C-Reactive Protein (CRP), High Sensitivity, Quantitative

C-Reactive Protein (CRP), High Sensitivity, Quantitative—also referred to as hs‑CRP, Cardio CRP, or ultra‑sensitive CRP—assesses subtle systemic inflammation relevant to cardiovascular disease. CRP rises within hours of an inflammatory trigger and broadly reflects inflammatory burden, often changing sooner than the erythrocyte sedimentation rate. In clinical practice, the hs‑CRP test is used to estimate cardiovascular risk in asymptomatic individuals in conjunction with other markers; to inform prognosis for adverse outcomes such as myocardial infarction, stroke, and sudden cardiac death among patients with coronary artery disease and hypertension; and to track response to preventive therapies, including statins and antiplatelet agents.

CRP is a hepatic acute‑phase glycoprotein whose synthesis is driven by proinflammatory cytokines, notably interleukin‑6, interleukin‑1, and TNF‑α. Production begins to increase approximately 6 hours after an inflammatory stimulus, and serum concentrations can rise 10–100‑fold within 24–48 hours. Levels >100 mg/L are typical of bacterial infections, whereas viral infections more often remain <20 mg/L. CRP also increases in the setting of tissue necrosis, exemplified by myocardial infarction, and with tumor necrosis. Functionally, CRP participates in complement activation, activation of monocytes, and upregulation of endothelial adhesion molecules (ICAM‑1, VCAM‑1, E‑selectin). It also binds and modifies LDL particles, mechanistically linking low‑grade vascular inflammation to atherogenesis. Baseline elevations detectable only with high‑sensitivity methods (hs‑CRP/Cardio CRP) reflect vascular inflammation and are associated with incident hypertension, myocardial infarction, stroke, sudden cardiac death, type 2 diabetes, and peripheral arterial disease. Among patients with established coronary artery disease, higher CRP associates with recurrent events and complications after revascularization. Lifestyle modification and pharmacologic therapy (eg, statins and aspirin) typically lower CRP in parallel with reduction of vascular inflammation. For risk assessment, baseline hs‑CRP should be measured at least 2 weeks after recovery from any acute illness or disease exacerbation. Markedly elevated values (>10 mg/L) prompt evaluation for active inflammatory or infectious conditions.