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Published on: March 15, 2022
Antiplatelet use and CADASIL: a retrospective observational analysis
Jayachandra Muppa1, Shadi Yaghi2, Eric D Goldstein3
1Department of Neurology, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Antiplatelet therapy did not significantly affect acute ischemic stroke or intracerebral hemorrhage rates in patients with Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL). Further research is needed for effective CADASIL treatments.
Area of Science:
- Neurology
- Vascular Neurology
- Genetics
Background:
- Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) involves microangiopathy and commonly uses antiplatelet medications for stroke prevention.
- The therapeutic benefit of antiplatelet agents in CADASIL remains unproven.
Purpose of the Study:
- To investigate the impact of antiplatelet therapy on the incidence of acute ischemic stroke (AIS) and intracerebral hemorrhage (ICH) in individuals diagnosed with CADASIL.
Main Methods:
- A retrospective analysis of anonymized data from the TriNetX Research Network (October 2015 - January 2021) was conducted.
- Individuals with an ICD-10 code for CADASIL (I67.850) were identified.
- The study assessed the incidence of AIS (I63) and ICH (I61) in relation to antiplatelet medication use for at least one month prior, using age-adjusted logistic regression.
Main Results:
- The study included 455 individuals, with 40 (8.8%) exposed to antiplatelet therapy.
- Antiplatelet users were older (61±12 years) than unexposed individuals (57±14 years).
- No significant difference was observed in AIS rates (23% vs. 14%) or ICH rates (3% vs. 5%) between the groups. Antiplatelet use did not significantly impact AIS likelihood (OR 1.62, p=0.23).
Conclusions:
- Current antiplatelet therapy does not appear to significantly alter the incidence of AIS or ICH in individuals with suspected CADASIL.
- The findings underscore the necessity for enhanced understanding of CADASIL pathophysiology to develop disease-modifying treatments.
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