Abstract Body: Introduction
Cervical artery dissection (CAD) is a significant etiology of ischemic stroke, especially in individuals under 50, accounting for up to 25% of cases in this age group. While antithrombotic therapy is the primary treatment for CAD, the role of statins in preventing recurrent ischemic strokes in these patients remains unclear. This study, a secondary analysis of the Antithrombotic Treatment for Stroke Prevention in Cervical Artery Dissection (STOP-CAD) trial, investigates the impact of statin therapy on subsequent ischemic stroke.

Methods
STOP-CAD was a multicenter retrospective observational study that included 4023 patients with non-major trauma-related CAD. For this substudy, we included 2610 patients with ischemic stroke, excluding those with non-ischemic presentations for example isolated horner’s syndrome and those lacking statin information (Figure 1.0). Patients were stratified based on statin use at hospital discharge and a sensitivity analysis was conducted based on intensity: high-intensity, moderate-intensity, low-intensity, or no statin.
Primary outcome assessed was the incidence of subsequent ischemic stroke, secondary outcomes were major hemorrhage, mortality and 90-day functional outcomes, defined by the Modified Rankin Scale (mRS ≤ 2). Statistical analyses included univariate analyses, Cox regression models to evaluate odds and hazard ratios.

Results
There was no significant difference in the incidence of subsequent ischemic strokes between the statin group (3.1%) and the no statin group (3.3%) with an adjusted hazard ratio (HR) of 0.736 (95% CI, 0.434-1.248, p=0.256). Similarly, the incidence of major hemorrhage, mortality and 90-day functional outcomes showed no significant differences between the groups (Table 1.0). However, a sensitivity analysis revealed a significantly lower mortality rate in the high-intensity statin group compared to the low-to-moderate intensity statin and no statin groups (p=0.009)(Table 2).

Conclusion
Statin therapy did not significantly reduce the risk of subsequent ischemic stroke, major hemorrhage, functional outcome, or mortality rates. This study underscores that while statin therapy is beneficial in reducing vascular events and improving outcomes in ischemic stroke population, its specific benefits in CAD-related ischemic strokes are less clear. These findings highlight the need for individualized treatment strategies and further research to optimize secondary prevention in CAD-related stroke.