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Optimized Management of Endovascular Treatment for Acute Ischemic Stroke
Published on: January 18, 2018
Antithrombotic therapy in the postacute phase of cervical artery dissection: the Italian Project on Stroke in Young
Debora Pezzini1, Mario Grassi2, Maria Luisa Zedde3
1Dipartimento di Scienze Cliniche e Sperimentali, Clinica Neurologica, Università degli Studi di Brescia, Brescia, Italia.
Insights
Discontinuing antithrombotic therapy after cervical artery dissection (CeAD) in the postacute phase did not increase the risk of stroke or recurrent dissection. Mid-term outcomes were similar for patients who stopped or continued antithrombotic treatment.
Area of Science:
- Neurology
- Vascular Medicine
- Clinical Research
Background:
- Cervical artery dissection (CeAD) is a significant cause of stroke in young adults.
- Optimal duration and necessity of antithrombotic therapy post-CeAD remain debated.
- Understanding mid-term outcomes after therapy discontinuation is crucial for clinical decision-making.
Purpose of the Study:
- To evaluate the impact of discontinuing antithrombotic therapy in the postacute phase of CeAD on mid-term patient outcomes.
- To compare the incidence of ischemic events and recurrent CeAD between patients who discontinued and continued antithrombotic treatment.
Main Methods:
- A cohort study of consecutive patients with first-ever CeAD was conducted.
- Outcomes beyond 6 months post-CeAD were compared between therapy discontinuation and continuation groups.
- Propensity score matching was used to control for confounding factors.
- Primary outcome: composite of ischemic stroke and transient ischemic attack. Secondary outcomes: ipsilateral brain ischemia and recurrent CeAD.
Main Results:
- Of 1390 patients, 201 (14.4%) discontinued antithrombotic therapy.
- In propensity score-matched samples (201 vs 201), the primary outcome incidence was comparable (5.0% vs 4.5%, p=0.526).
- Secondary outcomes, including ipsilateral brain ischemia (4.5% vs 2.5%, p=0.132) and recurrent CeAD (1.0% vs 1.5%, p=0.798), also showed no significant differences.
Conclusions:
- Discontinuation of antithrombotic therapy in the postacute phase of CeAD does not appear to elevate the risk of brain ischemia during follow-up.
- These findings suggest that carefully selected patients may safely discontinue antithrombotic treatment after the acute phase of CeAD.
Objective:
To explore the impact of antithrombotic therapy discontinuation in the postacute phase of cervical artery dissection (CeAD) on the mid-term outcome of these patients.
Methods:
In a cohort of consecutive patients with first-ever CeAD, enrolled in the setting of the multicentre Italian Project on Stroke in Young Adults Cervical Artery Dissection, we compared postacute (beyond 6 months since the index CeAD) outcomes between patients who discontinued antithrombotic therapy and patients who continued taking antithrombotic agents during follow-up. Primary outcome was a composite of ischaemic stroke and transient ischaemic attack. Secondary outcomes were (1) Brain ischaemia ipsilateral to the dissected vessel and (2) Recurrent CeAD. Associations with the outcome of interest were assessed by the propensity score (PS) method.
Results:
Of the 1390 patients whose data were available for the outcome analysis (median follow-up time in patients who did not experience outcome events, 36.0 months (25th-75th percentile, 62.0)), 201 (14.4%) discontinued antithrombotic treatment. Primary outcome occurred in 48 patients in the postacute phase of CeAD. In PS-matched samples (201 vs 201), the incidence of primary outcomes among patients taking antithrombotics was comparable with that among patients who discontinued antithrombotics during follow-up (5.0% vs 4.5%; p(log rank test)=0.526), and so was the incidence of the secondary outcomes ipsilateral brain ischaemia (4.5% vs 2.5%; p(log rank test)=0.132) and recurrent CeAD (1.0% vs 1.5%; p(log rank test)=0.798).
Conclusions:
Discontinuation of antithrombotic therapy in the postacute phase of CeAD does not appear to increase the risk of brain ischaemia during follow-up.
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