Intracranial atherosclerosis

doi:10.1016/S0140-6736(13)61088-0

The Lancet

Volume 383, Issue 9921, 15–21 March 2014, Pages 984-998

https://doi.org/10.1016/S0140-6736(13)61088-0 Get rights and content

Summary

Atherosclerotic disease often involves the intracranial arteries including those encased by cranial bones and dura, and those located in the subarachnoid space. Age, hypertension, and diabetes mellitus are independent risk factors for intracranial atherosclerosis. Intracranial atherosclerosis can result in thromboembolism with or without hypoperfusion leading to transient or permanent cerebral ischaemic events. High rates of recurrent ischaemic stroke and other cardiovascular events mandate early diagnosis and treatment. Present treatment is based on a combination of antiplatelet drugs, optimisation of blood pressure and LDL cholesterol values, and intracranial angioplasty or stent placement, or both, in selected patients.

Introduction

Atherosclerotic lesions ranging from slight wall thickening and non-stenosing plaques to severe luminal narrowing often involve intracranial arteries encased by cranial bones and dura, or those located in the subarachnoid space. The most common sites, in order, are the basilar artery, the internal carotid arteries, the middle cerebral arteries, the intracranial vertebral arteries, the posterior cerebral arteries, and the anterior cerebral arteries.¹ Intracranial atherosclerosis can occur in isolation or as part of systemic atherosclerotic disease involving the coronary, extracranial, and other peripheral arteries.2, 3 A disproportionately high rate of stroke mortality occurs in Asian countries such as China, Japan, and South Korea where intracranial atherosclerosis is highly prevalent.⁴ Therefore, intracranial atherosclerosis could be a major cause of regional variation in stroke mortality.

Section snippets

Epidemiology

Data for atherosclerotic disease prevalence are based on either studies of pathological changes in autopsy specimens or detection of arterial calcification or lumen narrowing by neuroimaging in population-based screening.⁵ In a study,⁶ atherosclerosis was evident in 10–30% of Europeans aged 20–29 years, and by the age of 65 years, 80–97% of the population had pathological evidence of intracranial atherosclerosis. In the population-based Rotterdam Study,⁶ intracranial internal carotid artery

Pathological appearance

Fatty streaks and fibrous plaques in intracranial arteries are evident by age 24 years,²⁷ followed by intimal necrosis and thickenings in older individuals.²⁸ Proliferative fibrosis of the intima or adventitia is more prevalent than is lipid infiltration in intracranial atherosclerosis, and changes appear later than those seen in coronary arteries.2, 29 Well defined plaques (figure 1) are most frequent in elderly people.14, 30 Vasa vasorum extending into the vascular media (neovascularisation)

Risk factors

Age, hypertension, and type 2 diabetes mellitus are consistently identified as independent risk factors for TCD-documented intracranial stenosis in studies that include asymptomatic8, 38, 39 or symptomatic patients.⁴⁰ Metabolic syndrome—a disorder of metabolic risk factors, insulin resistance, and vascular inflammation—is identified in almost half of patients.41, 42, 43 In the Barcelona Asymptomatic Intracranial Atherosclerosis (AsIA) study,⁴⁴ diabetes mellitus and metabolic syndrome increased

Clinical manifestations

Intracranial stenosis presents with one or many recurrent ischaemic strokes and transient ischaemic attacks (TIA).⁵⁴ Intracranial plaques and stenoses on autopsy are identified in 45–62% of patients who have had an ischaemic stroke,33, 50 and are causal in about 10% of ischaemic strokes.⁵⁰ Other ischaemic strokes are probably related to concomitant proximal extracranial stenosis or atrial fibrillation identified in 10–20% of patients with intracranial atherosclerosis.55, 56, 57 In the Northern

Diagnosis, quantification, and characterisation

Raised mean blood flow velocities on TCD or luminal narrowing and absence of flow, or both, on MRI, CT, and catheter angiography are used to identify and quantify the severity of intracranial atherosclerosis (table 1).87, 88, 89, 90, 91 Because of high negative predictive values, non-invasive methods are good screening tests, but might be inadequate to measure the severity of disease in some circumstances. Other appropriate features, such as the presence of multiple cardiovascular risk factors

Stroke, cardiovascular events, and mortality

After an initial TIA or ischaemic stroke, brain ischaemia can recur in the distribution of the stenotic artery and infrequently in another distribution in patients with intracranial stenosis. The high rate of vascular events emphasises the importance of timely diagnosis and treatment in these patients. Several studies have investigated patients given antithrombotic treatment but without intensive medical management. Early progression in deficits and mortality is underestimated in studies that

Antithrombotic treatment

The present treatment of patients with ischaemic events attributable to intracranial stenosis is based on a combination of antiplatelet drugs and optimisation of blood pressure and LDL cholesterol values through lifestyle modification and drug treatment (figure 4).

Early initiation of antiplatelet drugs is preferred over parenteral anticoagulation in patients who present with brain ischaemic events related to intracranial atherosclerosis because of easy administration, similar efficacy, and

Prevention of progression of stenosis

An increase in severity of stenosis due to continued inflammatory changes, lipid deposition, fibrosis, in-situ thrombus formation, and intraplaque haemorrhage is identified in 33% of patients during 2 years, and might result in occurrence of new ipsilateral ischaemic events.166, 167 In one study,¹²³ 457 patients with intracranial stenosis in the middle cerebral arteries or basilar artery and on aspirin were randomly assigned to either cilostazol or clopidogrel. The progression of intracranial

Conclusions

Intracranial atherosclerosis is a highly prevalent disorder that has gained recent attention because of the high risk of recurrent subclinical and clinical ischaemic events, and its association with cognitive deficits and dementia. Concurrent existence of extracranial and coronary artery atherosclerosis necessitates a targeted and global approach to reduce the risk of new or recurrent cerebral and coronary ischaemic events in patients with intracranial atherosclerosis.

Search strategy and selection criteria

We based our Seminar on personal knowledge of the subject supplemented by data derived from multicentre randomised trials and selected non-randomised or observational clinical studies that included ten or more patients. The information was identified by searches on Medline from January, 2004, to April, 2013, by cross-referencing keywords of “cerebral atherosclerosis”, “ischaemic stroke”, “intracranial stenosis”, “intracranial atherosclerosis”, “neuroimaging”, “clinical studies”, “randomised

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It remains unknown about the relationship between vertebrobasilar artery (VBA) calcification and plaque instability. We aimed to investigate the characteristics of VBA calcification using vessel wall magnetic resonance imaging (MRI) and computed tomography (CT) and its association with acute cerebral infarction (ACI).
Nine hundred and thirty patients with VBA stenosis who underwent vessel wall MRI and CT examinations were evaluated retrospectively. Calcification morphology was classified as either intimal or non-intimal predominant using a CT-pathology-validated grading method. Qualitative and quantitative plaque MRI variables and calcification characteristics were compared between culprit and non-culprit lesions. The association between VBA calcification and the occurrence of culprit lesions was investigated using multivariate logistic regression.
A total of 150 patients with ACI and 142 patients without ACI were eligible for subsequent analyses, respectively. In the qualitative analysis, T1 hyperintensity (p < 0.001) and intimal predominant calcification (p = 0.021) were more frequently observed in the culprit than non-culprit lesions. In the quantitative analyses, culprit lesions had a larger stenosis degree, plaque length, normal wall index, contrast enhancement ratio, lower calcification density and smaller calcification volume than non-culprit lesions (p all < 0.05). Intimal predominant calcification (odds ratio [OR], 2.51; 95 % confident interval [CI], 1.31–4.82, p = 0.006) and calcification density (OR, 0.53; 95 % CI, 0.35–0.78, p = 0.001) were independently associated with the presence of ACI after adjusting for clinical risk factors and plaque variables.
Intimal predominant calcification in vertebrobasilar atherosclerosis is associated with the likelihood of having caused acute cerebral infarction. The morphology and density of VBA calcification may provide insight into stroke risk stratification in the posterior circulation.
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Atherosclerotic plaques of carotid artery (CA) and middle cerebral artery (MCA) are important causes of acute ischemic stroke (AIS). This study was designed to jointly assess the plaque distribution and features of CA and MCA in AIS patients with pial infarction (PI) and perforating artery infarction (PAI), and to investigate the associations between plaque characteristics and ischemic infarction patterns.
Imaging data of sixty-five patients from a cross-sectional study were reviewed. All the patients had acute infarction in the MCA territory on diffusion weighted imaging (DWI) and underwent CA and MCA vessel wall imaging (VWI). The CA and MCA plaque presence and high-risk features on the ipsilateral side of infarction were analyzed. The brain infarction lesions were divided into PI group vs. non-PI group, and PAI group vs. non-PAI group. Different plaque distribution types and plaque features were compared in each two groups, and their associations were investigated using binary logistic regression.
Sixty-five patients (mean age, 54.6 ± 10.1 years; 61 men) were included. The CA high-risk plaque (OR: 5.683 [1.409–22.929], P = 0.015) and MCA plaque presence (OR: 3.949 [1.397–11.162], P = 0.010) were significantly associated with PI. MCA plaques that involved the orifice of the perforating arteries were significantly associated with PAI (OR: 15.167 [1.851–124.257], P = 0.011).
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SeminarIntracranial atherosclerosis

Summary

Introduction

Section snippets

Epidemiology

Pathological appearance

Risk factors

Clinical manifestations

Diagnosis, quantification, and characterisation

Stroke, cardiovascular events, and mortality

Antithrombotic treatment

Prevention of progression of stenosis

Conclusions

Search strategy and selection criteria

Atherosclerosis

Lancet Neurol

Atherosclerosis

Arch Gerontol Geriatr

Am J Hypertens

Atherosclerosis

J Neurol Sci

Am J Pathol

Am J Med

J Am Coll Cardiol

J Neurol Sci

J Am Coll Cardiol

Neurosci Lett

Alzheimers Dement

J Affect Disord

J Neurol Sci

Physical factors in the pathogenesis of cerebral atherosclerosis

Stroke

Correlation of the extent and severity of atherosclerosis in the coronary and cerebral arteries

Circulation

Epidemiology of intracranial stenosis

J Neuroimaging

Intracranial carotid artery atherosclerosis: prevalence and risk factors in the general population

Stroke

Prevalence of asymptomatic intracranial atherosclerosis in high-risk patients

Neurology

Prevalence and risk factors of middle cerebral artery stenosis in asymptomatic residents in Rongqi County, Guangdong

Cerebrovasc Dis

Estimated prevalence of acoustic cranial windows and intracranial stenosis in the US elderly population: ultrasound screening in adults for intracranial disease study

Neuroepidemiology

Joint study of extracranial arterial occlusion. II. Arteriography, techniques, sites, and complications

JAMA

Chinese-white differences in the distribution of occlusive cerebrovascular disease

Neurology

Racial differences in cerebrovascular disease. Angiographic evaluation of Japanese and American populations

Am J Roentgenol Radium Ther Nucl Med

Pattern of cerebral atherosclerosis in Hong Kong Chinese. Severity in intracranial and extracranial vessels

Stroke

Cerebral atherosclerosis in New Orleans. Comparisons of lesions by age, sex, and race

Lab Invest

Race, sex and occlusive cerebrovascular disease: a review

Stroke

Ischemic stroke subtype incidence among whites, blacks, and Hispanics: the Northern Manhattan Study

Circulation

Increasing severity of cardiovascular risk factors with increasing middle cerebral artery stenotic involvement in type 2 diabetic Chinese patients with asymptomatic cerebrovascular disease

Diabetes Care

Frequency and clinical correlates of occlusive lesions of cerebral arteries in Japanese patients without stroke. Evaluation by MR angiography

Cerebrovasc Dis

Ethnic differences in hypertension incidence among middle-aged and older adults: the multi-ethnic study of atherosclerosis

Hypertension

Racial differences in vascular risk factors and outcomes of patients with intracranial atherosclerotic arterial stenosis

Stroke

An explanation for variations in distribution of stroke and arteriosclerotic heart disease among populations and racial groups

Am J Epidemiol

An epidemiological study of cardiovascular and cardiopulmonary disease risk factors in four populations in the People's Republic of China. Baseline report from the P.R.C.–U.S.A. Collaborative Study

Circulation

Impact of body mass index on incident hypertension and diabetes in Chinese Asians, American Whites, and American Blacks: the People's Republic of China Study and the Atherosclerosis Risk in Communities Study

Am J Epidemiol

Cerebral atherosclerosis. Intimal proliferation and atherosclerosis in the cerebral arteries

Arch Pathol

Cerebrovascular disease. I. The large arteries of the circle of Willis

Neurology

Method dependent limits in a study on the natural history of coronary and cerebral atherosclerosis

Med Interne

Vasa vasorum of the intracranial arteries

Acta Neurochir (Wien)

Seminar
Intracranial atherosclerosis