ReviewCurrent atherosclerosis reports2026
Top 10 Concepts in Secondary ASCVD Prevention From the 2026 ACC/AHA Dyslipidemia Guideline: What Is New and Why It Matters.
Review in Current atherosclerosis reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purpose of reviewThe 2026 American College of Cardiology/American Heart Association (ACC/AHA) dyslipidemia guideline represents a major shift in secondary prevention of atherosclerotic cardiovascular disease (ASCVD), moving beyond a predominantly low-density lipoprotein cholesterol (LDL-C)-centered model toward earlier, lower, longer, and more individualized lipid-lowering strategies. This review summarizes 10 practice-changing concepts from the guideline with direct relevance to patients with clinical ASCVD. RECENT
findingsDespite high-intensity statin therapy, substantial residual cardiovascular risk may persist because of delayed treatment intensification, persistent apolipoprotein B (apoB)-containing lipoprotein burden, elevated lipoprotein(a) [Lp(a)], triglyceride-rich remnants, and high-risk cardiovascular-kidney-metabolic (CKM) comorbidities. Major updates include reintroduction of goal-directed therapy, lower LDL-C and non-high-density lipoprotein cholesterol (non-HDL-C) targets, and broader use of non-statin therapies, including ezetimibe, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, bempedoic acid, and inclisiran. In patients with clinical ASCVD at very high risk, LDL-C and non-HDL-C targets of < 55 mg/dL and < 85 mg/dL, respectively, are recommended. The guideline also emphasizes structured lipid monitoring and a systematic approach to statin-attributed muscle symptoms to reduce therapeutic inertia, preserve effective lipid-lowering therapy, and support sustained goal attainment. Collectively, these updates mark a transition toward precision lipidology, emphasizing individualized risk assessment, earlier treatment escalation, structured follow-up, preservation of effective therapy despite treatment-related symptoms, and more comprehensive reduction of residual cardiovascular risk in secondary prevention.
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