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Recent evidence has shifted emphasis from conventional lipid fractions to apolipoprotein B (ApoB)-containing lipoproteins, including lipoprotein(a) [Lp(a)], which more accurately reflect atherogenic particle burden than low-density lipoprotein cholesterol (LDL-C) alone and are increasingly used for stroke risk stratification. While the principle \u201cthe faster and the lower, the better\u201d underpins dyslipidemia management, evidence-based, subtype-specific lipid strategies in stroke remain limited. Intensive LDL-C reduction significantly lowers recurrent IS risk; however, uniform lipid targets are often applied without accounting for stroke etiology. High-intensity statins remain first-line therapy, with pleiotropic benefits extending beyond LDL-C reduction. For statin intolerance or suboptimal response, ezetimibe and PCSK9 inhibitors provide potent, bleeding-neutral LDL-C lowering. Inclisiran and bempedoic acid broaden therapeutic options, although stroke-specific efficacy data are still pending. Lp(a)-lowering agents, including pelacarsen, olpasiran, and lepodisiran, are under active evaluation and may address residual cardiovascular risk. For triglyceride lowering, recent randomized evidence supports icosapent ethyl for reducing IS risk. In intracerebral hemorrhage (ICH), the optimal intensity and thresholds of lipid lowering remain uncertain, warranting individualized weighting of ischemic against hemorrhagic risk, particularly in patients with lobar ICH or suspected cerebral amyloid angiopathy (CAA). In such cases, hydrophilic statins, ezetimibe, or PCSK9 inhibitors may represent reasonable options. This review synthesizes current evidence and proposes a phenotype-guided, individualized framework for dyslipidemia management across stroke subtypes. 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