Intracranial Carotid Calcification Research Articles

Assessment of relationship between extracranial and intracranial carotid calcifications—a retrospective cone beam computed tomography study

Cone beam CT scans in current day dental practice are highly collimated yet involve areas along the course of the extracranial carotid artery. Detecting an extracranial carotid calcification on small volume scans leaves the dentist with two questions: whether the patient is likely to have intracranial carotid calcifications and whether the patient warrants further medical attention. This study aimed to assess the presence of intracranial carotid artery calcifications (ICAC) in the presence of extracranial carotid artery calcifications (ECAC). 450 CBCT scans were retrospectively evaluated for ECAC and ICAC. Erby et al's classification was modified to classify calcifications as mild, moderate, and severe. The presence of ICAC when ECAC were present was evaluated in all three orthogonal planes. The risk of ICAC in the presence of ECAC was calculated as odds ratio and the association between the two was calculated using a χ2 test. The odds ratio for bilateral ICAC in the presence of bilateral ECAC was 15.09. The odds ratio for left ICAC/right ICAC in the presence of left/ right ECAC was 0.833 and 2.564, respectively. The number and severity of calcifications increased with age. The χ2 test showed that there was a strong association (p < 0.001) between bilateral ECAC with bilateral ICAC. The results of this group of patients showed that there is an increased presence of ICAC in the presence of ECAC.

ASSOCIATION BETWEEN INTERNAL AND EXTERNAL CAROTID ARTERY CALCIFICATIONS IN PATIENTS UNDERGOING DENTAL IMPLANT THERAPY

Background Vascular calcifications are often carefully assessed by oral and maxillofacial (OMF) radiologists on cone beam computed tomography (CBCT) scans. This is done because of the risk for cerebral ischemia and legal liabilities. Scans with a large field of view (FOV) often depict both extra- and intracranial carotid calcifications. Because of radiation dose concerns, the FOV is often reduced in certain examinations that tend to show extracranial carotid calcifications more often than intracranial vessels. It is valuable to predict the presence of intracranial carotid calcifications, which often pose a higher risk for cerebral ischemia in the presence of extracranial carotid calcification. Therefore, the current study aimed to assess the association between extra- and intracranial carotid calcifications. Materials and Methods Retrospective evaluation of 1000 CBCT scans of patients referred for dental implant therapy was done, and on the basis of FOV, 450 CBCT scans that included both the intra- and extracranial carotid calcifications were chosen for evaluation. The scans were evaluated for the presence/absence of vascular calcifications. The association between intra- and extracranial carotid calcifications was evaluated by using the χ2 test. Results Overall, 171 (38%) extracranial and 172 (38.2%) intracranial calcifications were detected. Of the 171 extracranial findings, 74 were bilateral, 45 were on the left, and 52 were on the right. Of the 172 intracranial findings, 112 were bilateral, 29 were on the left, and 31 were on the right. When extracranial calcification was present, intracranial calcifications were also noted in 61.9% cases. There was a strong association between extra- and intracranial calcifications (Pearson χ2 107.643; P Conclusions In this patient population, there is a significant association between extra- and intracranial carotid artery calcifications. Future studies should be performed on a larger patient population to better understand this association.

Severity of intracranial carotid artery calcification in intracranial atherosclerosis-related occlusion treated with endovascular thrombectomy

ObjectivesIntracranial atherosclerosis related large vessel occlusions (ICAS-O) are challenging to diagnose and manage. The degree of intracranial carotid artery calcification may assist pre-thrombectomy diagnosis of ICAS and guide treatment strategy. The aim of the study is to determine if intracranial carotid calcification is associated with ICAS-O. Patients and methodsConsecutive large vessel occlusion patients who underwent thrombectomy from 2006 to 2017 were retrospectively studied. Patients were classified into ICAS-O if pre-existing atherosclerotic lesion was identified as the etiology for large vessel occlusion during the thrombectomy. The degree of intracranial carotid artery calcification (ICAC), technical and clinical outcomes of ICAS-O was compared with non-ICAS-O patients. ResultsIn a retrospective cohort study of 64 thrombectomy patients, ICAS-O accounted for 14.1% of cases and was associated with higher degree of carotid calcification (mean Woodcock scale 2.8 vs 1.6, p = 0.044), need of stent-retreiver rescue (55.6% vs 5.5%, p = 0.001), and adjuvant stenting or angioplasty (33.3% vs 0%, p = 0.002) compared with non-ICAS-O. ConclusionThe severity of ICAC may be associated with ICAS-O as the underlying etiology amongst thrombectomy patients. Compared with large vessel occlusion of other causes, ICAS-O was associated with more failure of aspiration and a higher need of adjuvant stenting and angioplasty.

Intracranial atherosclerosis and cerebral small vessel disease in intracerebral hemorrhage patients

BackgroundThe association between cerebral small vessel diseases (cSVD) and intracranial atherosclerosis is debated and conflicting results have been reported. We sought to investigate this association in patients with intracerebral hemorrhage (ICH), due to severe cSVD. MethodsConsecutive ICH patients were divided into those meeting criteria for cerebral amyloid angiopathy (CAA) and those with deep hypertensive ICH consistent with hypertensive cSVD (HTN-SVD). White matter hyperintensity volumes (WMH) and microbleed counts (MB) were measured on MRI. CTA was rated for severity of intracranial carotid calcifications and for presence of >50% intracranial stenosis (ICS). Associations of intracranial atherosclerosis severity with type of SVD (CAA vs HTN-cSVD) and with imaging and clinical markers of cSVD burden were analyzed. ResultsThe cohort included 253 CAA and 90 HTN-SVD patients. In multivariable models, the type of cSVD (CAA vs. HTN-cSVD) was not associated with calcification severity (OR=1.04, 95% CI [0.62–3.5], p=0.37) or presence of ICS (OR=0.84, 95% CI [0.21–2.74], p=0.78).We found no association between intracranial atherosclerosis (calcifications and stenoses) and parenchymal markers of cSVD severity (WMH and MB, adjusted p≥0.2 for all comparisons) and no association with presence of dementia before ICH (adjusted p≥0.2 for both comparisons). ConclusionsWe found no association between intracranial atherosclerosis and parenchymal or clinical consequences of cSVD, suggesting that cSVDs while sharing some risk factors are not influenced by upstream larger vessel pathologies.

Liver fat is related to cardiovascular risk factors and subclinical vascular disease: the Rotterdam Study.

Increasing evidence suggests involvement of the amount of liver fat in the development of cardiovascular disease. We investigated the relation of liver fat with cardiovascular risk factors and subclinical vascular disease in the general population. Between 2003 and 2006, 2351 persons from the population-based Rotterdam Study (mean age 69.6 ± 6.7 years, 47.2% males) underwent non-enhanced computed tomography. We measured the mean liver attenuation value in Hounsfield units and quantified the following markers of subclinical vascular disease: epicardial fat volume and volumes of coronary (CAC), aortic (AAC), extracranial (ECAC), and intracranial carotid calcification (ICAC). Using linear regression, we investigated associations between traditional cardiovascular risk factors and mean liver attenuation. We also investigated relations of mean liver attenuation with markers of subclinical vascular disease, adjusting for cardiovascular risk factors. We found strong associations of waist circumference, diastolic blood pressure, and diabetes with lower mean liver attenuation [multivariable-adjusted beta per unit increase in waist circumference: -2.54 (95% CI: -3.10; -1.99); diastolic blood pressure: -0.52 (95% CI: -0.88; -0.17); and the presence of diabetes: -21.91 (95% CI: -31.76; -12.06)]. Moreover, we found that larger mean liver attenuation values were associated with smaller volumes of epicardial fat and CAC, independent of cardiovascular risk factors [beta per 1-SD increase in mean liver attenuation value: -0.05 (95% CI: -0.08; -0.02) and -0.05 (95% CI: -0.10; -0.01), respectively]. Larger amounts of liver fat are related to larger volumes of epicardial fat and CAC, independent of traditional cardiovascular risk factors, providing important novel insights into the role of liver fat as a marker of vascular disease.

Intracranial Carotid Calcification on Cranial Computed Tomography: Visual Scoring Methods, Semiautomated Scores, and Volume Measurements in Patients With Stroke.

Intracranial internal carotid artery calcification is associated with cerebrovascular risk factors and stroke, but few quantification methods are available. We tested the reliability of visual scoring, semiautomated Agatston score, and calcium volume measurement in patients with recent stroke. We used scans from a prospective hospital stroke registry and included patients with anterior circulation ischemic stroke or transient ischemic stroke whose noncontrast cranial computed tomographic scans were available electronically. Two raters measured semiautomatic quantitative Agatston score, and calcium volume, and performed qualitative visual scoring using the original 4-point Woodcock score and a modified Woodcock score, where each image on which the internal carotid arteries appeared was scored and the slice scores summed. Intra- and interobserver coefficient of variations were 8.8% and 16.5% for Agatston, 8.8% and 15.5% for calcium volume, and 5.7% and 5.4% for the modified Woodcock visual score, respectively. The modified Woodcock visual score correlated strongly with both Agatston and calcium volume quantitative measures (both R(2)=0.84; P<0.0001); calcium volume increased by 0.47-mm/point increase in modified Woodcock visual score. Intracranial internal carotid artery calcification increased with age by all measures (eg, visual score, Spearman ρ=0.4; P=0.005). Visual scores correlate highly with quantitative intracranial internal carotid artery calcification measures, with excellent observer agreements. Visual intracranial internal carotid artery scores could be a rapid and practical method for epidemiological studies.

Is Calcification of Intracranial Arteries Important and How?

Intracranial atherosclerosis is a well-recognized and common cause of stroke in Asian, black, and Hispanic individuals.1,2 Recent studies showed that intracranial occlusive disease is also a more common cause of stroke in white individuals than previously thought.3 In this issue of JAMA Neurology, Bos and colleagues4 provide evidence that intracranial carotid artery calcification is an important risk factor for stroke in an elderly white Dutch population. As part of the prospective, population-based Rotterdam study, the authors followed up 2323 individuals to determine the incidence of stroke (parenchymal brain hemorrhage or ischemic) after they had nonenhanced computed tomography (CT) scanning that imaged the coronary arteries, aortic arch, extracranial carotid arteries, and intracranial carotid arteries. The authors used calcification volume in these arteries as an indicator of atherosclerosis and correlated this with the risk for all stroke and ischemic stroke. They found that larger intracranial carotid calcification volume was independently associated with all stroke and that intracranial carotid calcification was a more important risk factor for stroke than aortic arch calcification or extracranial carotid calcification. The apparent discrepancy between the importance of intracranial carotid calcification as a major risk factor for stroke in this study and the low frequency of stroke caused by intracranial atherosclerosis in most studies of white patients is largely explained by the different design of these studies. Prior studies identified consecutive patients with stroke and determined the frequency of proximal intracranial atherosclerotic arterial stenosis. In the current study, intracranial carotid calcification (not stenosis) was measured and correlated with subsequent stroke regardless of the territory of the stroke. Data on the size, location (cortical or subcortical), and vascular territory of brain infarcts were not collected. While the current study suggests that intracranial carotid artery calcification is an important, previously seldom considered, risk factor for subsequent stroke in any vascular territory in white patients, the study did not show that the intracranial vascular lesions were the cause of the strokes. Many of the ischemic strokes in this study were almost surely not caused by intracranial carotid atherosclerosis because the strokes were either in a different vascular territory or were caused by other vascular diseases (eg, coexisting penetrating artery disease,5 a cardiac source of embolism). Moreover, at least 11% of the strokes in the study were hemorrhagic and no causal relationship has been established between intracranial arterial calcification and parenchymal brain hemorrhage. Recent interest in calcification of arteries has been spurred on by the strong association between coronary calcification detected by cardiac CT and the risk for future cardiac events.6 The situation appears to be different in relation to carotid artery disease in the neck where the presence of heavy calcification on spiral CT has been correlated with stable, noninflammatory, asymptomatic plaques.7 Whether intracranial arterial calcification is also associated with stable plaque that is unlikely to cause a distal stroke is unknown. What is known is that severe stenosis of an intracranial artery is strongly associated with a high risk for stroke distal to the stenosis in patients presenting with a transient ischemic attack or stroke.8 If the presence of severe intracranial carotid calcification implied coexistent severe arterial stenosis of the artery, that would provide some evidence of a potential causal link between calcification and risk for stroke attributable to the affected artery. However, the relationship between calcification of the intracranial carotid artery and coexistent stenosis is unsettled. Older pathological studies found that heavy calcification of the carotid siphon did not necessarily indicate stenosis of the lumen9; however, a more recent neuroimaging study showed that the positive predictive value of severe carotid siphon calcification on CT for a stenosis of greater than 50% on angiography was 86% using bone window measurements.10 It is also possible that intracranial carotid calcification may cause stroke without the presence of coexistent stenosis if calcification is associated with unstable plaque features that predispose to distal embolism. This study by Bos and colleagues4 raises important questions about the role of calcification in the pathophysiology of intracranial atherosclerosis and should reawaken interest in intracranial atherosclerosis as a cause of stroke inwhite individuals. The study indicates that intracranial carotidcalcification isamajor risk factor for stroke inwhite individuals but does not establish a pathophysiologic causal relationshipbetweenthe two.Establishing thatwill require further prospective studies that correlate the association between intracranial arterial calcification and stenosis more clearly, identifyatheroscleroticplaque featuresassociatedwith calcification thatmay be associatedwith a high risk for distal embolism, and classify ischemic strokes that occur in patientswith intracranial carotid calcification according to size, location (cortical or subcortical), vascular territory, and thecoexistenceofotherpotential causesof stroke.Muchworkneeds to be done. Related article page 405 Opinion

Atherosclerotic calcification relates to cognitive function and to brain changes on magnetic resonance imaging

Increasing evidence suggests a role of atherosclerosis in the pathogenesis of cognitive impairment and dementia. Calcification volume measured with computed tomography (CT) is a valid marker of atherosclerosis. This study investigates associations of atherosclerosis (measured using CT) at four locations with cognition and brain changes on magnetic resonance imaging (MRI). To quantify calcification volume, 2414 nondemented people from the Rotterdam Study underwent CT of the coronary arteries, aortic arch, extracranial carotid arteries, and intracranial carotid arteries. To assess global cognition and performance on memory, executive function, information processing speed, and motor speed, they also underwent neuropsychological tests. In a random subgroup of 844 participants, brain MRI was performed. Automated segmentation and quantification of brain MRI scans yielded brain tissue volumes in milliliters. Diffusion tensor imaging was used to measure the microstructural integrity of the white matter. Relationships of atherosclerotic calcification with cognition, brain tissue volumes, and diffusion tensor imaging measures were assessed with linear regression models and adjusted for relevant confounders. With larger calcification volumes, lower cognitive scores were observed. When calcification volumes were larger, total brain volumes were also smaller. Specifically, larger coronary artery calcification volumes related to smaller gray matter volumes, and extracranial and intracranial carotid calcification volumes related to smaller white matter volumes. Larger calcification volume in all vessel beds was accompanied by worse microstructural integrity of the white matter. Larger calcification volume is associated with worse cognitive performance. It also relates to smaller brain tissue volumes and worse white matter microstructural integrity, revealing possible mechanisms through which atherosclerosis may lead to poorer cognition.

Calcification in Major Vessel Beds Relates to Vascular Brain Disease

Calcification in atherosclerotic plaques is a novel marker of atherosclerosis and is related to cardiovascular disease. However, its relationship with cerebrovascular disease has not been investigated extensively. We investigated the relationship between calcification in various vessel beds outside the brain and imaging markers of vascular brain disease. A total of 885 community-dwelling people (mean age, 66.7 years) underwent computed tomography of the coronary arteries, aortic arch, and extracranial and intracranial carotid arteries to assess arterial calcification. Brain magnetic resonance imaging scans were performed to assess cerebral infarcts, microbleeds, and white matter lesions (WMLs). Calcification in each vessel bed was associated with presence of cerebral infarcts and with larger WML volume. The most prominent associations were found between intracranial carotid calcification and WML volume and between extracranial carotid calcification and infarcts. Adjustment for cardiovascular risk factors or ultrasound carotid plaque scores did not change these results. No associations were found between calcification and cerebral microbleeds. Arterial calcification in major vessel beds is associated with vascular brain disease on magnetic resonance imaging. Most notably, larger intracranial carotid calcification load relates to larger WML volumes, and larger extracranial carotid calcification load relates to the presence of cerebral infarcts, independently of ultrasound carotid plaque score. This suggests that calcification of atherosclerotic plaque yields other information in addition to merely the presence of plaques, providing novel insights into the etiology of vascular brain disease.

Intracranial carotid calcification on CT images as an indicator of atheromatous plaque: analysis of high-resolution CTA images using a 64-multidetector scanner

Intracranial arterial wall calcifications are frequently observed on routine head computed tomography (CT) images. The purpose of this study was to evaluate whether calcification of the intracranial carotid artery on CT images could predict atheromatous plaque and luminal stenosis. A total of 259 patients were examined using three-dimensional CT angiography using high-resolution 64 detector scanners. We examined patients from the petrous portion to the top of the internal carotid arteries. We evaluated the existence of calcification and atheromatous plaque based on our criteria retrospectively. The thickness of calcification was measured in each vessel, and the shape of calcification was classified into three types. There was low correlation between the thickness of the calcification and luminal stenosis, but the shape of the calcification corresponded well to the stenosis. The population of patients with >50% stenosis of the intracranial carotid artery differed statistically significantly for each calcification shape. There was a high negative predictive value (97.7%) in the correlation between the existence of calcification and atheromatous plaque on the multidetector CT images. Calcification of the intracranial carotid artery on CT images shows a high negative predictive value for the existence of atheromatous plaque in the same artery. The thickness of the calcification did not correlate well with luminal stenosis, but its shape seemed to predict luminal stenosis.