High-Sensitivity C-Reactive Protein and Atherogenic Lipid Phenotypes in Early Acute Coronary Syndromes: Inflammatory-Lipid Interactions, Plaque Instability, and Prognostic Implications for Precision Cardiovascular Risk Stratification

Abstract Background: Acute coronary syndromes (ACS) represent a critical manifestation of cardiovascular disease, driven by complex interactions between inflammation and lipid metabolism. High-sensitivity C-reactive protein (hs-CRP) serves as a key biomarker of systemic inflammation, while atherogenic lipid phenotypes, including elevated low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), and apolipoprotein B (apoB), contribute to plaque formation and instability. This review explores the interplay between hs-CRP and atherogenic lipids in early ACS, their role in plaque vulnerability, and implications for prognostic risk stratification in precision medicine. Methods: A comprehensive literature review was conducted using databases such as PubMed, Scopus, and Web of Science, focusing on studies from 2000 to 2026. Inclusion criteria encompassed prospective cohort studies, randomized controlled trials (RCTs), and meta-analyses examining hs-CRP, lipid profiles, and ACS outcomes. Data synthesis involved qualitative and quantitative analysis of inflammatory-lipid interactions, plaque instability mechanisms, and prognostic models. Results: Elevated hs-CRP levels (>2 mg/L) independently predict adverse outcomes in early ACS, with synergistic effects when combined with atherogenic lipids (e.g., LDL-C >100 mg/dL). Inflammatory processes enhance lipid oxidation, monocyte recruitment, and matrix degradation, leading to thin-cap fibroatheroma (TCFA) and plaque rupture. Prognostic models incorporating hs-CRP and lipid indices (e.g., atherogenic index of plasma [AIP]) improve risk stratification, identifying high-risk patients for targeted therapies like statins and anti-inflammatory agents. Conclusion: The integration of hs-CRP and atherogenic lipid phenotypes enhances understanding of ACS pathogenesis and enables precision risk stratification. Future research should focus on novel therapeutics modulating these pathways to reduce residual inflammatory and lipid risks. Keywords: High-sensitivity C-reactive protein, Atherogenic lipids, Acute coronary syndromes, Inflammation, Plaque instability, Risk stratification