Imaging of intracranial arterial disease: a comparison between MRI and unenhanced CT.

Background and purpose: Arterial calcifications on unenhanced CT scans and vessel wall lesions on MRI are often used interchangeably to portray intracranial arterial disease. However, the extent of pathology depicted with each technique is unclear. We investigated the presence and distribution of these two imaging findings in patients with a history of cerebrovascular disease. Materials and methods: We analyzed CT and MRI data from 78 patients admitted for stroke or TIA at our institution. Vessel wall lesions were assessed on 7 T MRI sequences, while arterial calcifications were assessed on CT scans. The number of vessel wall lesions, severity of intracranial internal carotid artery (iICA) calcifications, and overall presence and distribution of the two imaging findings were visually assessed in the intracranial arteries. Results: At least one vessel wall lesion or arterial calcification was assessed in 69 (88%) patients. Only the iICA and vertebral arteries (VA) showed a substantial number of both calcifications and vessel wall lesions. The other vessels showed almost exclusively vessel wall lesions. The number of vessel wall lesions was associated with the severity of iICA calcification (p = 0.013). Conclusions: The number of vessel wall lesions increases with the severity of iICA calcifications. Nonetheless, the distribution of vessel wall lesions on MRI and arterial calcifications on CT shows remarkable differences. These findings support the need for a combined approach to examine intracranial arterial disease.

The correlation between medial pattern of intracranial arterial calcification and white matter hyperintensities.

BACKGROUND AND AIMS: Despite reported correlations between intracranial arterial calcification (IAC) and white matter hyperintensities (WMH), little is known about the relationship between IAC pattern and WMH. By differentiating intimal and medial IAC, we aimed to investigate the relationship between IAC pattern and WMH. METHODS: Consecutive acute stroke patients were included. IAC pattern was categorized as intimal or medial on plain brain CT. The number of cerebral arteries involved by IAC for each patient was recorded. IAC severity was defined as focal or diffuse. On brain MRI, the burden of WMH was visually graded and classified as absent mild, moderate and severe. Multiple logistic regression was performed to examine the relationship between IAC and WMH. RESULTS: Among 265 patients, intimal IAC was detected in 54.7% patients and medial IAC in 48.5% patients. Diffuse IAC was present in 27.9% patients, all of which were medial. WMH was found in 75.5% patients, including 39.6% patients with mild WMH, 26.0% with moderate WMH, and 9.8% with severe WMH. The severity of medial IAC was correlated with WMH occurrence (p < 0.001). Chi-square linear trend suggested the number of arteries involved by medial IAC (p < 0.001) and the severity of medial IAC (p < 0.001) were correlated with WMH burden. Multiple ordinal logistic regression demonstrated a positive correlation of WMH burden with the number of arteries involved by medial IAC (p < 0.001) and the severity of medial IAC (p < 0.001). CONCLUSIONS: Medial IAC was correlated with WMH. The dose-effect relationship between medial IAC and WMH suggests underlying shared mechanisms of intracranial large artery disease and small vessel disease.

Brachial-ankle pulse wave velocity is associated with intracranial artery calcification in acute stroke patients.

BACKGROUND: Intracranial artery calcification (IAC) is closely associated with cerebrovascular disease. Brachial-ankle pulse wave velocity (baPWV) is a noninvasive method for estimating arterial stiffness, which reflects the stiffness of peripheral arteries. This study aimed to examine the association of baPWV with the presence and degree of IAC in patients with acute ischemic stroke. METHODS: A total of 143 ischemic stroke subjects were recruited. A head computed tomography (CT) scan was used to assess the presence and severity of IAC. The oscillometric method was used to simultaneously measure bilateral brachial and posterior tibial arterial pulse waveforms and arterial BP. Multiple logistic regression analysis was used to identify the independent relationship between baPWV and IAC. RESULTS: 143 subjects were included in this study. The demographic and clinical characteristics of the study population were classified according to the baPWV quartile. A higher prevalence of IAC was noted across increasing baPWV quartiles (Q1: 53 %, Q2: 69 %, Q3: 86 %, Q4: 94 %, P < 0.001). IAC scores were also increased with elevated ccPWV values (1.60 ± 1.71; 2.56 ± 1.99; 3.44 ± 1.91; 4.64 ± 1.58. P < 0.001). After an additional adjustment for age and hypertension, the odds ratio (95 % confidence interval) for the IAC scores was 1.61 (1.06-2.45; P = 0.025) in the top quartile of baPWV compared with those in the lowest quartile. CONCLUSIONS: Arterial stiffness as defined by baPWV was positively associated with the degree of IAC in patients with acute ischemic stroke, suggesting the severity of IAC may also be a marker of peripheral or systemic arterial stiffness.

Cerebral Arterial Stiffness as Measured Based on the Pulse Wave Velocity is Associated With Intracranial Artery Calcification in Patients With Acute Stroke.

BACKGROUND AND PURPOSE: By measuring a newly defined parameter, the carotid-cerebral pulse wave velocity (ccPWV), this study aimed to determine the association of intracranial artery calcification (IAC) with arterial stiffness as reflected by the pulse wave velocity between the carotid and middle cerebral arteries using transcranial Doppler sonography in patients with acute stroke. METHODS: We recruited 146 patients with ischemic stroke from our stroke center. Computed tomography of the head was used to assess the presence and severity of IAC. Arterial stiffness was evaluated using ccPWV. Data are presented as quartiles of ccPWV. A multivariable logistic regression model was used to assess the independent relationship between ccPWV and IAC. RESULTS: The IAC prevalence increased with the ccPWV quartile, being 54%, 76%, 83%, and 89% for quartiles 1, 2, 3, and 4, respectively (p<0.001) as did IAC scores, with median [interquartile range] values of 0 [0-2], 3 [2-4], 4 [2-5], and 5 [4-6], respectively (p<0.001). After additionally adjusting for age and hypertension, a significant correlation was only found between quartiles 3 and 4 of ccPWV and IAC scores. The odds ratio (95% confidence interval) for the IAC scores was 1.78 (1.28-2.50) (p=0.001) in quartile 4 of ccPWV and 1.45 (1.07-1.95) (p=0.015) in quartile 3 compared with quartile 1. CONCLUSIONS: We found that in patients with acute ischemic stroke, ccPWV was positively related to the degree of IAC. Future longitudinal cohort studies may help to identify the potential role of IAC in the progression of cerebral arterial stiffness.

Intracranial Arterial Calcification and Intracranial Atherosclerosis: Close but Different.

BACKGROUND AND PURPOSE: Intracranial arterial calcification (IAC) may be present in the intimal or medial arterial layer. This study aimed to elucidate the link between the calcification and atherosclerotic disease in the intracranial vasculature. METHODS: Consecutive patients with acute ischemic stroke were included. Bilateral intracranial segment of the internal carotid artery, M1 segment of the middle cerebral artery, intracranial segment of the vertebral artery, and the basilar artery were visualized by the multi-detector computed tomography (CT) and vessel-wall magnetic resonance imaging (vwMRI) within 14 days after stroke onset. IAC was into the intimal or medial pattern. Subsequently, on the vwMRI, we assessed the luminal stenosis, eccentricity, plaque burden, and intraplaque hemorrhage (IPH) as markers of atherosclerosis at each IAC site. RESULTS: Among 69 patients with stroke, IAC was identified in 35% of (161/483) artery segments, of which 61.5% were predominantly intimal calcification and 38.5% were predominantly medial calcification. About 79.8% of intimal calcifications and 64.5% of medial calcifications co-existed with atherosclerotic plaques. Intimal calcification was associated with luminal stenosis (p = 0.003) caused by atherosclerotic lesions. Compared with the medial IAC, intimal IAC was more often accompanied by eccentric plaques (p = 0.02), larger plaque burden (p = 0.001), and IPH (p = 0.001). CONCLUSION: Our multimodal imaging-based comparison study on intracranial arteriosclerosis demonstrated that intimal IAC, compared with medial IAC, was more often accompanied by the luminal stenosis, larger plaque burden, eccentricity, and IPH, providing strong evidence for clinical evaluation on the mechanism, risk, and prognosis of ischemic stroke.

Intracranial Arterial Calcification Relates to Long-Term Risk of Recurrent Stroke and Post-stroke Mortality.

Background: Intracranial arterial calcification (IAC) is highly prevalent in ischemic stroke patients. However, data on the association of IAC with stroke recurrence and mortality remains limited. We examined the effect of IAC on the long-term recurrence of stroke and the risk of post-stroke mortality. Methods: Using a prospective stroke registry, we recruited 694 patients (mean age 71.6 ± 12.4; male sex 50.3%) since December 2004. IAC was visualized using the computed tomography exam that was made at hospital admission and was quantified with the Agatston method. All patients were regularly followed up till July 2016. The impacts of IAC on stroke recurrence and mortality were assessed using Cox-regression models with adjustments for age, sex, and relevant cardiovascular risk factors. Results: During a median follow-up period of 8.8 years, 156 patients (22.5%) suffered a recurrent stroke and 84 died (12.1%). We found that a higher IAC Agatston score related to a higher risk of stroke recurrence (HR per 1-SD increase in IAC: 1.30; 95% CI, 1.08-1.56, p = 0.005) and a higher risk of post-stroke mortality (HR per 1-SD increase, 1.44; 95% CI, 1.06-1.96, p = 0.019). After investigating etiology-specific risks of stroke-recurrence, we found that a higher IAC Agatston score specifically associated with small-vessel occlusive stroke. Conclusions: IAC is a strong risk factor for recurrent stroke and post-stroke mortality. Among stroke subtypes, IAC relates to higher risk of stroke recurrence among patients with small-vessel disease, which indicates chronic calcification detected in large cerebral arteries may have potential effects on the cerebrovascular beds extending to small vessels.

Intracranial Arterial Calcification: Prevalence, Risk Factors, and Consequences: JACC Review Topic of the Week.

Intracranial large and small arterial calcifications are a common incidental finding on computed tomography imaging in the general population. Here we provide an overview of the published reports on prevalence of intracranial arterial calcifications on computed tomography imaging and histopathology in relation to risk factors and clinical outcomes. We performed a systematic search in Medline, with a search filter using synonyms for computed tomography scanning, (histo)pathology, different intracranial arterial beds, and calcification. We found that intracranial calcifications are a frequent finding in all arterial beds with the highest prevalence in the intracranial internal carotid artery. In general, prevalence increases with age. Longitudinal studies on calcification progression and intervention studies are warranted to investigate the possible causal role of calcification on clinical outcomes. This might open up new therapeutic directions in stroke and dementia prevention and the maintenance of the healthy brain.

Correlation Between Intracranial Arterial Calcification and Imaging of Cerebral Small Vessel Disease.

Background and Purpose: Vascular calcification is part of the atherosclerotic process. Intracranial artery calcification is closely associated with cerebral small vessel disease (SVD). The present study aimed to investigate the distribution pattern of intracranial arterial calcification and its association with magnetic resonance imaging (MRI) markers of SVD in patients with acute ischemic cerebrovascular disease. Methods: Two hundred and seventy six consecutive patients with transient ischemic attack (TIA) or acute ischemic stroke who underwent both computed tomography (CT) angiography and MRI were enrolled in this study. Intracranial arterial calcium scores were evaluated using Agatston method. MRI was performed to assess cerebral infarction, white matter hyperintensities (WMHs), lacunes, cerebral microbleeds (CMBs), and enlarged perivascular spaces (EPVSs). Results: Intracranial artery calcification was present in 200 (72.46%) patients, with the highest prevalence in the internal carotid arteries (ICA) (64.8%). The severity of intracranial arterial calcification was associated with the presence of WMHs (P = 0.0001), lacunes (P = 0.0001), and CMBs (P = 0.0001); however, there was no association between calcifications and the presence of EPVSs (P = 0.058). The correlation coefficients (rs) were 0.350, 0.142, 0.285, and 0.251 for WMHs, EPVSs, lacunes, and CMBs, respectively. The adjusted odds ratios (ORs) of intracranial arterial calcification were: 2.747 for WMH (grade 1-2), 3.422 for WMH (grade 3), 2.902 for lacunes, 2.449 for CMB, 0.88 for EPVS (grade 1), and 0.295 for EPVS (grade 2-4). Conclusion: Intracranial artery calcification is common in patients with ischemic cerebrovascular disease and the intracranial carotid artery is most frequently affected. Intracranial arterial calcifications might be associated with imaging markers of SVD and are highly correlated with WMHs, lacunes, and CMBs. Quantification of calcification on CT provides additional information on the pathophysiology of SVD. Intracranial arterial calcification could act as a potential marker of SVD.

Impact of intracranial artery calcification on cerebral hemodynamic changes.

PURPOSE: Intracranial artery calcification (IAC) has been demonstrated to be correlated with ischemic stroke, cognitive decline, and other vascular events by accumulating evidences from both Western and Asian populations. The proposed study aimed to investigate its potential mechanisms by evaluating the blood flow velocity and pulsatility index (PI) of cerebral arteries. METHODS: Consecutive ischemic stroke patients admitted to the Prince of Wales Hospital were recruited after excluding those with atrial fibrillation or poor temporal window. Quantitative measurements of IAC severity were assessed on brain CT scans. Transcranial Doppler (TCD) ultrasonography was performed to evaluate the blood flow velocity of the middle cerebral artery (MCA) and vertebral-basilar artery (VBA). RESULTS: In total, 318 patients were analyzed. Spearman's correlation analysis demonstrated both high MCA systolic flow velocity and high MCA PI were correlated with IAC Agatston score, p < 0.001 individually. Similar correlation was also found between IAC Agatston score and high VBA velocity/high VBA PI, p ≤ 0.001 individually. Multiple logistic regression analysis showed IAC Agatston score was an independent risk factor for high MCA velocity (OR 1.533; 95% CI 1.235-1.903), high VBA velocity (OR 1.964; 95% CI 1.381-2.794), and high VBA PI (OR 1.200; 95% CI 1.016-1.418), respectively. CONCLUSION: Heavier IAC might cause generalized artery flow velocity changes and increased pulsatility index, which may indicate high resistance within cerebrovasculature.

High Extent of Intracranial Carotid Artery Calcification Is Associated with Downstream Microemboli in Stroke Patients.

BACKGROUND: Intracranial arterial calcification (ICAC) is frequently detected on head computed tomography and has been found to be associated with ischemic stroke by recent clinical studies. AIMS: Based on a hospital-based study, we aimed to compare the occurrence of cerebral microembolic signals (MES) among stroke patients with different degrees of ICAC, which may indicate the potential mechanisms linking ICAC and ischemic stroke in intracranial atherosclerosis patients. METHODS: This is a post-hoc analysis of our previous clinical study in 2005-2007, recruiting consecutive ischemic stroke patients with middle cerebral artery territory infarctions and good temporal window for MES monitoring. The degrees of ICAC in the Circle of Willis, especially calcification in the ipsilateral intracranial internal carotid artery (iICA), were evaluated both qualitatively and quantitatively on unenhanced head computed tomography. RESULTS: Among the 68 recruited patients, MES was detected in 26 patients (38.24%). The overall degree of ICAC in the Circle of Willis was similar between patients with and without MES. For calcification in ipsilateral iICA, the presence of MES was more frequent in the high extent group (widest arc of calcification ≥90°) than in the low extent group (54.2% versus 29.5%, P = .046). Logistic regression found that a high extent ipsilateral iICA calcification was an independent risk factor of MES (odds ratio: 3.134; 95% confidence interval, 1.029-9.543; P = .044). CONCLUSIONS: MES is frequently detected in patients with a high extent of ipsilateral iICA calcification, which suggests that a high extent of iICA calcification indicates artery vulnerability and accounts for the occurrence of microemboli in the corresponding artery.

Calcifications in the carotid siphon inversely associate with cognitive performance in stroke-free community dwellers living in rural Ecuador (The Atahualpa Project).

We aimed to assess whether carotid siphon calcifications (as seen on computed tomography) are associated with worse performance in the Montreal Cognitive Assessment in 584 stroke-free individuals living in rural Ecuador. Using mean Montreal Cognitive Assessment score of subjects with Grade 1 calcifications (23.1 ± 4.2) as the referent category, fully adjusted generalized linear models showed significant associations between severity of carotid siphon calcifications and cognitive performance (mean Montreal Cognitive Assessment scores: 20.2 ± 4.8 for Grade 2 (p = 0.004), 19.7 ± 5.3 for Grade 3 (p = 0.0001), and 18.8 ± 4.1 for Grade 4 (p = 0.02)). Predictive Montreal Cognitive Assessment score margins were higher in individuals with Grade 1 calcifications than in other groups. This study shows an inverse relationship between calcium content in the carotid siphon and cognitive performance in Amerindians.

Intracranial Artery Calcification and Its Clinical Significance.

Intracranial arterial calcification (IAC) is an easily identifiable entity on plain head computed tomography scans. Recent studies have found high prevalence rates for IAC worldwide, and this may be associated with ischemic stroke and cognitive decline. Aging, traditional cardiovascular risk factors, and chronic kidney disease have been found to be associated with IAC. The severity of IAC can be assessed using different visual grading scales or various quantitative methods (by measuring volume or intensity). An objective method for assessing IAC using consistent criteria is urgently required to facilitate comparisons between multiple studies involving diverse populations. There is accumulating evidence from clinical studies that IAC could be utilized as an indicator of intracranial atherosclerosis. However, the pathophysiology underlying the potential correlation between IAC and ischemic stroke-through direct arterial stenosis or plaque stability-remains to be determined. More well-designed clinical studies are needed to explore the predictive values of IAC in vascular events and the underlying pathophysiological mechanisms.

Calcifications in the carotid siphon correlate with silent cerebral small vessel disease in community-dwelling older adults: A population-based study in rural Ecuador.

AIM: Using a population-based, cross-sectional design, we aimed to assess whether the presence of calcifications in the carotid siphon (as seen on computed tomography) is associated with silent markers of cerebral small vessel disease (on magnetic resonance imaging) in apparently healthy older adults living in Atahualpa, a rural Ecuadorian village. METHODS: Stroke-free Atahualpa residents aged ≥60 years identified during a door-to-door survey underwent head computed tomography for assessment of carotid siphon calcifications, and brain magnetic resonance imaging for identification of white matter hyperintensities and silent lacunar infarcts. We evaluated the association between calcifications and markers of small vessel disease using logistic regression models adjusted for demographics and cardiovascular risk factors. RESULTS: The mean age of the 236 participants was 71 ± 8 years, and 139 (59%) were women. Computed tomography readings showed high calcium content in the carotid siphon in 64 individuals (27%), and magnetic resonance imaging showed moderate-to-severe white matter hyperintensities in 51 (30%) and lacunar infarcts in 28 (12%). In the univariate analysis, individuals with high calcium content were older and were more likely to have high fasting glucose levels than those with low calcium content. After adjusting for confounding variables, we found an independent association between high calcium content in the carotid siphon and moderate-to-severe white matter hyperintensities (OR 2.3, 95% CI 1.1-4.9, P = 0.035) as well as lacunar infarcts (OR 3.1, 95% CI 1.3-7.6, P = 0.013). CONCLUSIONS: The present study shows a direct relationship between calcium content in the carotid siphon and silent small vessel disease in an indigenous Latin American population. Geriatr Gerontol Int 2016; 16: 1063-1067.

Intracranial Artery Calcification and Its Clinical Significance

Intracranial arterial calcification (IAC) is an easily identifiable entity on plain head computed tomography scans. Recent studies have found high prevalence rates for IAC worldwide, and this may be associated with ischemic stroke and cognitive decline. Aging, traditional cardiovascular risk factors, and chronic kidney disease have been found to be associated with IAC. The severity of IAC can be assessed using different visual grading scales or various quantitative methods (by measuring volume or intensity). An objective method for assessing IAC using consistent criteria is urgently required to facilitate comparisons between multiple studies involving diverse populations. There is accumulating evidence from clinical studies that IAC could be utilized as an indicator of intracranial atherosclerosis. However, the pathophysiology underlying the potential correlation between IAC and ischemic stroke-through direct arterial stenosis or plaque stability-remains to be determined. More well-designed clinical studies are needed to explore the predictive values of IAC in vascular events and the underlying pathophysiological mechanisms.

Intracranial Artery Calcification and Its Clinical Significance

Intracranial arterial calcification (IAC) is an easily identifiable entity on plain head computed tomography scans. Recent studies have found high prevalence rates for IAC worldwide, and this may be associated with ischemic stroke and cognitive decline. Aging, traditional cardiovascular risk factors, and chronic kidney disease have been found to be associated with IAC. The severity of IAC can be assessed using different visual grading scales or various quantitative methods (by measuring volume or intensity). An objective method for assessing IAC using consistent criteria is urgently required to facilitate comparisons between multiple studies involving diverse populations. There is accumulating evidence from clinical studies that IAC could be utilized as an indicator of intracranial atherosclerosis. However, the pathophysiology underlying the potential correlation between IAC and ischemic stroke-through direct arterial stenosis or plaque stability-remains to be determined. More well-designed clinical studies are needed to explore the predictive values of IAC in vascular events and the underlying pathophysiological mechanisms.