C-reactive protein and residual cardiovascular risk in hypertension: a prospective cohort study

Abstract

Control of systolic blood pressure (SBP) is important to prevent major adverse cardiovascular events (MACE) in hypertension. However, many individuals with controlled SBP still experience MACE, and the mechanisms remain relatively unknown. We sought to investigate whether elevated C-reactive protein (CRP), indicator of systemic inflammation, was associated with residual MACE risk in hypertensive individuals with controlled SBP. Community hypertensive individuals without cardiovascular disease (CVD) at baseline were included from UK Biobank study (n = 200243; mean age 58.3 years; females 50.3%; median CRP 1.6 mg/L). Baseline CRP was categorized into < 2 mg/L (normal) and ≥ 2 mg/L (elevated); and baseline SBP was categorized into < 120, 120-129, 130-139 and ≥ 140 mmHg. Primary outcome was MACE, a composite of coronary heart disease, myocardial infarction, stroke and cardiovascular death. Among included individuals, 40.4% had CRP ≥ 2 mg/L. During a median follow-up of 12.4 years, incidence rates of MACE were higher in CRP ≥ 2 mg/L group (12.01 vs 9.27 per 1000 person-years; P < 0.0001). CRP ≥ 2 mg/L in reference to CRP < 2 mg/L was associated with 17% (95% CI 14-22%) higher adjusted risk of MACE. This association was attenuated when SBP was below 120 mmHg but remained significant when SBP was at the range of 120-139 mmHg (P-interaction=0.004), irrespective of baseline antihypertensive therapy status. Elevated CRP was significantly associated with residual MACE risk in community hypertensive individuals with controlled SBP. Future studies may be warranted to evaluate whether CRP is a potential therapeutic target to reduce residual MACE risk.