Multivariable logistic regression analysis for the ability of previously defined clinical stroke scale cutoffs to predict large-vessel occlusion in the examined cohort
| Stroke Scale | Crude OR (95% CI) | P Value | Adjusted OR (95% CI)a | P Value |
|---|---|---|---|---|
| 3I/SS ≥4 | 4.736 (1.513–14.826) | .008 | 5.389 (0.856–33.908) | .073 |
| VAN ≥2 | 3.918 (1.979–7.760) | <.001 | 2.468 (0.845–7.206) | .098 |
| CPSSS ≥2 | 2.710 (1.388–5.290) | .003 | 2.794 (0.973–8.028) | .056 |
| RACE ≥5 | 5.706 (2.881–11.299) | <.001 | 3.236 (1.099–9.527) | .033 |
| FAST-ED ≥4 | 4.749 (2.447–9.217) | <.001 | 3.740 (1.291–10.839) | .015 |
↵a Each model was adjusted for leukoaraiosis burden (as determined by the Fazekas scale score) as well as Leukoaraiosis × Stroke Scale Interaction. When additionally entered into the model, the prestroke modified Rankin Scale, age, sex, hypertension, history of stroke/transient ischemic attack, and atrial fibrillation were not retained in the final step of the analysis. In all analyses, leukoaraiosis and stroke scales were entered as dichotomized variables. When all analyses were repeated by entering the Fazekas scale score and stroke scale scores as ordinal variables, the VAN (P = .029), CPSSS (P = .024), FAST-ED (P = .003), RACE (P = .002), and 3I/SS (P = .006) scores predicted LVO independent of the leukoaraiosis burden (not shown). There was no Leukoaraiosis × Stroke Scale Interaction in any of the examined models (P > .05, each).