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Correlation analysis of hematocrit level and coronary heart disease in patients with chest pain: a case-control study
Jiahong Xie1,2, Hongshuai Cao3, Dongxu Jin2
1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Insights
Hematocrit (HCT) is an independent risk factor for coronary heart disease (CHD). Elevated HCT levels increase the risk of CHD, potentially through hemodynamic mechanisms like increased wall shear stress.
Area of Science:
- Cardiology
- Biomedical Engineering
- Hemodynamics
Background:
- Controversy exists regarding hematocrit (HCT) as a risk factor for coronary heart disease (CHD).
- Investigating the impact of low or high HCT on CHD development is crucial.
- Understanding the hemodynamic mechanisms underlying HCT's effect on CHD is needed.
Purpose of the Study:
- To explore the effect of low or high hematocrit (HCT) on coronary heart disease (CHD).
- To analyze the underlying hemodynamic mechanisms.
- To determine if HCT is an independent risk factor for CHD.
Main Methods:
- Retrospective analysis of 3,200 patients undergoing coronary angiography or CTA.
- Coronary artery stenosis ≥50% defined as CHD.
- Logistic regression for HCT and CHD relationship; computational fluid dynamics (CFD) for wall shear stress (WSS).
Main Results:
- Hematocrit (HCT) is an independent risk factor for coronary heart disease (CHD) (RR 1.108, P<0.001).
- HCT demonstrated predictive ability for CHD events (AUC 0.726, cut-off 44.13).
- Increased HCT positively correlated with wall shear stress (WSS), potentially causing plaque rupture.
Conclusions:
- Hematocrit (HCT) is confirmed as a risk factor for coronary heart disease (CHD).
- Combining HCT with traditional risk factors may aid non-invasive CHD diagnosis.
- HCT levels may predict prognosis in patients with coronary artery stenosis, offering a new therapeutic target.
Background:
At present, there is controversy about whether hematocrit (HCT) is a risk factor for coronary heart disease (CHD). We try to explore the effect of low or high HCT on CHD, and analyze its mechanism from the perspective of hemodynamics.
Methods:
According to the exclusion criteria, a total of 3,200 patients who underwent coronary angiography or coronary computed tomography angiography (CTA) for typical post-exercise chest pain/dyspnea; atypical chest pain; or noncardiac chest pain or asymptomatic at Beijing Anzhen Hospital Affiliated to Capital Medical University from October 2019 to October 2021 were selected as research subjects. A coronary artery stenosis of 50% was used as the criterion for determining CHD. A total of 1,660 patients with coronary artery stenosis greater than 50% were selected as the CHD group and 1,540 adults with coronary artery stenosis less than 50% were selected as the non-CHD group. The clinical data, including HCT, were subjected to non-parametric tests and chi-square tests. The relationship between HCT and CHD was statistically analyzed using logistic regression. Wall shear stress (WSS) is obtained through fluent software combined with Navier-Stokes (NS) equation calculation.
Results:
Multivariate logistic regression analysis showed that HCT was an independent risk factor for CHD [risk ratio (RR) 1.108, 95% confidence interval (CI): 1.084-1.133, P<0.001]. The area under the receiver operating characteristic (ROC) curve for the ability of HCT to predict CHD events was 0.726. The cut-off value was 44.13, with specificity of 0.701 and sensitivity of 0.702. The results of a computational fluid dynamics simulation demonstrated that the magnitude of HCT is positively correlated with the WSS. When HCT exceeds 50%, the WSS of the stenosis site reaches 42 Pa, which may lead to endothelial denudation and further damage to the blood vessel, resulting in plaque rupture.
Conclusions:
HCT is one of the risk factors for CHD. Combining HCT with traditional risk factors may be helpful for non-invasive diagnosis of CHD. In addition, the level of HCT may also help to judge the future prognosis of patients with coronary artery stenosis greater than 50% without revascularization, providing a new potential target for future clinical treatment of CHD.
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