Should patients with lacunar stroke and severe carotid artery stenosis undergo endarterectomy?

Kelly, James

doi:10.1093/qjmed/95.5.313

Cited by 4 publications

(4 citation statements)

References 85 publications

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“…The similarity of RRs for ipsilateral and contralateral carotid stenosis supports the concept that carotid stenosis is unlikely to cause most lacunar infarctions. However, the benefit from carotid endarterectomy among patients with lacunar infarction and severe carotid stenosis suggests that artery-to-artery emboli and low flow resulting from carotid stenosis may play an etiological role in some lacunar infarcts 53…”

Section: Discussionmentioning

confidence: 99%

Are Lacunar Strokes Really Different?

Jackson

Sudlow

2005

Stroke

232

117

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Background and Purpose-Differences in risk factors between lacunar and nonlacunar infarcts might support a distinct arterial pathological process underlying lacunar infarction. Methods-We did a systematic review of studies comparing risk factors in patients with lacunar versus nonlacunar infarction. For each risk factor, we calculated study-specific and pooled relative risks (RRs) for lacunar versus nonlacunar infarction. Results-A total of 16 of 28 studies included risk factors in their ischemic stroke subtype definitions. Hypertension and diabetes appeared commoner among patients with lacunar versus nonlacunar infarction. However, analyses confined to studies using risk factor-free ischemic subtype definitions found only a marginal excess of hypertension with lacunar versus nonlacunar infarction (RR, 1.11; 95% CI, 1.04 to 1.19) and no difference for diabetes (RR, 0.95; 95% CI, 0.83 to 1.09). Atrial fibrillation and carotid stenosis were associated more with nonlacunar than lacunar infarction but less so when only studies using risk factor-free classifications were considered. Otherwise, there was no evidence of differences in risk factor profiles. Conclusions-Risk factor-free ischemic stroke subtype classification methods should be used for comparing risk factor profiles between lacunar and nonlacunar subtypes.

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Section: Discussionmentioning

confidence: 99%

Are Lacunar Strokes Really Different?

Jackson

Sudlow

2005

Stroke

232

117

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“…Recently, it has been proposed that this type of stroke may be ‘a manifestation of non-atherothrombotic occlusive small vessel disease'. Further, these infarcts may require different investigations and treatment [6,7,8]. The mechanism of these infarcts is a point of controversy with other investigators pointing to atherosclerotic disease involving the larger arteries [7,9,10] or embolism [11,12].…”

Section: Introductionmentioning

confidence: 99%

Dimensions of Subcortical Infarcts Associated with First- to Third-Order Branches of the Basal Ganglia Arteries

Phan

Voort²,

Beare³

et al. 2013

Cerebrovasc Dis

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Background: It has been described that lacunar infarct is characterized by its smallish size (15-20 mm) in the axial plane. However, the size of the basal ganglia artery responsible for this type of infarct is uncertain. Detection of small arterial occlusion is not possible with current angiography, hindering correlation of arterial occlusion with subcortical infarct size. Recently, investigators have published microangiographic templates of arteries supplying the basal ganglia. These templates display first-order (proximal) to third-order (distal) branching of these arteries and can help with estimating the likely site of arterial disease in subcortical infarcts. We correlated the dimensions of subcortical infarcts with the order of arterial branching described in a microangiographic template. Such data may provide further clues about the type of arteries associated with subcortical infarcts and assist in refining the concept of lacunar infarction. Method: Patients with subcortical infarcts on MR imaging (MRI) admitted to our institution between 2009 and 2011 were included in the study. Infarcts were manually segmented and registered to a standard brain template. These segmented infarcts were scaled and overlapped with published microangiographic templates, and used by 6 raters who independently estimated the branching order of arterial disease that might result in these infarcts. We used regression analysis to relate these ratings to infarct dimensions. Results: Among 777 patients, there were 33 (58% male) patients with subcortical infarcts. The mean age was 63.1 ± 15.1 years. Infarct dimensions for the groups were as follows: group 1 (first-order branch): height 37.6 ± 7.4 mm, horizontal width 21.2 ± 11.6 mm, anterior-posterior length 36.8 ± 20.1 mm; group 2 (second-order branch): height 25.2 ± 7.9 mm, horizontal width 16.6 ± 22.8 mm, anterior-posterior length 16.1 ± 8.0 mm; group 3 (third-order branch): height 11.6 ± 5.7 mm, axial width 5.3 ± 3.1 mm, anterior-posterior length 5.5 ± 3.8 mm. Increasing vessel branching order (from large to small vessels) was linearly and negatively associated with infarct height (β = -16.7 mm per change in branching order disease, 95% CI -20.3, -13.1 mm, p < 0.01) and anterior-posterior length (β = -16.8 mm per change in branching order disease, 95% CI -23.2, -10.5 mm, p < 0.01). Discussion: Based on MRI infarct dimensions and a microangiographic template, it may be possible to estimate the branching order of the artery involved in subcortical infarcts. Further, our small data set suggests that reliance on an axial dimension of 15-20 mm may not be the best approach to classifying lacunar infarct. This finding needs to be confirmed in a larger data set.

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“…Trials of endarterectomy for symptomatic carotid stenosis included patients with recent symptomatic small subcortical ischemic strokes. Post hoc analyses of the trial data suggest benefit for these patients 48 ; therefore, carotid endarterectomy or stenting should be performed in patients with carotid stenosis and recent small subcortical stroke in the carotid perfusion territory.…”

Section: Secondary Prevention Of Symptomatic Small Subcortical Ischemmentioning

confidence: 99%

Prevention of Cerebral Small Vessel Disease

Smith

2017

Semin Neurol

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Cerebral small vessel disease can cause either ischemic stroke or intracerebral hemorrhage. Accounting for up to 25% of all strokes, it is also the second biggest contributor to the risk of dementia, and is the most common incidentally discovered finding on brain imaging. There are two main causes of cerebral small vessel disease: arteriolosclerotic small vessel disease (with hypertension as the main modifiable risk factor) and cerebral amyloid angiopathy (predominantly caused by β-amyloid deposits limited to the cerebral small arteries, arterioles, and capillaries). Prevention should include the treatment of hypertension and diabetes, if present, and the modification of lifestyle factors such as obesity and poor nutrition. Patients with small subcortical ischemic strokes should be treated with antithrombotics; dual antiplatelet therapy may be more effective than aspirin for the first 3 weeks following acute stroke, but is not more effective than aspirin for long-term prevention. Unresolved questions include the effectiveness of nonaspirin prevention strategies to prevent early recurrence or stroke extension in small subcortical ischemic stroke, and whether symptomatic or silent small vessel disease should influence decisions regarding selection for carotid revascularization or anticoagulation for atrial fibrillation. There is an unmet need for disease-modifying preventive therapies for cerebral amyloid angiopathy, the second most-common cause of spontaneous intracerebral hemorrhage.

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Should patients with lacunar stroke and severe carotid artery stenosis undergo endarterectomy?

Cited by 4 publications

References 85 publications

Are Lacunar Strokes Really Different?

Are Lacunar Strokes Really Different?

Dimensions of Subcortical Infarcts Associated with First- to Third-Order Branches of the Basal Ganglia Arteries

Prevention of Cerebral Small Vessel Disease

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