Intracranial Artery Calcification Research Articles

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

BackgroundIntracranial 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. MethodsA 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. Results143 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. ConclusionsArterial 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.

Correlation Between Intracranial Calcification and Extracranial Stenosis of the Internal Carotid Artery.

Intracranial artery calcification is a marker of vascular atherosclerosis and has a high prevalence worldwide. Both atherosclerosis of the internal carotid artery at the carotid sinus in the neck and intracranial calcification have been associated with ischemic stroke. The relationship between the two has not been well studied. The present study investigated how carotid sinus narrowing could relate to calcification located in the distal intracranial artery at the cavernous carotid. We examined a population not selected for cerebral disease. This retrospective study contained 179 subjects aged 18 years and older from the Hawaii Diagnostic Radiology database. Extracranial internal carotid artery stenosis was determined using the absolute diameter, North American Symptomatic Carotid Endarterectomy Trial, and common carotid artery methods. Calcification was scored using the modified Woodcock method. A positive correlation between intracranial calcification and extracranial carotid stenosis was found using all three methods. Individuals with intracranial calcification were more likely to be older, have a smaller internal carotid artery diameter, and have a greater percent stenosis at the internal carotid artery than those without intracranial artery calcification (p<0.001 for all). These results may help refocus interest in calcification in studies of cerebral vasculature and its correlation with extracranial carotid stenosis.

AORTIC STIFFNESS IS INDEPENDENTLY ASSOCIATED WITH INTRACRANIAL CAROTID ARTERY CALCIFICATION IN PATIENTS WITH ISCHEMIC STROKE

Objective: Intracranial carotid artery calcification (ICAC), as a strong contributor to the occurrence of ischemic stroke, might be present in the medial or intimal arterial layer. Traditional vascular risk factors are associated with ICAC; however, its association with new markers of vascular function are less understood. The paper aims to evaluate the relationship between carotid-femoral pulse wave velocity (CF-PWV) and ICAC subtypes. Design and method: We enrolled 65 patients with acute ischemic stroke. CF-PWV, systolic, diastolic and mean blood pressure, and pulse pressure (SBP, DBP, MBP, PP) were measured within 6±2 days of stroke onset. CT was performed within 24 hours of stroke onset and ICAC on the stroke site was classified by two methods: volume- and score-based. Tertiles of ICAC volume were determined, and low-grade ICAC (T1) was regarded as a reference. According to the score-based method, medial and intimal ICAC subtypes were determined. Data were analyzed with multivariate logistic regression. Results: Medial and intimal ICAC subtypes were found in 34 (52%) and 24 (37%) patients, respectively. In 11% of patients no ICAC calcifications were found. CF-PWV was higher in patients with high-grade ICAC (OR = 1.56, 95%CI = 1.03-2.35, p = 0.035). CF-PWV was higher in patients with the medial ICAC subtype than in patients with the intimal ICAC subtype (OR = 1.60, 95%CI = 1.00-2.55, p = 0.049) after adjustment for age, MBP, diabetes mellitus, arterial hypertension, hyperlipidemia, and smoking status. Conclusions: Our study demonstrates that among patients with ischemic stroke, aortic stiffness is independently associated with ICAC, and that medial ICAC, compared with intimal ICAC, is accompanied by more advanced aortic stiffness.

Changes in intra- and extracranial carotid plaque calcification: a 2-year follow-up study

Extra- and intracranial carotid plaque calcification might have plaque-stabilizing effects, yet information on changes in plaque calcification remains scarce. We evaluated changes in carotid plaque calcification over 2 years follow-up in patients with symptomatic carotid artery disease. This study is based on the PARISK-study, a multicenter cohort study, with TIA/minor stroke patients with ipsilateral mild-to-moderate carotid artery stenosis (< 70%). We included 79 patients (25% female, mean age 66 years) who underwent CTA imaging with 2 year interval. We assessed the volume of extra- and intracranial carotid artery calcification (ECAC and ICAC) and calculated the difference between baseline and follow-up ECAC and ICAC volume. We performed multivariable regression analyses to investigate the association between change of ECAC or ICAC with cardiovascular determinants. ECAC. We found increase (46.2%) and decrease (34%) in ECAC volume during 2 year follow-up, both significantly correlation with baseline ECAC volume (OR = 0.72, 95% CI 0.58–0.90 respectively OR = 2.24, 95% CI 1.60–3.13).We found significant correlation for change in ECAC volume with diabetes (β = 0.46, 95% CI 0.03–0.89) and baseline ECAC volume (β = 0.81, 95% CI 0.73–0.88). ICAC. We found increase (45.0%) and decrease (25.0%) in ICAC volume. The ICAC decrease was significantly correlated with baseline ICAC volume (OR = 2.17, 95% CI 1.48–3.16), age (OR = 2.00, 95% CI 1.19–3.38) and use of antihypertensive drugs (OR = 3.79, 95% CI 1.20–11.96]).The overall change of ICAC volume was also significantly correlated with diabetes (β = 0.92, 95% CI 1.59–7.02), use of oral hypoglycemic drugs (β = 0.86, 95% CI 0.12–1.59) and baseline ICAC volume (β = 0.71, 95% CI 0.55–0.87). We provide novel insights into the dynamics of carotid plaque calcification in symptomatic stroke patients.

The role of intracranial artery calcification (IAC) in stroke subtype and risk of vascular events

ObjectiveTo test the hypothesis that intracranial arterial calcification (IAC) is associated with intracranial large artery stenosis (ILAS) and a higher risk of vascular events and mortality. MethodWe leveraged data from two cohorts, the New York-Presbyterian Hospital/Columbia University Irving Medical Center Stroke Registry Study (NYP/CUIMC-SRS) and the Northern Manhattan Study (NOMAS) to test our hypotheses. We measured IAC using CT scans of participants in both cohorts and expressed IAC as present (vs not) and in tertiles. For the CUIMC-SRS, demographic, clinical and ILAS status was collected retrospectively. In NOMAS, we used research brain MRI and MRA to define asymptomatic ILAS and covert brain infarcts(CBI). We built models adjusted for demographics and vascular risk factors for cross-sectional and longitudinal analyses. ResultsCross-sectionally, IAC was associated with ILAS in both cohorts (OR 1.78, 95% CI: 1.16-2.73 for ILAS-related stroke in the NYP/CUIMC-SRS and OR 3.07, 95%CI 1.13-8.35 for ILAS-related covert brain infarcts in NOMAS). In a meta-analysis of both cohorts, IAC in the upper (HR 1.25, 95%CI 1.01-1.55) and middle tertile (HR 1.27, 95%CI 1.01-1.59) was associated with higher mortality compared with participants with no IAC. There were no longitudinal associations between IAC and risk of stroke or other vascular events. ConclusionIn these multiethnic populations, IAC is associated with symptomatic and asymptomatic ILAS as well as higher mortality. IAC may be a useful marker of higher mortality, the role of IAC as an imaging marker of risk of stroke is less certain.

Systemic arterial calcium burden in patients with chronic limb-threatening ischemia

Introduction5-year mortality of chronic limb-threatening ischemia (CLTI) is 50–60% and coronary artery disease (CAD) is the main cause of death of CLTI patients, followed by stroke. The aim of this study is to quantify and qualify the calcium load in different arterial territories in patients with CLTI. MethodsProspectively, 60 patients with CLTI were included and received a full-body CT scan. 6 patients were excluded. Different arterial territories (the peripheral lower extremity arteries, coronary arteries, extracranial and intracranial carotid arteries, thoracic and abdominal aorta) were analyzed. Analysis and interrelations of both quantitative and semi-quantitative CT measurements was performed. ResultsMean age was 72 years (range 47–95; SD 11.4). Almost all CLTI patients had calcified arterial beds (femoropopliteal 100%, crural 98.1%, coronary 100%, carotid bifurcation 96.2%, internal carotid artery 98.1%, thoracic aorta 96.2%, abdominal aorta 92.3%). Nearly all arterial territories had severe calcifications. 57% had a very high coronary Agatston score (>1000), and 35% extremely high (>2000). Calcifications in the lower extremity were significantly correlated to CAC score, carotid artery bifurcation calcification score, and to a lesser extent correlated to annular calcifications in the aorta. Very high and extremely high total CAC scores were strongly correlated with severe lower extremity arterial calcifications and severe carotid and intracranial internal carotid artery, thoracic and abdominal aorta calcifications in patients with CLTI patients. ConclusionsIn CLTI patients nearly all arterial territories are severely calcified, suggesting that systemic calcification plays an important role in the poor outcome of this disease.

The correlation between intracranial arterial calcification and the outcome of reperfusion therapy.

Intracranial arterial calcification (IAC) is a risk factor of ischemic stroke. However, the relationship between IAC patterns and clinical outcome of ischemic stroke remains controversial. We aimed to investigate the correlation between IAC patterns and the effects of reperfusion therapy among acute stroke patients. Consecutive acute ischemic stroke patients who underwent reperfusion therapy were included. IAC was categorized as intimal or medial. Based on its involvement, IAC was further classified as diffuse or focal. Neurologic dysfunction was assessed by the National Institute of Health stroke scale (NIHSS). Clinical outcome including favorable neurologic outcome (FNO) and early neurologic deterioration (END) were assessed. Of 130 patients, 117 had IAC. Intimal IAC was identified in 74.6% of patients and medial IAC was present in 64.6% of patients. Diffuse IAC was present in 31.5% of patients. All diffuse IACs were medial pattern. Diffuse IAC was associated with higher baseline NIHSS (p = 0.011) and less FNO (p = 0.047). Compared with patients with focal or single diffuse IAC, patients with multiple diffuse IAC had higher baseline NIHSS (p = 0.002) and less FNO (p = 0.024). Multivariable linear regression (p < 0.001) and logistic regression (p = 0.027) suggested that multiple diffuse IAC was associated with higher baseline NIHSS and less FNO. No significant association was found between END and different IAC patterns. Multiple diffuse medial IAC may predict severer neurologic dysfunction and less favorable neurologic outcome after reperfusion therapy in acute stroke patients.

Lipoprotein(a) is associated with a larger systemic burden of arterial calcification.

Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for cardiovascular disease. However, population-based evidence on the link between Lp(a) and subclinical arteriosclerosis is lacking. We assessed associations of Lp(a) concentrations with arteriosclerosis in multiple arteries. From the population-based Rotterdam study, 2354 participants (mean age: 69.5 years, 52.3% women) underwent non-contrast computed tomography to assess arterial calcification as a hallmark of arteriosclerosis. We quantified the volume of coronary artery calcification (CAC), aortic arch calcification (AAC), extracranial (ECAC), and intracranial carotid artery calcification (ICAC). All participants underwent blood sampling, from which plasma Lp(a) concentrations were derived. The association of plasma Lp(a) levels was assessed with calcification volumes and with severe calcification (upper quartile of calcification volume) using sex-stratified multivariable linear and logistic regression models. Higher Lp(a) levels were associated with larger ln-transformed volumes of CAC [fully adjusted beta 95% confidence interval (CI) per 1 standard deviation (SD) in women: 0.09, 95% CI 0.04-0.14, men: 0.09, 95% CI 0.03-0.14], AAC (women: 0.06, 95% CI 0.01-0.11, men: 0.09, 95% CI 0.03-0.14), ECAC (women: 0.07, 95% CI 0.02-0.13, men: 0.08, 95% CI 0.03-0.14), and ICAC (women: 0.09, 95% CI 0.03-0.14, men: 0.05, 95% CI -0.02 to 0.11]. In the highest Lp(a) percentile, severe ICAC was most prevalent in women [fully adjusted odds ratio (OR) 2.41, 95% CI 1.25-4.63] and severe AAC in men (fully adjusted OR 3.29, 95% CI 1.67-6.49). Higher Lp(a) was consistently associated with a larger calcification burden in all major arteries. The findings of this study indicate that Lp(a) is a systemic risk factor for arteriosclerosis and thus potentially an effective target for treatment. Lp(a)-reducing therapies may reduce the burden from arteriosclerotic events throughout the arterial system. In 2354 participants from the Rotterdam study, we assessed the link between Lp(a) concentrations and arterial calcifications, as proxy for arteriosclerosis, in major arteries. We found that higher Lp(a) levels were consistently associated with larger volumes of calcification in the coronary arteries, aortic arch, extracranial carotid arteries, and intracranial carotid arteries. The findings of our study indicate that Lp(a) is a systemic risk factor for arteriosclerosis, suggesting that the systemic burden of arteriosclerosis throughout the arterial system could be reduced by targeting Lp(a).

Evaluation of prophylactic efficacy of sodium thiosulfate in combating I/R injury in rat brain: exploring its efficiency further in vascular calcified brain slice model.

Cerebral ischemia reperfusion injury (CIR) is one of the clinical manifestations encountered during the management of stroke. High prevalence of intracranial arterial calcification is reported in stroke patients. However, the impact of vascular calcification (VC) in the outcome of CIR and the efficacy of mechanical preconditioning (IPC) and pharmacological conditioning with sodium thiosulphate (STS) in ameliorating IR remains unclear. Two experimental models namely carotid artery occlusion (n=36) and brain slice models (n=18) were used to evaluate the efficacy of STS in male Wistar rats. IR was inflicted in rat by occluding carotid artery for 30min followed by 24-h reperfusion after STS (100mg/kg) administration. Brain slice model was used to reconfirm the results to account blood brain barrier permeability. Further, brain slice tissue was utilised to evaluate the efficacy of STS in VC rat brain by measuring the histological alterations and biochemical parameters. Pre-treatment of STS prior to CIR in intact animal significantly reduced the IR-associated histopathological alterations in brain, declined oxidative stress and improved the mitochondrial function found to be similar to IPC. Brain slice model data also confirmed the neuroprotective effect of STS similar to IPC in IR challenged tissue slice. Higher tissue injury was noted in VC brain IR tissue than normal IR tissue. Therapeutic efficacy of STS was evident in VC rat brain tissues and normal tissues subjected to IR. On the other hand, IPC-mediated protection was noted only in IR normal and adenine-induced VC brain tissues not in high-fat diet (HFD) induced VC brain tissues. Based on the results, we concluded that similar to IPC, STS was effective in attenuating IR injury in CIR rat brain. Vascular calcification adversely affected the recovery protocol of brain tissues from ischemic insult. STS was found to be an effective agent in ameliorating the IR injury in both adenine and HFD induced vascular calcified rat brain, but IPC-mediated neuroprotection was absent in HFD-induced VC brain tissues.

Is there a correlation between dizziness and intracranial artery calcification?

This study aimed to investigate the correlation between dizziness and intracranial artery calcification. A total of 107 consecutive patients were recruited for this study. These patients were categorized into first (case) and second (control) groups. The first and second groups had complaints of dizziness and headache, respectively. All the patients had noncontrast cranial computed tomography images. Bilateral internal carotid arteries, bilateral vertebral arteries, and basilar arteries were evaluated for detecting burden of intracranial artery calcification. Finally, demographic characteristics, stroke risk factors, and burden of intracranial artery calcification of these two groups were compared. The Mann-Whitney U test, chi-square test, and Spearman's correlation were performed to analyze the study. It was found that the first and second groups included 39 and 68 patients, respectively. The mean age of the first group was significantly higher than that of the second group. The mean burden of intracranial artery calcification of the posterior circulation in the first and second groups were not statistically different from each other (p=0.555). The mean burden of intracranial artery calcification of the anterior circulation in the first group was found to be significantly higher than the second group (p=0.005). However, no significant difference was found between the two groups in terms of burden of intracranial artery calcification of anterior or posterior circulation, when the age variable was synchronized in both groups. Although this study found a limited correlation between dizziness and intracranial artery calcification, this situation was basically related to aging.

Intracranial carotid artery calcification morphology differs in patients with lacunar and nonlacunar acute ischemic strokes.

Intracranial carotid artery calcifications (ICACs) are a common finding on noncontrast computed tomography (NCCT) and have been associated with an increased risk of ischemic stroke. However, no data are available about the association between ICAC patterns and stroke etiology. We investigated the association between ICAC patterns and etiological subtypes of ischemic stroke. We retrospectively analyzed a single center cohort of patients admitted for ischemic stroke with known etiology. Each carotid artery was evaluated separately on NCCT scans to define the ICAC pattern (intimal, medial, mixed). The association between ICAC patterns and stroke etiology was investigated using logistic regression models adjusting for relevant confounders. A total of 485 patients were included (median age=78 [interquartile range (IQR) = 70-85] years, 243 [50%] female, median National Institutes of Health Stroke Scale=6 [IQR=3-12]). Frequencies of ICAC patterns were: intimal, n= 96 (20%); medial, n= 273 (56%); mixed, n= 51 (11%), indistinct/absent, n= 65 (13%) patients. Intimal pattern was more frequent in lacunar compared with nonlacunar (33% vs. 16%, p< 0.001) stroke etiology, whereas medial pattern was less frequent in lacunar compared with nonlacunar stroke (36% vs. 62%, p< 0.001). After adjustment for confounders, intimal ICAC predominant pattern remained associated with lacunar stroke etiology in two multivariate models (Model 1: adjusted odds ratio [aOR]=2.08, 95% confidence interval [CI]=1.20-3.56; Model 2: aOR=2.01, 95% CI=1.16-3.46). Our study suggests that intimal ICAC pattern is associated with lacunar stroke and may serve as a marker for lacunar stroke etiology, possibly strengthening the relation between endothelial dysfunction and lacunar stroke.

Intracranial Artery Calcifications Profile as a Predictor of Recanalization Failure in Endovascular Stroke Treatment.

Acute ischemic stroke with large or medium-vessel occlusion associated with intracranial artery calcification (IAC) is an infrequent phenomenon presumably associated with intracranial atherosclerotic disease. We aimed to characterize IAC and its impact on endovascular treatment outcomes. We performed a retrospective cross-sectional study of consecutive patients with stroke treated with thrombectomy from January 2020 to July 2021 in our institution. We described IAC findings (length, density, and location pattern) on baseline noncontrast computed tomography. Patients were divided into 3 groups: IAC related to the occlusion location (symptomatic-IAC group), unrelated to the occlusion (asymptomatic-IAC group), and absence of any IAC (non-IAC group). We analyzed the association between the IAC profile and outcomes using logistic regression models. Intracranial angioplasty and stenting were considered rescue treatments. Of the 393 patients included, 26 (6.6%) patients presented a symptomatic-IAC, 77 (19.6%) patients an asymptomatic-IAC, and in 290 (73.8%) patients no IAC was observed. The rate of failed recanalization (expanded Thrombolysis in Cerebral Infarction 0-2a) before rescue treatment was higher in symptomatic-IAC (65.4%) than in asymptomatic-IAC (15.6%; P<0.001) or non-IAC (13.4%; P<0.001). Rescue procedures were more frequently performed in symptomatic-IAC (26.9%) than in asymptomatic-IAC (1.3%; P<0.001) and non-IAC (4.1%; P<0.001). After adjusting for identifiable clinical and radiological confounders, symptomatic-IAC emerged as an independent predictor of failed recanalization (odds ratio, 11.89 [95% CI, 3.94-35.91]; P<0.001), adoption of rescue procedures (odds ratio, 12.38 [95% CI, 2.22-69.09]; P=0.004), and poor functional outcome (90-day modified Rankin Scale score ≥3; odds ratio, 3.51 [95% CI, 1.02-12.00]; P=0.046). The presence of IAC related to the occlusion location is associated with worse angiographic and functional outcomes. Therefore, identification of symptomatic-IAC on baseline imaging may guide optimal endovascular treatment strategy, predicting the need for intracranial stenting and angioplasty.

Intracranial artery calcification as an independent predictor of ischemic stroke: a systematic review and a meta-analysis

Background and purposeThe association between intracranial artery calcification (IAC) and the risk of ischemic stroke occurrence or poor prognosis had not yet been fully understood. In this study, we conducted a meta-analysis of existing studies aimed to assess whether IAC can be used to predict future ischemic stroke and post-stroke mortality.MethodsMedline, Cochrane, Web of Science and Google Scholar databases were searched up to June 30, 2022. Studies were included if they reported risk ratio (RR) or odds ratios (OR) and corresponding 95% confidence intervals (CI) of stroke concerning the presence of IAC. Random or fixed effects model meta-analyses were performed. Meta-analysis was conducted by using Stata version 16.0.ResultsTwelve studies involving 9346 participants were included. Compared with those without IAC, patients with IAC had a higher risk of stroke occurrence (adjusted OR 1.62, 95% CI 1.18–2.23, P = 0.001) and stroke recurrence (adjusted OR 1.77, 95% CI 1.25–2.51, P = 0.003). However, we did not find a significant correlation between IAC and post-stroke mortality (pooled OR 1.12, 95% CI 0.80–1.56, P = 0.504).ConclusionsOur meta-analysis demonstrated that the presence of IAC was identified as an independent risk factor for ischemic stroke occurrence and recurrence but is not a predictor of post-stroke mortality.

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

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. 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. 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. 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 Carotid Arteriosclerosis Mediates the Association Between Blood Pressure and Cerebral Small Vessel Disease.

Intracranial arteriosclerosis could explain the association between blood pressure (BP) and cerebral small vessel disease (CSVD). Therefore, we tested whether intracranial carotid artery calcification (ICAC) mediates the association between BP and CSVD and determined pathophysiological mechanisms based on ICAC subtypes. One thousand four hundred fifty-eight stroke-free participants from the Rotterdam Study (mean age, 68 years; 52% women) underwent nonenhanced computed tomography scans to quantify ICAC volume (mm3) between 2003 and 2015. ICAC was categorized into intimal and internal elastic lamina calcifications. CSVD included white matter hyperintensities volume, the presence of lacunes, and cerebral microbleeds visualized on magnetic resonance imaging. Office BP included systolic BP, diastolic BP, pulse pressure, and mean arterial pressure. Mediation analysis included a 2-way decomposition to determine the direct association between BP and CSVD and the indirect or mediated effect (negative or positive mediations expressed in %) of log-ICAC volume on such association. BP and log-ICAC were correlated and were also associated with CSVD. In all participants, total log-ICAC volume mediated the association of diastolic BP (-14.5%) and pulse pressure (16.5%) with log-white matter hyperintensities. Internal elastic lamina log-ICAC volume mediated -19.5% of the association between diastolic BP and log-white matter hyperintensities; intimal log-ICAC volume did not mediate associations. For lacunes, total and internal elastic lamina log-ICAC volume mediated the association of diastolic BP (-40% and -45.8%) and pulse pressure (26.9% and 18.2%). We did not observe mediations for cerebral microbleeds. Intracranial arteriosclerosis mediates the association between BP and CSVD. Internal elastic lamina calcification, considered a proxy of arterial stiffness, is the leading mechanism explaining the link between BP and CSVD.

The association of renal impairment with different patterns of intracranial arterial calcification: Intimal and medial calcification

Background and aimsIncreasing knowledge about calcification together with improved imaging techniques provided evidence that intracranial arterial calcification (IAC) can be divided into two distinct entities: intimal and medial calcification. The purpose of this study was to investigate the association between kidney function and the two patterns of IAC, which could clarify the underlying mechanisms of intimal or medial calcification and its clinical consequence. MethodsA total of 516 participants were enrolled in this study. Kidney function was assessed using the estimated glomerular filtration rate (eGFR) based on modified glomerular filtration rate estimating equation. The degree of IAC measured by IAC scores was evaluated on non-contrast head computed tomography (CT) images and IAC was classified as intimal or medial calcification. Associations of kidney function with IAC scores and patterns were assessed sing multivariate logistic regression analysis. ResultsIn 440 patients (85.27%) with IAC, 189 (42.95%) had predominant intimal calcifications and 251 (57.05%) had predominant medial calcifications. Multivariate analysis revealed that lower eGFR level (eGFR <60 ml/min/1.73 m2) was associated with higher IAC scores (odds ratio [OR] 2.01; 95% confidence interval [CI], 1.50–2.71; p < 0.001). Medial calcification was more frequent in the lower eGFR group (eGFR <60 ml/min/1.73 m2) compared to the other two groups with eGFR 60 to 89 and eGFR >90 ml/min/1.73 m2 (78.72% vs. 53.65%, p < 0.001; 78.72% vs. 47.78%, p < 0.001). In multivariable analysis, impaired kidney function was associated with an increased odds of medial calcification presence in patients with eGFR <60 ml/min/1.73 m2 (OR, 1.47; 95% CI, 1.05 to 2.06). ConclusionsOur findings demonstrated that impaired renal function was independently associated with a higher degree of calcification in intracranial arteries, especially medial calcification, which reflects a distinction between two types of arterial calcification and raise the possibility for specific prevention of lesion formation.

Abstract 10309: Susceptibility-Weighted Imaging is Not Inferior to CT in Detecting Intracranial Vertebral Artery Calcification

Susceptibility-Weighted Imaging is not inferior to CT in detecting intracranial vertebral artery calcification Hon-Man Liu. Department of Medical Imaging, Fu-Jen Catholic University Hospital, Fu-Jen Catholic University, New Taipei City, Taiwan Introduction: Microcalcification is vulnerable and ready to rupture, and macrocalcification is more stable. CT is more sensitive to detect calcification than conventional MR. We demonstrated that the advance MR technique, susceptibility-weighted imaging (SWI), is not inferior to CT in detecting calcification of intracranial vertebral artery. Hypothesis: Susceptibility-weighted imaging can detect paramagnetic blood clots and diamagnetic calcification. Materials and methods: We reviewed the patients’ brain SWI imaging between January 2021 to March 2022 in our institute. The inclusion criteria were patients had SWI and brain CT done within 3 months. The exclusion criteria were poor imaging quality, insufficient study, and incomplete study. We defined that vessel wall calcification as void signal on SWI and hyper-attenuation (&gt; or =100 HU) on CT. We compared the incidence and location of the calcification shown on CT and the void signal on SWI in the intracranial vertebral artery wall. Results: A total of 817 patients is eligible for this study. They were aged between 25 years to 90 years old and 393 were females. A 3.0T MR scanner was used in 486 patients, and 1.5T in 331. On CT, intracranial vertebral artery calcification was shown in 613 vertebral arteries. Susceptibility-weighted imaging could depict 98.5% (n=604) void signal at the corresponding intracranial vertebral artery segment shown on CT. Void signal on SWI is conspicuous in 12 foci that not shown as hyper-attenuation on CT. Conclusion: Susceptibility-weighted imaging is not inferior to CT in detecting intracranial vertebral artery calcification. SWI can play a role in the research about intracranial atherosclerosis in the future.

Arterial calcification over time in pseudoxanthoma elasticum: a repeated measurements study

Abstract Background Pseudoxanthoma elasticum (PXE) is a rare genetic disorder, characterized by progressive systemic arterial calcification and an elevated cardiovascular disease risk. Although arterial calcification is an established risk factor of cardiovascular morbidity and mortality, insights into its artery-specific changes over time in PXE remain lacking. Objectives To assess artery-specific changes in arterial calcification over time in PXE and to investigate the associations of cardiovascular risk factors with these changes. Methods We prospectively included 311 PXE patients (mean age 53.1 years, 185 [59.5%] females). During a median follow-up of 3.7 (25th–75th percentiles 1.3–4.2) years patients underwent 472 full-body, non-contrast computed tomography (CT) scans (maximum of 6 CTs per patient) to quantify the volume (μL) of intracranial carotid artery calcification (ICAC), extracranial carotid artery calcification (ECAC), coronary artery calcification (CAC), aortic calcification (AoC), iliac artery calcification (IAC), and leg artery calcification (LAC) and total body calcification (sum of all arteries). We calculated absolute yearly change (follow-up volume × baseline volume / time difference) and relative yearly change (absolute change divided by baseline volume × 100%) in calcification. The correlations amongst arteries in absolute and relative calcification change were assessed using Spearman's correlation coefficients. Risk factors for change in arterial calcification were assessed using linear mixed models (including age as time variable and with all risk factors entered simultaneously into models). Results Calcification volume change ranged from 3% to 12% increase per year, with a total body calcification progression of 11% per year. The correlations amongst arteries in absolute and relative yearly progression of calcification were only weak to moderate (correlation coefficients ranged from 0.23 between CAC and ECAC to 0.38 between CAC and LAC). Hypertension was markedly associated with increased AoC (multiplicative change in calcification per 5 years of age 1.46 [95% CI 1.13–1.89]). Moreover, the strongest predictor of ICAC change was ever smoking (1.23 [95% CI 1.03–1.46]) and of ECAC change was hypercholesterolemia (1.21 [95% CI 1.02–1.43]). Conclusions Arterial calcification volume progressed with 11% per year in PXE, with considerable variation between and only moderate correlation amongst arteries. Moreover, we found several modifiable, artery-specific risk factors for the progression of calcification. Although both PXE and risk factor presence are considered systemic in nature, our findings highlight that considerable differences exist between arteries in susceptibility to calcification. As such, our results provide important insights into the mechanisms underlying arterial calcification in PXE, which might be used for more targeted treatment and prevention. Funding Acknowledgement Type of funding sources: None.

Intracranial Arterial Calcifications: Potential Biomarkers of Stroke Risk and Outcome.

Intracranial artery calcifications (IAC), a common and easily identifiable finding on computed tomorgraphy angiography (CTA), has gained recognition as a possible risk factor for ischemic stroke. While atherosclerosis of intracranial arteries is believed to be a mechanism that commonly contributes to ischemic stroke, and coronary artery calcification is well-established as a predictor of both myocardial infarction (MI) and ischemic stroke risk, IAC is not currently used as a prognostic tool for stroke risk or recurrence. This review examines the pathophysiology and prevalence of IAC, and current evidence suggesting that IAC may be a useful tool for prediction of stroke incidence, recurrence, and response to acute ischemic stroke therapy.

Comparison of Intracranial and Extracranial Carotid Artery Calcifications between Obstructive Sleep Apnea Patients and Healthy Individuals: A Combined Cone-Beam Computed Tomography and Polysomnographic Study.

Purpose This study aimed to compare the presence and grades of intra- and extracranial carotid artery calcifications between obstructive sleep apnea (OSA) and non-OSA patients. Methods CBCT records of 190 patients (95 OSA patients and 95 non-OSA patients) were retrospectively collected and analyzed. Patient demographic data, including age and gender for both study groups and body mass index (BMI), and apnea-hypopnea index (AHI) for OSA patients were recorded. The presence of intra- and extracranial carotid artery calcifications and the number of calcifications were noted according to the grading scale. Results There was a significant difference in carotid artery calcifications between OSA patients and healthy individuals. A total of 56.8% of the OSA patients showed at least one carotid artery calcification, whereas 13.8% of healthy individuals showed at least one carotid artery calcification (p < 0.05). For intracranial calcifications, OSA patients showed a significantly higher prevalence than healthy individuals (p < 0.05). The results showed that as the apnea-hypopnea index increases in OSA patients, the incidence of carotid artery calcification increases simultaneously. AHI > 30 patients showed the highest percentage of calcifications. Conclusion In conclusion, OSA patients showed a higher prevalence of calcified carotid artery calcifications than healthy individuals. The results can be interpreted as the higher AHI, the more carotid artery calcification occurs. As these lesions can be a precursor of future strokes, 3D MDCT/CBCT images should evaluate meticulously not only extracranial but also intracranially, especially in OSA patients.