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Published on: November 23, 2017
Relationship between stroke recurrence, infarct pattern, and vascular distribution in patients with symptomatic
Karthikram Raghuram1, Aditya Durgam1, Jennifer Kohlnhofer1
1Department of Radiology, University of Texas Medical Branch, Galveston, Texas, USA.
Insights
Stroke recurrence risk varies by stenosis location and infarct pattern. Optimized medical therapy is crucial, especially for plaque destabilization and watershed infarcts, to reduce recurrent stroke events.
Area of Science:
- Neurology
- Vascular Medicine
- Radiology
Background:
- Recent literature links stroke recurrence and intervention risks to plaque physiology and instability.
- Understanding the relationship between stenosis anatomy, presentation, and stroke patterns is critical.
Purpose of the Study:
- To determine stroke patterns and recurrence rates based on the anatomy and presentation of intracranial stenosis.
- To investigate the influence of plaque physiology on stroke recurrence.
Main Methods:
- Retrospective review of patient charts and angiographic imaging (CT and MR).
- Analysis of 39 patients' risk factors, medical therapy optimization, and clinical follow-up.
- Evaluation of infarct patterns (embolic, perforator, watershed) and vascular distribution.
Main Results:
- Basilar artery stenosis was associated with perforator stroke and low recurrence.
- Suboptimal medical therapy doubled the risk of recurrent stroke.
- Optimized therapy showed no recurrence in embolic infarcts but 57% in watershed infarcts.
Conclusions:
- Intracranial stenosis may require tailored medical or endovascular therapy based on hemodynamic factors, plaque stability, and territory.
- Aggressive risk factor control and understanding vascular territory are key to reducing stroke recurrence.
Objective:
In view of recent literature suggesting that stroke recurrence and risks related to intervention may be related to plaque physiology/instability, our study sought to discern the pattern of stroke and rates of stoke recurrence as they relate to the anatomy and presentation of the underlying stenosis.
Methods:
Retrospective chart as well as CT and MR angiographic imaging review of patients in the institutional stroke database was performed, including identification of patient risk factors, medical therapeutic optimization, compliance, serum cholesterol (low density lipoprotein) levels, blood pressure, physical therapy referrals, follow-up clinical status (using the modified Rankin Scales), and rate of recurrent stroke. 39 patients met the inclusion criteria. We evaluated infarct pattern (embolic, adjacent perforator, or watershed) and vascular distribution.
Results:
Basilar artery stenosis was most likely to present as a perforator stroke and least likely to recur. Patients discharged with suboptimal medical therapy were twice as likely to have a recurrent stroke. Among patients with optimized medical therapy, no recurrent strokes were seen in patients with an embolic infarct pattern, while a 57% recurrence rate was seen in patients with a watershed infarct pattern.
Conclusions:
Our results suggest that hemodynamic intracranial vascular stenoses may be less responsive to medical therapy, while stenotic lesions caused by plaque destabilization or in perforator territories may benefit from aggressive medical management with delayed or staged endovascular therapy. Recurrence of stroke may be affected both by vascular territory and by aggressive risk factor control, although the latter remains difficult to evaluate.
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