Elevated C-reactive protein and cardiovascular risk

Purpose of review This review critically examines the evolving role of C-reactive protein (CRP) in cardiovascular disease (CVD), addressing its pathogenesis and relationship with various CVDs including coronary artery disease (CAD), heart failure, and atrial fibrillation. Recent findings CRP is mechanistically implicated in endothelial dysfunction, oxidative stress, and plaque destabilization. Recent studies demonstrate that lipid-lowering agents (statins, bempedoic acid) and anti-inflammatory therapies (canakinumab, colchicine) reduce CRP levels and improve outcomes in CAD. In heart failure, elevated CRP predicts adverse events, though evidence on phenotypes varies, and novel therapies (glucagon-like peptide-1 agonists, sodium-glucose cotransporter-2 inhibitors) lower CRP independently of weight loss. For atrial fibrillation, CRP correlates with postoperative incidence and recurrence postablation, though data remain inconsistent. Guidelines offer differing opinion with the American College of Cardiology and the American Heart Association (ACC/AHA) guidelines cautiously endorsing CRP for risk stratification in intermediate-risk individuals, while European guidelines advise against its routine use for primary prevention, reflecting unresolved questions about CRP's additive value. Summary CRP remains a pivotal inflammation biomarker in CVD, yet its causal role and clinical applicability require clarification. While CRP-guided therapies show promise, discrepancies in guidelines highlight the need for robust trials to determine whether targeting CRP directly improves outcomes. Future research should focus on CRP's pathophysiological mechanisms and validate its utility in personalized CVD management.