apoA, apoB, and lpa in patients with vs. without ≥ 50% ICAS were 133.7 vs. 137.3 mg/dl (p=0.17), 95.1 vs. 89.6 mg/dl (p=0.02), and 109.2 vs. 97.7 ug/mL (p=0.19). The levels of apoA, apoB, and lpa in patients with vs. without IS were 131.6 vs. 137.1 mg/dl (p=0.19), 99.7 vs. 89.8 mg/dl (p=0.01), and 109.5 vs. 98.4 ug/mL (p=0.43). ApoA and lpa were not associated with our outcomes in  multivariate models. The highest quartile of apoB had an odds ratio of 1.74 for ≥50% ICAS (95% CI, 1.04-2.92, p=0.037) and hazard ratio of 2.50 for ischemic stroke (95% CI, 1.04-2.92, p=0.037).

ApoB is associated with ICAS and IS over two decades of follow-up, which has implications for primary prevention efforts.