HDL subfractions determined by microfluidic chip electrophoresis predict the vulnerability of intracranial plaque: A HRMRI study

High-density lipoprotein (HDL) can be divided into several subfractions based on density, size and composition. Accumulative evidence strongly suggests that the subfractions of HDL have very different roles in the pathogenesis of atherosclerosis. The purpose of this study was to further delineate the relationship between HDL subfractions extracted by microfluidic chip electrophoresis and the vulnerability of plaques in patients with intracranial atherosclerosis with a high-resolution magnetic resonance imaging (HRMRI) study.We prospectively enrolled patients with single atherosclerotic plaque in the middle cerebral artery (MCA) or basilar artery (BA) between July 2020 and Dec 2022 and performed 3-tesla HRMRI on the relevant artery. The HDL cholesterol concentration and HDL subfractions (HDL-2a, HDL-2b and HDL-3) percentage were analyzed in serum samples from the same patients by electrophoresis on a microfluidics system.A total of 81 MCA or BA plaques [38 (46.9%) symptomatic and 43 (53.1%) asymptomatic] in 81 patients were identified on HRMRI. Patients with symptomatic plaques had a significantly lower HDL-2b level than asymptomatic plaques [symptomatic vs. asymptomatic: 0.16 (0.10-0.18) vs. 0.27(0.21-0.34), p = 0.001]. After adjusting for demographics and vascular risk factors, logistic regression showed that HDL-2b was inversely associated with asymptomatic plaques (B = -0.04, P = 0.017). According to receiver operating characteristic (ROC) curve model analysis, the cutoff point of HDL-2b in predicting asymptomatic plaques was 0.21 mmol/L (Area under curve: 0.719, specificity: 73.7%, sensitivity: 72.1%). Furthermore, plaque enhancement on HRMRI (P < 0.001), positive remodeling (P < 0.001), plaque load (P < 0.001) and luminal stenosis (P < 0.001) were superior among patients with HDL-2b < 0.21 mmol/L.Our data showed that serum HDL-2b levels may serve as a biomarker for predicting vulnerability in intracranial atherosclerotic plaques.