Why the study?
Traditional ASCVD risk factors fail to fully reflect residual risk driven by chronic low-grade inflammation. More information was needed on whether longitudinal inflammatory burden, quantified by changes in serial hsCRP levels, provides prognostic information on how persistent inflammation drives residual risk.
Does longitudinal assessment of serial hsCRP trajectories improve prediction of all-cause and cardiovascular death in adults without known ASCVD?
Cohort (n=15,967)
Yes
Does longitudinal assessment of serial hsCRP trajectories improve prediction of all-cause and cardiovascular death in adults without known ASCVD?
Sustained or newly developed low-grade inflammation assessed via serial hsCRP measurements independently identifies individuals without known ASCVD at higher long-term risk of all-cause and cardiovascular death.
Background Traditional risk factors for atherosclerotic cardiovascular disease (ASCVD) fail to fully reflect the residual risk, driven by chronic low-grade inflammation, observed in many. Generally, high-sensitivity C-reactive protein (hsCRP) concentrations remain stable, but some individuals may experience increases. More information on whether longitudinal inflammatory burden, quantified by changes in serial hsCRP levels, provides prognostic information may improve our understanding of how persistent inflammation drives residual risk. Methods In this population-based cohort study, sequential hsCRP measurements were available in 15,967 UK Biobank participants without known history of ASCVD. The hsCRP cutoff value of 2 mg/L defined individuals with low-grade inflammation. The primary outcomes were all-cause and cardiovascular death. Results Median time between baseline (T0) and follow-up (T1) hsCRP measurement was 4.4 years. During a median follow-up of 15.3 years, 884 participants died. Compared with participants with consistently low inflammation, individuals with persistently elevated hsCRP had the highest risk of death (Hazard ratio (HR): 2.19; 95% confidence interval (CI):1.87, 2.56; p<0.001), followed by those with newly increased hsCRP (HR: 1.65; 95% CI: 1.35, 2.01; p<0.001), while participants whose hsCRP decreased (HR: 1.41; 95% CI: 1.13, 1.75; p<0.001) and those with consistently low hsCRP showed the lowest risk. Similar results were observed for cardiovascular death. These results were largely independent of age, sex, body mass index, type 2 diabetes mellitus, smoking, systolic blood pressure, low-density lipoprotein cholesterol and estimated glomerular filtration rate. Conclusion In this longitudinal assessment of hsCRP, sustained or newly developed low-grade inflammation independently identified individuals at higher risk of death. These findings emphasize the prognostic importance of cumulative persistent inflammation as a marker of residual cardiovascular risk and highlight the potential clinical value of serial hsCRP measurements to improve long-term risk stratification and preventive strategies.
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Kahles et al. (2026) conducted a cohort in Low-grade inflammation / Atherosclerotic cardiovascular disease (ASCVD) prevention (n=15,967). Persistently elevated hsCRP (≥2 mg/L) vs. Consistently low hsCRP (<2 mg/L) was evaluated on All-cause death and cardiovascular death (HR 2.19, 95% CI 1.87-2.56, p=<0.001).
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