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Association of high sensitive C-reactive protein with coronary heart disease: a Mendelian randomization study
Qian Zhuang1, Chong Shen2, Yanchun Chen1
1Department of Cardiology, Affiliated Yixing People's Hospital of Jiangsu University, Yixing, China.
Insights
High sensitivity C-reactive protein (hs-CRP) is not causally linked to coronary heart disease (CHD). However, hs-CRP may serve as a predictor for CHD incidence in the general population.
Area of Science:
- Cardiovascular Disease Epidemiology
- Genetic Epidemiology
- Biomarker Research
Background:
- The causal relationship between high sensitivity C-reactive protein (hs-CRP) and coronary heart disease (CHD) remains uncertain.
- Investigating this link is crucial for understanding cardiovascular disease (CVD) risk factors.
Purpose of the Study:
- To determine the causal effect of hs-CRP on the risk of developing CHD.
- To evaluate hs-CRP as a potential predictor for CHD incidence.
Main Methods:
- Utilized Mendelian Randomization (MR) analysis with specific CRP gene polymorphisms (rs1205, rs876537) as instrumental variables.
- Employed linear regression, survival ROC curve analysis, and Cox regression models.
- Recruited 3802 subjects for a follow-up study with a median duration of 5.01 years.
Main Results:
- Identified a hs-CRP cut-off value of 1.08 mg/L for CHD prediction with optimal sensitivity and specificity.
- Observed an increased risk of CHD incidence in participants with hs-CRP ≥ 1.08 mg/L (adjusted HR: 1.69, 95% CI: 1.11-2.60).
- Mendelian Randomization analysis revealed no significant causal association between hs-CRP and CHD (P = 0.777).
Conclusions:
- The association between hs-CRP and CHD is unlikely to be causal.
- hs-CRP may function as a valuable predictor for CHD incidence in the general population.
Objectives:
Whether high sensitivity C-reactive protein (hs-CRP) has a causal effect on coronary heart disease (CHD) is unclear. This study investigated the causal effect of hs-CRP on CHD risk using Mendelian Randomization (MR) analysis.
Methods:
A total of 3802 subjects were recruited in the follow-up study. Linear regression model was used to evaluate the relationship between CRP polymorphisms and hs-CRP. Survival receiver operator characteristic curve method was used to explore the cut-off of hs-CRP on CHD incidence. Cox regression model was applied to detect the association of hs-CRP with CHD by calculating the hazard ratio (HR) and 95% confidence interval (CI). Rs1205 and rs876537 in CRP were selected as instrumental variables in MR analysis.
Results:
During a median follow-up time of 5.01 years, 98 CHD incidence was identified (47.03/104 person-years). Hs-CRP was significantly increased among rs1205 and rs876537 genotypes with r values of 0.064 and 0.066, respectively. Hs-CRP 1.08 mg/L was identified as the cut-off value with a maximum value of sensitivity and specificity on prediction of CHD. Participants with ≥1.08 mg/L of hs-CRP has a higher risk of CHD incidence than that of participants with < 1.08 mg/L, the adjusted HR (95% CI) was 1.69 (1.11-2.60) with a P value of 0.016. No significant casual association was observed between hs-CRP and CHD with a P value of 0.777.
Conclusions:
The association between hs-CRP and CHD is unlikely to be causal, hs-CRP might be a predictor for incidence of CHD in general population.
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