Current health sciences journal · 2025
Statin Use in Cervical Artery Dissection and Subsequent Ischemic Stroke.
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Lodhi Omair Ul Haq, Yaghi Shadi, Shu Liqi, Chung Natali, Guerrero Christopher Robert Leon, Kaufman Josefin Emily, Engelter Stefan, Traenka Christopher, Kam Wayneho, Zubair Adeel S, Almajali Mohammad, Marto João Pedro, Affan Muhammad
Аннотация
BACKGROUND AND PURPOSE: The role of statins in preventing recurrent ischemic strokes in the setting of non-traumatic cervical artery dissection remains unclear. This study, a secondary analysis of Antithrombotic Treatment for Stroke Prevention in Cervical Artery Dissection (STOP-CAD) study, investigates the impact of statin therapy on subsequent ischemic stroke.
METHODS: STOP-CAD, a multicenter retrospective observational study, included 4023 patients with non-major trauma-related CAD. For this sub study, we included 2610 patients with ischemic stroke, excluding those with non-ischemic presentations and missing statin information. 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 was the incidence of subsequent ischemic stroke after hospital discharge. Secondary outcomes included major hemorrhage, mortality and 90-day functional outcomes. Statistical analyses included univariate analyses, Cox regression models to evaluate odds and hazard ratios.
RESULTS: There was no significant difference in subsequent ischemic strokes after hospital discharge between the statin group (3.1%) and no statin group (3.3%) (aHR 0.73 95% CI, 0.43-1.24, p=0.25). Similarly, the incidence of major hemorrhage, mortality and 90-day functional outcomes showed no significant differences between the groups.
CONCLUSION: Statin therapy did not significantly reduce the risk of subsequent ischemic stroke, major hemorrhage, functional outcome, or mortality. While statins are beneficial in reducing vascular events and improving outcomes in ischemic stroke, its 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.
METHODS: STOP-CAD, a multicenter retrospective observational study, included 4023 patients with non-major trauma-related CAD. For this sub study, we included 2610 patients with ischemic stroke, excluding those with non-ischemic presentations and missing statin information. 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 was the incidence of subsequent ischemic stroke after hospital discharge. Secondary outcomes included major hemorrhage, mortality and 90-day functional outcomes. Statistical analyses included univariate analyses, Cox regression models to evaluate odds and hazard ratios.
RESULTS: There was no significant difference in subsequent ischemic strokes after hospital discharge between the statin group (3.1%) and no statin group (3.3%) (aHR 0.73 95% CI, 0.43-1.24, p=0.25). Similarly, the incidence of major hemorrhage, mortality and 90-day functional outcomes showed no significant differences between the groups.
CONCLUSION: Statin therapy did not significantly reduce the risk of subsequent ischemic stroke, major hemorrhage, functional outcome, or mortality. While statins are beneficial in reducing vascular events and improving outcomes in ischemic stroke, its 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.