Prognostic impact of neurological dysfunction assessed by modified Rankin Scale in acute myocardial infarction

Figures

• 

  Fig. 1. Identification of cases for analysis among patients with acute myocardial infarction from November 17, 2015, to October 15, 2021, and followed up until February 18, 2024a. amRS, modified Rankin Scale.

• 

  Fig. 2. Stacked bar chart of the distribution of all-cause death across mRS subgroupsa. amRS, modified Rankin Scale. This stacked bar chart shows the proportion of all-cause death and survival in AMI patients across the non-stroke group, prior ischemic stroke with mRS 0–1 group, and prior ischemic stroke with mRS 2–5 group during the median 5.26-year follow-up.

• 

  Fig. 3. Kaplan-Meier curve illustrates survival free of all-cause, cause-specific mortality in acute myocardial infarction patients without prior ischemic stroke vs. admission mRS 0–1 and mRS 2–5a. aAMI, acute myocardial infarction; CVD, cardiovascular diseases; mRS, modified Rankin Scale. Kaplan-Meier curves were used to compare the event-free survival rate of all-cause death (3a), CVD death (3b), non-CVD death (3c), AMI-specific death (3d), stroke-specific death (3e), and other CVD-related death (3f) among the three study groups. The log-rank test was performed to compare the differences in survival curves between the mRS 0–1/mRS 2–5 group and the non-stroke reference group.

• 

  Fig. 4. Cumulative incidence curves of CVD death and non-CVD death across mRS subgroups (Fine-Gray competing risk model) a. aAMI, acute myocardial infarction; CVD, cardiovascular diseases; mRS, modified Rankin Scale. Cumulative incidence curves were generated by the Fine-Gray competing risk model, with non-CVD death set as the competing event for CVD death. Solid lines represent the cumulative incidence of CVD death, and dashed lines represent the cumulative incidence of non-CVD death. The number of patients at risk at each follow-up time point is listed below the figure.

• 

  Fig. 5. Subgroup analysis of the association between mRS subgroups and all-cause mortality (adjusted HR, 95% CI) a. aCI, confidence interval; HR, hazard ratio; mRS, modified Rankin Scale; NSTEMI, non-ST-elevation myocardial infarction; STEMI, ST elevation myocardial infarction. This forest plot shows the subgroup analysis of the association between mRS subgroups and all-cause mortality during the median 5.26-year follow-up. The non-stroke group was set as the reference. The model was adjusted for age (years), thrombolysis before admission, STEMI, anterior wall infarction location, hypertension, diabetes mellitus, old myocardial infarction, chronic kidney disease, atrial flutter/fibrillation, malignant tumor, anemia, heart failure, primary percutaneous coronary intervention, aspirin, ticagrelor, tirofiban, statin, and angiotensin-converting enzyme inhibitor. The P value for interaction was calculated by the Wald chi-square test to assess the heterogeneity of treatment effects across subgroups.

• 

  Fig. 6. Subgroup analysis of the association between mRS subgroups and cardiovascular mortality (adjusted HR, 95% CI) a. aCI, confidence interval; CVD, cardiovascular diseases; HR, hazard ratio; mRS, modified Rankin Scale; NSTEMI, non-ST-elevation myocardial infarction; STEMI, ST elevation myocardial infarction. This forest plot shows the subgroup analysis of the association between mRS subgroups and CVD mortality during the median 5.26-year follow-up. The non-stroke group was set as the reference. The model was adjusted for the same covariates as the all-cause mortality model (detailed in Fig. 5 legend). The P value for interaction was calculated by the Wald chi-square test to assess the heterogeneity of treatment effects across subgroups.