Program

Lecture Abstract：
Traditional lipid panels often underestimate residual cardiovascular risk, particularly in ischemic stroke etiology. Apolipoprotein B (ApoB) and Lipoprotein(a) [Lp(a)] have emerged as critical, independent biomarkers that refine risk stratification and guide targeted prevention strategies.
Every atherogenic particle—including LDL, VLDL, and IDL—carries exactly one molecule of ApoB. Consequently, ApoB provides an accurate measure of total atherogenic particle number. It outperforms traditional LDL cholesterol (LDL-C) in predicting ischemic stroke risk, particularly in patients with metabolic syndrome or discordant lipid levels where cholesterol mass misrepresents true particle burden. Data from major epidemiological studies identify the ApoB/ApoA1 ratio as a premier lipid predictor for stroke.
Concurrently, Lp(a) is a highly atherogenic, pro-inflammatory, and pro-thrombotic particle. Because plasma levels are predominantly genetically determined, standard lipid-lowering therapies like statins fail to reduce them. Elevated Lp(a) (≥50 mg/dL or ≥125 nmol/L) acts as a potent lifelong risk-enhancing factor, driven primarily by its strong association with large-artery atherosclerosis.
While intensive LDL-C and ApoB lowering remains the cornerstone of secondary prevention—utilizing high-intensity statins, ezetimibe, and PCSK9 inhibitors—the therapeutic landscape for Lp(a) is rapidly evolving. Novel RNA-targeted therapies, such as antisense oligonucleotides and siRNAs, can lower Lp(a) by up to 90%. However, the clinical outcome benefits need to be evaluated from current ongoing clinical trials.
I will review the pathophysiological mechanisms of ApoB and Lp(a) in cerebrovascular disease, discuss their integration into current clinical guidelines, including Taiwan’s 2026 consensus from TSLA and evaluate emerging targeted therapeutics aimed at mitigating residual stroke risk.