The relation between C-reactive protein (CRP) and risk of incident heart failure in patients with cardiovascular disease: a narrative review.

Cardiovascular disease (CVD) remains a leading global cause of morbidity and mortality, with heart failure (HF) significantly contributing to this burden. Elevated C-reactive protein (CRP), a biomarker of systemic inflammation, has been implicated in the pathogenesis of various cardiovascular conditions, including HF. This narrative review examines the relationship between CRP levels and the risk of incident HF in patients with pre-existing CVD. By synthesizing findings from prospective cohort studies, clinical trials, and meta-analyses, we aim to assess the potential role of CRP as a predictive biomarker for HF onset. Inflammation is a critical component in HF pathophysiology, contributing to myocardial remodeling, fibrosis, and endothelial dysfunction. High-sensitivity CRP (hs-CRP) assays allow for the detection of low-grade inflammation, offering improved risk stratification for cardiovascular events. Studies indicate that elevated hs-CRP levels correlate with an increased risk of myocardial infarction, stroke, and HF development. However, CRP's specificity as a marker remains a challenge due to its association with various systemic inflammatory conditions. Recent research has explored CRP's role in HF subtypes, particularly HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Despite growing evidence linking CRP to HF, gaps remain in understanding its mechanistic role, optimal clinical thresholds, and therapeutic implications. Future research should focus on mechanistic studies elucidating CRP's direct impact on myocardial dysfunction, subgroup-specific analyses, and interventional trials targeting CRP-driven inflammation. Addressing these gaps could significantly improve HF prevention and management by leveraging CRP as a viable prognostic and therapeutic target.