Deep subcortical infarct burden in relation to apolipoprotein B/AI ratio in patients with intracranial atherosclerotic stenosis
Correspondence: J.-H. Park, Department of Neurology, Kwandong University Myongji Hospital, 697-24 Hwajeong-dong, Deokyang-gu Goyang, Gyeonggi-do 412-270, Korea (tel.: +82-31-810-5417; fax: +82-31-969-0500; e-mail: email@example.com).
Background and purpose
Pre-existing brain infarct (PBI), frequently seen on magnetic resonance imaging and usually silent, is recognized as a risk factor for future stroke. Increased apolipoprotein B (apoB)/apoAI ratio is known to be a risk predictor of ischaemic stroke and is associated with intracranial atherosclerotic stenosis (ICAS). However, little is known about the association of apoB/apoAI ratio with PBI.
A total of 522 statin-/fibrate-naïve Korean patients, who experienced acute ischaemic stroke, were categorized into three groups: ICAS (n = 254), extracranial (n = 51), and no cerebral atherosclerotic stenosis (n = 217). We explored the association between apoB/apoAI ratio and PBI lesions according to atherosclerosis type (ICAS, ECAS, and NCAS), PBI location (deep subcortical [ds-PBI] versus hemispheric [h-PBI]), and symptomatic PBI (s-PBI) which was relevant to a prior clinical stroke event.
Pre-existing brain infarct(+) patients showed a higher apoB/apoAI ratio than PBI(−) patients (0.81 ± 0.28 vs. 0.72 ± 0.23, P < 0.001). In ICAS group, patients with higher apoB/apoAI ratio quartiles had more PBIs, ds-PBIs, and s-PBIs (P = 0.020, P = 0.025, and P = 0.001, respectively). With multivariable analyses, the highest apoB/apoAI ratio quartile was associated with PBI (OR, 2.56; 95% CI, 1.39–4.73), ds-PBI (2.48; 1.33–4.62), and advanced (≥3) ds-PBIs (2.68; 1.27–5.63) in ICAS group, but not with h-PBI. s-PBI had a dose–response relationship with apoB/apoAI ratio quartiles (6.18; 1.31–29.13 for the second; 5.34; 1.06–26.83 for the third; and 12.17; 2.50–59.19 for the fourth quartile), when referenced to the first quartile.
ApoB/apoAI ratio is associated with asymptomatic deep subcortical ischaemic burden as well as with symptomatic lesion in patients with ICAS.