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Purpose <p>This study aims to explore the connection between the Monocyte to High-Density Lipoprotein Cholesterol Ratio (MHR) and the formation of carotid artery plaque (CAP) in individuals who have experienced a cerebral infarction (CI). Additionally, it examines the relationship between CAP and varying blood pressure and glucose metabolism stratifications.</p> Method <p>The investigation involved 10,627 individuals with cerebral infarction. Participants were categorized based on their blood pressure levels and glucose metabolism profiles, and then sorted into tertiles according to their MHRs. Logistic regression analysis was used to assess the relationship between MHR and carotid plaque in CI patients, adjusting for potential confounders and applying FDR correction. Discrimination performance was evaluated using ROC curves, NRI, and IDI. Restricted cubic splines and threshold analysis were employed to explore dose-response relationships and identify inflection points.</p> Result <p>MHR demonstrated a significant positive association with carotid artery plaque (CAP) in patients with cerebral infarction. For each one-standard deviation increase in standardized MHR, the adjusted OR was 1.154 (95% CI: 1.079–1.235, <i>P</i> &lt; 0.001). The strongest association was found in the T3 group (MHR &gt; 0.552) (OR = 1.392, <i>P</i> &lt; 0.001), which remained significant after FDR correction. Subgroup analysis indicated that this association was significant in individuals with prehypertension (OR = 1.169, <i>P</i> = 0.020), hypertension (OR = 1.180, <i>P</i> &lt; 0.001), prediabetes (OR = 1.158, <i>P</i> &lt; 0.05), and diabetes (OR = 1.137, <i>P</i> &lt; 0.05). After FDR adjustment, the association remained robust in the hypertension group (FDR-adjusted <i>P</i> = 0.004) and the prediabetes group (FDR-adjusted <i>P</i> = 0.030). MHR displayed a nonlinear association with CAP (P for nonlinear = 0.04) and a threshold effect, with an inflection point at 0.89 (OR = 2.47, <i>P</i> &lt; 0.001 when MHR &lt; 0.89). Incorporating MHR improved the model’s AUC to 0.746 (<i>P</i> = 0.049), with NRI = 0.095 and IDI = 0.002 (both <i>P</i> &lt; 0.001).</p> Conclusion <p>In patients with cerebral infarction, MHR is significantly associated with carotid plaque. This association remains robust in hypertensive and prediabetic patients after FDR adjustment. Furthermore, MHR exhibits a nonlinear relationship with carotid plaque and a threshold effect at an inflection point of 0.89, significantly enhancing plaque discrimination performance.</p>

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Investigating the relationship between monocyte to high-density lipoprotein cholesterol ratio and carotid artery plaque in cerebral infarction patients under different blood pressure and glucose metabolic conditions

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月7日

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  • Shencheng Luo,
  • Kun Ma,
  • Ting Liu,
  • Jiawen Dong,
  • Lin Zhu,
  • Sitong Shen,
  • Bernhard Kolberg,
  • Jing Li,
  • Jiangwei Shi,
  • Junhua Zhang

摘要

Purpose

This study aims to explore the connection between the Monocyte to High-Density Lipoprotein Cholesterol Ratio (MHR) and the formation of carotid artery plaque (CAP) in individuals who have experienced a cerebral infarction (CI). Additionally, it examines the relationship between CAP and varying blood pressure and glucose metabolism stratifications.

Method

The investigation involved 10,627 individuals with cerebral infarction. Participants were categorized based on their blood pressure levels and glucose metabolism profiles, and then sorted into tertiles according to their MHRs. Logistic regression analysis was used to assess the relationship between MHR and carotid plaque in CI patients, adjusting for potential confounders and applying FDR correction. Discrimination performance was evaluated using ROC curves, NRI, and IDI. Restricted cubic splines and threshold analysis were employed to explore dose-response relationships and identify inflection points.

Result

MHR demonstrated a significant positive association with carotid artery plaque (CAP) in patients with cerebral infarction. For each one-standard deviation increase in standardized MHR, the adjusted OR was 1.154 (95% CI: 1.079–1.235, P < 0.001). The strongest association was found in the T3 group (MHR > 0.552) (OR = 1.392, P < 0.001), which remained significant after FDR correction. Subgroup analysis indicated that this association was significant in individuals with prehypertension (OR = 1.169, P = 0.020), hypertension (OR = 1.180, P < 0.001), prediabetes (OR = 1.158, P < 0.05), and diabetes (OR = 1.137, P < 0.05). After FDR adjustment, the association remained robust in the hypertension group (FDR-adjusted P = 0.004) and the prediabetes group (FDR-adjusted P = 0.030). MHR displayed a nonlinear association with CAP (P for nonlinear = 0.04) and a threshold effect, with an inflection point at 0.89 (OR = 2.47, P < 0.001 when MHR < 0.89). Incorporating MHR improved the model’s AUC to 0.746 (P = 0.049), with NRI = 0.095 and IDI = 0.002 (both P < 0.001).

Conclusion

In patients with cerebral infarction, MHR is significantly associated with carotid plaque. This association remains robust in hypertensive and prediabetic patients after FDR adjustment. Furthermore, MHR exhibits a nonlinear relationship with carotid plaque and a threshold effect at an inflection point of 0.89, significantly enhancing plaque discrimination performance.