Introduction/Purpose Intracranial atherosclerotic disease remains a challenging condition to manage in the post-SAMMPRIS era. Recent studies indicate that stroke recurrence and risks associated with intervention are related to the underlying characteristics of the stenosis (such as plaque instability). The purpose of this study is to discern the pattern of stroke and rates of stoke recurrence as they relate to the anatomy and presentation of the underlying stenosis.
Materials and Methods Retrospective chart as well as CT and MR angiographic imaging review of patients in the institutional stroke database was performed to identify patients with stroke caused by significant (>50%) intracranial stenosis. Only patients with CT or MR documented infarcts were included in the study. Patient clinical data was reviewed to identify risk factors, discharge medications (with optimal therapy being defined by at least dual antiplatelet therapy and statin therapy), medication compliance, follow-up clinical status (by Modified Rankin Score), and rate of recurrence stroke with statistical analysis to identify correlations between the data points.
Results A total 1007 cases were included from the stroke database, with a total of 39 patients meeting inclusion criteria. 95% medication compliance rate was reported. We evaluated infarct pattern (embolic, adjacent perforator, or watershed) and vascular distribution (basilar, ICA, and MCA). We also determined the correlation between infarct pattern and recurrence rate. Stroke recurrence rate with and without optimal medical therapy was also determined.
Conclusion We determined that basilar artery stenosis was most likely to present as a perforator stroke. As expected, patients discharged with suboptimal medical therapy were twice as likely to have a recurrent stroke (29% versus 13%). Among patients with optimal medical therapy, no recurrent strokes were seen in patients with embolic infarct pattern, while 57% recurrence rate was seen in patients with a watershed infarct pattern, suggesting that an embolic infarct pattern on initial presentation is possibly related to underlying plaque instability that is modifiable with optimal medical therapy. On the other hand, initial watershed infarct pattern may be related to underlying hemodynamic insufficiency which is not easily modified by medical therapy
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Disclosures K. Raghuram: None. J. Kohlnhofer: None. A. Durgam: None.
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