Relationship between carotid atherosclerotic plaques and 90-day prognosis after acute ischemic stroke mediated by multiple inflammatory factors: A cohort and Mendelian randomization study
Tonglong Jin1, Yuan Zhu1, Hui Huang1
1Department of Neurology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China; Department of Neurology, Jiangsu Province Hospital of Chinese Medicine, Nanjing 210029, China.
Insights
Maximum carotid plaque thickness correlates with poor outcomes after acute ischemic stroke, with inflammatory factors mediating this effect. Carotid intima-media thickness also causally increases stroke risk, though oncostatin M may mitigate this.
Area of Science:
- Cardiovascular Medicine
- Neurology
- Inflammation Research
Background:
- Investigated the link between carotid plaque thickness (cPTmax) and carotid intima-media thickness (cIMT) with 90-day prognosis in acute ischemic stroke (AIS) patients.
- Explored the mediating roles of inflammatory factors in this relationship.
Purpose of the Study:
- To determine the prognostic value of cPTmax and cIMT in AIS.
- To elucidate the mediating mechanisms involving inflammatory markers and oncostatin M (OSM).
Main Methods:
- Enrolled 951 AIS patients, measuring cPTmax, monocytes (Mono), lymphocyte-monocyte ratio (LMR), and monocyte-to-high-density lipoprotein ratio (MHR).
- Utilized ROC curve analysis for mediating variables and two-sample Mendelian randomization (MR) to assess cIMT's causal effect on ischemic stroke (IS) and OSM's mediation.
Main Results:
- cPTmax positively correlated with poor 90-day outcomes (p < 0.001).
- Mono, LMR, and MHR acted as positive mediators. MR showed cIMT positively associated with IS (β = 3.115).
- OSM demonstrated a negative mediating role with a 7.5% mediating effect value.
Conclusions:
- cPTmax predicts poor prognosis post-AIS, mediated by inflammatory factors like Mono, LMR, and MHR.
- cIMT has a causal relationship with increased IS risk.
- OSM may play a protective role by reducing IS risk.
Background:
We explored the relationship between maximum carotid plaque thickness (cPTmax), carotid intima-media thickness (cIMT), and the 90-day prognosis of patients with acute ischemic stroke (AIS), as well as the mediating roles of inflammatory factors.
Methods:
We enrolled 951 patients with AIS who underwent carotid artery ultrasonography between June 2019 and November 2023. cPTmax, monocytes (Mono) and the calculated lymphocyte-monocyte ratio (LMR) and monocyte-to-high-density lipoprotein ratio (MHR) values were obtained. Receiver operating characteristic (ROC) curve analysis was used to determine the sensitivity and specificity of Mono, LMR, and MHR as mediating variables, and their predictive value for poor prognosis was evaluated. We then performed two-sample Mendelian randomization to estimate the independent effect of cIMT on IS and explored the mediation effect of oncostatin M (OSM).
Results:
cPTmax was positively correlated with the poor outcomes (p < 0.001). Mediation analysis revealed that multiple inflammatory factors, including Mono, LMR, and MHR, acted as positive mediators. In the two-sample Mendelian randomization, we found that cIMT was positively associated with ischemic stroke (β = 3.115, 95 % CI: 1.519-4.710), whereas OSM played a negative mediating role, with a mediating effect value of 7.5 %.
Conclusions:
Our cohort study showed a positive correlation between cPTmax and poor prognosis 90 days after acute stroke, with Mono, LMR, and MHR mediating this process. A Mendelian randomization (MR) study showed a causal relationship between an increase in cIMT and an increased risk of IS. The mediating role of OSM in this process can reduce the risk of IS.
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