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C-reactive protein and residual cardiovascular risk in hypertension: a prospective cohort study
Anping Cai1, Junguo Zhang2, Stephen A Clarkson3
1Department of Cardiology, Hypertension Research Laboratory, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, China.
Insights
Elevated C-reactive protein (CRP), a marker of inflammation, is linked to increased risk of major adverse cardiovascular events (MACE) in hypertensive patients even with controlled systolic blood pressure (SBP). This suggests inflammation plays a role in residual cardiovascular risk.
Area of Science:
- Cardiovascular Medicine
- Inflammation Research
- Public Health
Background:
- Systolic blood pressure (SBP) control is crucial for preventing major adverse cardiovascular events (MACE) in hypertension.
- However, residual MACE risk persists in many hypertensive individuals with controlled SBP, with underlying mechanisms unclear.
- Systemic inflammation, indicated by C-reactive protein (CRP), is a potential contributor to this residual risk.
Purpose of the Study:
- To investigate the association between elevated CRP levels and residual MACE risk in hypertensive individuals with controlled SBP.
- To determine if CRP is an independent predictor of MACE in this population.
- To explore the interaction between CRP levels and SBP control on MACE risk.
Main Methods:
- Utilized data from the UK Biobank study, including 200,243 community-dwelling hypertensive individuals without baseline cardiovascular disease.
- Categorized baseline CRP as normal (<2 mg/L) or elevated (≥2 mg/L) and SBP into <120, 120-129, 130-139, and ≥140 mmHg.
- Assessed the primary outcome of MACE (composite of coronary heart disease, myocardial infarction, stroke, cardiovascular death) over a median follow-up of 12.4 years.
Main Results:
- 40.4% of participants had elevated CRP levels (≥2 mg/L).
- Higher incidence rates of MACE were observed in the elevated CRP group (12.01 vs 9.27 per 1000 person-years).
- Elevated CRP was associated with a 17% higher adjusted risk of MACE, particularly significant when SBP ranged from 120-139 mmHg, independent of antihypertensive therapy.
Conclusions:
- Elevated CRP is significantly associated with residual MACE risk in hypertensive individuals, even with controlled SBP.
- Systemic inflammation may be a key factor driving cardiovascular events in this population.
- CRP warrants further investigation as a potential therapeutic target to mitigate residual cardiovascular risk in hypertension.
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.
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