Table 4.
Independent variable | OR (95% CI) | P-value |
---|---|---|
Model 1*,† | ||
WMH lesion burden | 1.80 (1.18–2.76) | 0.007 |
Non-SVD SSI mechanism | 6.51 (1.52–27.94) | 0.012 |
| ||
Model 2*,†,‡ | ||
WMH lesion burden | 2.28 (1.04–4.99) | 0.040 |
Pre-admission mRS score, per point | 8.96 (2.65–30.27) | <0.001 |
Infarct volume, per mL | 1.98 (1.14–3.44) | 0.016 |
Age, per year | 0.91 (0.82–1.01) | 0.063 |
Non-SVD SSI mechanism | 9.20 (1.04–81.39) | 0.046 |
Hosmer-Lemeshow for model 1: χ2=7.758, p=0.457. Hosmer-Lemeshow for model 2: χ2=3.059, p=0.931.
Entering the infarct volume as mean or total infarct volume did not meaningfully change the results, respectively.
The interaction term of white matter hyperintensity (WMH) lesion burden x infarct volume and presence of multiple SSI were not retained. Finally, entering large artery atherosclerosis, cardioaortic embolism, and small arterial occlusion in lieu of the non-small vessel disease (SVD) small subcortical infarct (SSI) mechanism did not meaningfully change the models whereby presence of SVD-related SSI etiology was associated with a favorable outcome (p<0.05 in each model).
The National Institutes of Health Stroke Scale score was not retained in model 2. Further, restricting the analysis to patients with a modified Rankin Scale (mRS) of <6, did not meaningfully change the results.