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The Combination of Hyperuricemia and Elevated High-Sensitivity C-Reactive Protein Increased the Risk of Cardiac

Na Li1, Liufu Cui1, Gary Tse2,3

  • 1Department of Rheumatology and Immunology, Kailuan General Hospital, Tangshan, Hebei Province, People's Republic of China.

Journal of Inflammation Research
|June 17, 2024
PubMed

Insights

High uric acid (HUA) and high-sensitivity C-reactive protein (hs-CRP) significantly increase cardiac conduction block (CCB) risk, particularly atrioventricular block. hs-CRP partially mediates the link between uric acid and CCB development.

Area of Science:

  • Cardiology
  • Biochemistry
  • Epidemiology

Background:

  • Hyperuricemia (HUA) and elevated high-sensitivity C-reactive protein (hs-CRP) are independently associated with cardiovascular disease.
  • The combined impact of HUA and low-grade inflammation on cardiac conduction block (CCB) risk is not well understood.
  • Investigating the potential mediating role of hs-CRP in the relationship between uric acid (UA) and CCB is crucial for understanding disease mechanisms.

Purpose of the Study:

  • To examine the association between combined hyperuricemia and elevated hs-CRP levels with the incidence of cardiac conduction block (CCB).
  • To determine if hs-CRP mediates the effect of uric acid on the risk of developing CCB.

Main Methods:

  • A prospective cohort study of 81,896 individuals without baseline CCB from the Kailuan cohort.
  • Participants were stratified into four groups based on HUA and hs-CRP levels (low-grade inflammation defined as hs-CRP > 3 mg/L).
  • Cox regression and mediation analyses were used to assess CCB risk and the mediating role of hs-CRP.

Main Results:

  • The combination of HUA and low-grade inflammation was associated with increased risks of CCB (HR: 1.56), atrioventricular block (AVB) (HR: 1.88), and right bundle branch block (HR: 1.47) compared to the low UA/low CRP group.
  • In individuals with HUA, the overall risk of CCB increased by 14.0% compared to those without HUA.
  • Mediation analysis indicated that 10.3% of the increased CCB risk in the HUA group was attributable to hs-CRP.

Conclusions:

  • Concomitant hyperuricemia and elevated hs-CRP significantly elevate the risk of cardiac conduction block, with a notable impact on atrioventricular block.
  • The association between uric acid levels and CCB risk is partly explained by the mediating effect of hs-CRP.
  • These findings highlight the importance of managing both HUA and inflammation for cardiovascular protection.
Abstract

Keywords:
cardiac conduction blockcombined exposurehyperuricemiainflammationmediationrisk factors

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