Intracranial Carotid Artery Calcification Research Articles

Clinical and imaging features associated with intracranial internal carotid artery calcifications in patients with ischemic stroke.

Intracranial internal carotid artery calcifications (ICAC), a frequent finding on imaging studies, are predictive of future stroke risk in population-based studies. The clinical significance of this observation among ischemic stroke patients is however less clear. In this study, we analyzed ICAC burden in relation to vascular risk factor profile, stroke etiology, and extent of craniocervical vascular calcifications in a consecutive series of ischemic stroke patients. The burden of ICAC was determined both on non-contrast CT and CT-angiography source images by semiquantitative scoring algorithms. The distribution of vascular risk factors, etiologic stroke subtype, and calcification burden in other craniocervical arteries was assessed among patients with no ICAC, mild-moderate ICAC, and severe ICAC. Of 319 patients included into the study, 28% had no ICAC, 35% had mild-moderate ICAC, and 37% had severe ICAC on CT angiography. Independent factors associated with ICAC burden in multivariate analysis included age (p < 0.001), diabetes mellitus (p = 0.006), and coronary artery disease (p < 0.001). Furthermore, a stroke etiology of large artery atherosclerosis or cardioaortic embolism was significantly related to higher ICAC burden (p = 0.006). Patients with severe ICAC were more likely to harbor calcifications in other vascular beds (p < 0.001). All of these findings persisted when analyses were repeated with CT-based ICAC burden assessments. ICAC burden reflects a continuum of atherosclerotic disease involving carotid arteries together with other craniocervical vascular beds. ICAC is significantly associated with stroke of large vessel or cardioembolic origin. This information might help the clinician in prioritizing etiologic work-up in the acute period.

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

Carotid siphon calcification impact on revascularization and outcome in stroke intervention

ObjectiveThe degree of coronary artery calcification has been shown to predict outcomes in coronary artery disease. The impact of intracranial carotid artery calcification on the prognosis of acute ischemic stroke (AIS) is unknown. The authors sought to examine if the degree of intracranial carotid artery calcification influences reperfusion or outcomes in AIS intervention. MethodsAll anterior circulation large vessel occlusion AIS cases that underwent intra-arterial therapy from January 2009 to July 2012 were reviewed. Clinical and radiographic data were collected. Non-contrast brain CT scans were assigned a Calcium Extent Score (degree of calcification of the carotid wall circumference), Calcium Thickness Score (thickness of the calcified plaque), and total Carotid Siphon Calcium (CSC) Score (8-point scale). ResultsOne-hundred seventeen patients met inclusion criteria. The mean age was 65.4±15.6 years and 36% were male. Calcification was present in the intracranial carotid artery of 84 patients (71%). Inter-rater agreement for total CSC score was strong (Spearman's rho=0.883, p<0.001). The mean Calcium Extent Score was 1.5±1.3, Calcium Thickness Score 1.3±1.0 and total CSC Score 2.8±2.2. Reperfusion and mRS were not associated with CSC. Multivariate linear regression analysis revealed that older age, history of coronary disease and cervical internal carotid occlusion/near-occlusion were independently associated with higher total CSC scores. ConclusionExtensive calcification on the intracranial carotid artery does not have impact on reperfusion or clinical outcomes in AIS patients undergoing endovascular therapy. Higher CSC scores are associated with coronary artery disease, increasing age and cervical internal carotid artery occlusion/near-occlusion.

Association Between Arterial Calcifications and Nonlacunar and Lacunar Ischemic Strokes

Nonlacunar cerebral infarcts are presumed to be caused by thromboembolism from the heart or extracranial arteries, whereas lacunar infarcts are thought to be caused by small vessel disease. We investigated to what extent arterial calcifications differ between nonlacunar and lacunar ischemic strokes. We studied 820 consecutive patients with transient ischemic attack or ischemic stroke in the anterior circulation who underwent multidetector computed tomography angiography and had no rare cause of stroke. The presence of likely cardioembolic pathogenesis was determined according to the Trial of Org 10172 in Acute Stroke Treatment criteria. The remaining 708 patients were categorized as nonlacunar or lacunar strokes, either transient ischemic attacks or strokes, based on clinical symptoms corrected by brain imaging results. We measured volume of calcifications in the aortic arch, symptomatic extracranial and intracranial carotid artery using multidetector computed tomography angiography. The difference in calcifications between nonlacunar and lacunar strokes was assessed with a multivariable logistic regression analysis. We adjusted for degree of symptomatic carotid artery stenosis and cardiovascular risk factors. We found an independent association between volume of aortic arch calcifications and nonlacunar ischemic strokes (adjusted odds ratio [95% confidence interval], 1.11 [1.02-1.21]). No independent associations between extracranial and intracranial carotid artery calcifications and nonlacunar strokes were present. The only difference we found between nonlacunar and lacunar strokes was a higher calcification volume in the aortic arch in nonlacunar strokes. Our findings only partially confirm the notion of distinct etiologies and suggest that the potential role of other plaque components, plaque morphology, and aortic arch calcifications in ischemic stroke subtypes awaits further evaluation.

Intracranial Carotid Artery Atherosclerosis and the Risk of Stroke in Whites

Intracranial atherosclerosis represents a relatively unexplored, but potentially important, cause of stroke in a white population. To investigate the relationship between intracranial carotid artery calcification (ICAC) as a marker of intracranial atherosclerosis and the risk of stroke in whites. A population-based cohort study in the general community with 6 years of follow-up was conducted (the Rotterdam Study). Between 2003 and 2006, a random sample of 2323 stroke-free persons (mean age, 69.5 years) underwent computed tomography scanning to quantify ICAC volume. All participants were continuously monitored for the occurrence of stroke until January 1, 2012. Atherosclerotic calcification in the intracranial internal carotid arteries. Incident stroke. During 14,055 person-years of follow-up, 91 participants had a stroke, of which 74 were ischemic. Larger ICAC volume was related to a higher risk of stroke, independent of cardiovascular risk factors, ultrasound carotid plaque score, and calcification in other vessels (fully adjusted hazard ratio per an increase of 1 SD in ICAC volume, 1.43 [95% CI, 1.04-1.96]). Intracranial carotid artery calcification contributed to 75% of all strokes; for aortic arch and extracranial carotid artery calcification this incidence was only 45% and 25%, respectively. Our findings establish intracranial atherosclerosis as a major risk factor for stroke in the general white population and suggest that its contribution to the proportion of all strokes may be greater than that of large-artery atherosclerosis in more proximally located vessel beds.

Cone beam CT incidental findings: intracranial carotid artery calcification—a cause for concern

You may wonder why, as an exception, this editorial is co-authored by Arthur Friedlander from UCLA Dental School, LA. Well, he is currently actively involved in a discussion of obvious importance to the DMFR community. A recently published article noted that intracranial carotid artery calcifications (ICACs) were identified in 4 (2.4%) individuals (statistics recalculated by this correspondent) who were likely nested in the oldest cohort (n=169; age range, 50–85 years) of dental school clinic attendees having cone beam CT scans, in the main for implant placement.1 Using the best available evidence at the time, the authors concluded that no referral or intervention was warranted for these individuals because a study involving 406 (mainly Caucasian) patients (males, 60%; mean age, 62 ± 14 years) with ischaemic cerebrovascular symptoms (amaurosis fugax, transient ischaemic attack, stroke) could not associate the presence or volume of ICAC (as determined by multidetector CT angiography) with the patients’ symptomatic side.2 A review of more recent research, however, demonstrates the need to refer such patients to a physician because the data demonstrate that ICAC is a risk indicator of atherosclerotic disease burden across ethnic lines in both the cerebrovascular and cardiovascular distribution of healthy and symptomatic individuals. Specifically, the results of a recent study completed in Rotterdam, Netherlands, demonstrated that ICAC evidenced on non-contrast enhanced CT was prominently associated with the concomitant presence of MRI markers of vascular brain disease in healthy individuals.3 This investigation, conducted amongst 885 community-dwelling adults (males, 49.2%; mean age, 66.7 ± 5.5 years), demonstrated that higher calcification load and volume in the ICAC were prominently associated with MRI-determined increasing volume of white matter lesions known to be associated over time with development of cognitive impairment. These findings are substantiated by a study conducted in the USA which evaluated 108 consecutive multiethnic (African-American, Hispanic, Caucasian) patients (males 46%; mean age, 57.3 ± 12 years) admitted to the stroke service at Parkland Hospital in Dallas, TX.4 The researchers noted that extensive calcification of the ICAC on head CT was associated with high-grade stenosis (greater than or equal to 50%) on follow-up catheter-based cerebral angiographic study. These findings are supported by two other studies conducted in the Republic of Korea among groups of Asian patients admitted to major medical centers with symptomatic (acute ischaemic stroke/transient ischaemic attack) cerebrovascular disease. In the first project conducted amongst 159 consecutively treated patients (males, 61%; mean age, 66 ± 12 years), the extent of ICAC calcifications (as determined by unenhanced CT) was significantly associated with MRI-demonstrated periventricular and deep white matter hyperintensities and lacunar lesions.5 In the second Korean study evaluated, 314 patients (males, 65%; mean age, 66.3 ± 12.6 years), the severity of ICAC calcification on brain CT was significantly correlated with coronary artery calcium scores as determined by CT coronary angiography among patients previously believed free of atherosclerotic heart disease.6 Atherosclerosis is a generalized process affecting multiple vascular beds with arterial calcifications associated with more advanced states of disease. Cerebral calcification is a validated risk indicator of a diffuse atherosclerotic process in cerebral circulation and coronary artery atherosclerosis. The intention of this editorial is to make oral and maxillofacial radiologists aware that ICAC is a severe incidental finding that should definitely result in referral of these patients to physicians for further evaluation.

The Impact of Intracranial Carotid Artery Calcification on the Development of Thrombolysis-Induced Intracerebral Hemorrhage

We aimed to assess whether intracranial carotid artery calcification (ICAC) evident on head computed tomography is a risk factor for symptomatic intracerebral hemorrhage (sICH) following tissue plasminogen activator (tPA) treatment for acute stroke. We classified 297 consecutive patients into 2 groups (no to mild ICAC and moderate to severe ICAC) according to ICAC severity. Outcome measures included detection of intracerebral hemorrhage and assessment using a modified Rankin scale (mRS) at 1 month and 1 year after stroke. ICH (any type) was significantly more common in patients with moderate to severe ICAC than in patients with no to mild ICAC (22.5% versus 12%; relative risk [RR], 1.67; 95% confidence interval [CI], 1.1-2.5; P<.05). The moderate to severe ICAC group tended to have a higher percentage of sICH, but this association was not statistically significant (RR, 1.57; 95% CI, .75-3.3, P>.05). Multivariate adjusted regression analysis revealed that moderate to severe ICAC was an independent risk factor for ICH following tPA treatment (odds ratio, 2.52; 95% CI, 1.07-5.94; P=.04). Dependent functional outcome (mRS score 3-6) at 1-month and 1-year follow-up was significantly associated with moderate to severe ICAC (RR, 1.56; 95% CI, 1.06-2.27; and RR, 1.56; 95% CI, 1.06-2.33; P<.05). However, ICAC was not an independent factor of functional dependency at 1-month and 1-year follow-up in the final multivariate regression model. A significantly higher percentage of patients with moderate to severe ICAC developed ICH following tPA administration for stroke. ICAC severity is an independent risk factor for ICH events. ICAC severity can help predict short-term and long-term functional dependency in tPA-treated patients, although this can be confounded by other cardiovascular risk factors and stroke severity.

Increased Pulsatility Index Is Associated with Intracranial Arterial Calcification

Background/Aims: An increase in the pulsatility index (PI) has been suggested to reflect distal vascular resistance. The purpose of the present study was to investigate the association between intracranial arterial calcification and intracranial PIs. Methods: Consecutive patients with acute ischemic stroke or transient ischemic attack were included. The PIs of both middle cerebral arteries (MCAs) were measured by transcranial Doppler ultrasonography. Intracranial carotid artery calcification (ICAC) was assessed on computed tomography angiography, and then compared with the mean PI of both MCAs. Patients with internal carotid artery steno-occlusion were excluded from this study. Results: A total of 156 patients were finally enrolled. The prevalence of diabetes increased as the PI value increased (p for trends; p = 0.025). PI was correlated with ICAC score (r = 0.413, p < 0.001) and age (r = 0.507, p < 0.001). Multiple linear regression analysis indicated that aging and ICAC were independent determinants of the PI of MCA after adjusting for sex, systolic blood pressure, smoking, and the presence of diabetes. Conclusions: This study shows that an increase in PI was correlated with the severity of ICAC, which suggests calcification-related vascular resistance might have a role in the elevation of PI.

Quantification of intracranial internal carotid artery calcification on brain unenhanced CT: evaluation of its feasibility and assessment of the reliability of visual grading scales

Previous studies have evaluated intracranial internal carotid artery calcifications (ICACs) qualitatively using different visual grading scales, which could lead to inconsistent results. The purpose of this study was to evaluate the feasibility of ICAC volume measurement and to correlate the volume with visual grading scales. We included 49 patients (>50 years) who underwent unenhanced cranial CT. Two observers evaluated four visual grading scales and measured ICAC volumes semi-automatically, and interobserver agreements were assessed. Differences in ICAC volume between visual grades of each scale were tested. The relationship between the visual grading and volume was assessed. Interobserver agreements ranged from 0.841 to 0.901 for visual grading and 0.997 for volume measurement. Mean volumes were not significantly different between the visual grades (P > 0.05) except when comparing grade 4 with the other grades. The grades of each visual grading correlated well with ICAC volumes (Spearman's ρ = 0.849-0.881, P < 0.001). The relationship between the visual grades and volume was described by a quadratic model (R (2), 0.31-0.50, P < 0.01). ICAC volume measurement is feasible and reproducible, whereas visual grades poorly reflect the actual volume; therefore, volume measurement may be warranted for future research.

Intracranial Carotid Artery Atherosclerosis

Intracranial atherosclerosis is worldwide one of the leading causes of stroke. However, surprisingly little is known about its prevalence and risk factors in a community-dwelling population of white descent. In this study, we determined the prevalence and investigated risk factors of intracranial internal carotid artery calcification (ICAC) as a marker of intracranial atherosclerosis. To quantify the volume of ICAC, 2495 participants (mean age, 69.6 years) from the population-based Rotterdam Study underwent a nonenhanced computed tomography of the intracranial internal carotid arteries. We calculated the prevalence of ICAC. Next, we defined sex-specific quartiles and defined the upper quartile as severe ICAC. Risk factors of ICAC were investigated by linear and logistic multivariate modeling and were stratified by sex. The overall prevalence of ICAC was 82.2%. The median volume of ICAC was 44 mm3 and was larger in men. Age was independently associated with ICAC in both men and women. In men, excessive alcohol intake and smoking (OR, 1.74 [95% CI, 1.28-2.37] and 1.72 [95% CI, 1.10-2.70]) were strong risk factors of ICAC, whereas diabetes and hypertension were in women (OR, 2.02 [95% CI, 1.29-3.17] and 1.79 [95% CI, 1.20-2.68]). A low high-density-lipoprotein concentration was not associated with ICAC. ICAC is highly prevalent and occurs in over 80% of older, white persons. Conventional cardiovascular risk factors are associated with ICAC, but risk factor profiles differ between men and women.

Semi-automatic quantitative measurements of intracranial internal carotid artery stenosis and calcification using CT angiography

IntroductionIntracranial carotid artery atherosclerotic disease is an independent predictor for recurrent stroke. However, its quantitative assessment is not routinely performed in clinical practice. In this diagnostic study, we present and evaluate a novel semi-automatic application to quantitatively measure intracranial internal carotid artery (ICA) degree of stenosis and calcium volume in CT angiography (CTA) images.MethodsIn this retrospective study involving CTA images of 88 consecutive patients, intracranial ICA stenosis was quantitatively measured by two independent observers. Stenoses were categorized with cutoff values of 30% and 50%. The calcification in the intracranial ICA was qualitatively categorized as absent, mild, moderate, or severe and quantitatively measured using the semi-automatic application. Linear weighted kappa values were calculated to assess the interobserver agreement of the stenosis and calcium categorization. The average and the standard deviation of the quantitative calcium volume were calculated for the calcium categories.ResultsFor the stenosis measurements, the CTA images of 162 arteries yielded an interobserver correlation of 0.78 (P < 0.001). Kappa values of the categorized stenosis measurements were moderate: 0.45 and 0.58 for cutoff values of 30% and 50%, respectively. The kappa value for the calcium categorization was 0.62, with a good agreement between the qualitative and quantitative calcium assessment.ConclusionsQuantitative degree of stenosis measurement of the intracranial ICA on CTA is feasible with a good interobserver agreement ICA. Qualitative calcium categorization agrees well with quantitative measurements.

Intracranial Internal Carotid Artery Calcification: A Representative for Cerebral Artery Calcification and Association with White Matter Hyperintensities

Background: Our aim was to investigate the distribution pattern of cerebral artery calcification and its association with white matter hyperintensities (WMH). Methods: We identified 159 consecutive patients with acute ischemic stroke. Calcifications of cerebral arteries and WMH were graded. Results: Cerebral artery calcification was found in 137 patients (86.2%). The intracranial internal carotid artery (I-ICA) was the most frequently affected artery with calcification (76.7%) and moderate-to-severe calcification (38.1%). Spearman’s rank test revealed that the grade of I-ICA calcification was correlated with those of periventricular WMH (r = 0.417, p < 0.001) and deep WMH (r = 0.388, p < 0.001). The adjusted ORs of I-ICA were 2.62 (p <0.05) for periventricular WMH and 3.25 (p <0.05) for deep WMH. Conclusions: Cerebral artery calcification is common in patients with ischemic stroke. I-ICA is the most frequently and most severely affected cerebral artery and its calcification is associated with WMH.

Intracranial Internal Carotid Artery Calcifications: Association with Vascular Risk Factors and Ischemic Cerebrovascular Disease

Intracranial Internal Carotid Artery Calcifications: Association with Vascular Risk Factors and Ischemic Cerebrovascular Disease

Intracranial Internal Carotid Artery Calcifications: Association with Vascular Risk Factors and Ischemic Cerebrovascular Disease

Atherosclerotic calcifications are present not only in the extracranial carotid bifurcation but also in the intracranial part of the internal carotid artery. We assessed the association between intracranial internal carotid artery calcifications and cardiovascular risk factors in patients with ischemic cerebrovascular disease and the association between calcifications and the presence of this disease. Patients undergoing multidetector CT (MDCT) angiography of the carotid arteries for assessment of stenosis degree were included in the study. A semiautomatic custom-made system to quantify calcifications was developed. The associations between the volume of calcifications and cardiovascular risk factors and the type of ischemic cerebrovascular symptoms were assessed with logistic regression. MDCT angiography was performed in 406 patients (age, 62 +/- 14 years; 242 men). Men had a significantly higher calcification volume (66 mm(3)) than women (33 mm(3)). Calcification volume was positively associated with age in both men and women. Smoking, hypercholesterolemia, and a history of cardiac disease were independently related to the presence of calcifications. A history of cardiac disease and ischemic cerebrovascular disease were independently related to the volume of calcifications. No association was found between calcifications and the presence or type of ischemic cerebrovascular disease in the vascular territory of the intracranial internal carotid artery. Calcifications were associated with higher age and male gender. The presence and volume of calcifications were independently associated with cardiovascular risk factors. Calcifications were not related to the presence or type of ischemic cerebrovascular disease.

Intracranial carotid artery calcification on head CT and its association with ischemic changes on brain MRI in patients presenting with stroke-like symptoms: retrospective analysis

Intracranial carotid artery calcification on head CT and its association with ischemic changes on brain MRI in patients presenting with stroke-like symptoms: retrospective analysis

Intracranial carotid artery calcification on head CT and its association with ischemic changes on brain MRI in patients presenting with stroke-like symptoms: retrospective analysis

Our purpose was to study the association between the intracranial arterial calcifications observed on head CT and brain infarcts demonstrated by MRI in patients presenting with acute stroke symptoms. Institutional review board approval was obtained for this retrospective study which included 65 consecutive patients presenting acutely who had both head CT and MRI. Arterial calcifications of the vertebrobasilar system and the intracranial cavernous carotid arteries (intracranial carotid artery calcification, ICAC) were assigned a number (1 to 4) in the bone window images from CT scans. These four groups were then combined into high calcium (grades 3 and 4) and low calcium (grades 1 and 2) subgroups. Brain MRI was independently evaluated to identify acute and chronic large-vessel infarcts (LVI) and small-vessel infarcts (SVI). The relationship between ICAC and infarcts was evaluated before and after adjusting for demographics and cardiovascular risk factors. Statistical analysis could not be performed for the vertebrobasilar system due to an insufficient number of patients in the high calcium group. Of the 65 patients, 46 (71%) had a high ICAC grade on head CT. They were older and had a higher prevalence of cardiovascular risk factors. Acute SVI (P = 0.006), chronic SVI (P = 0.006) and acute LVI (P = 0.04) were associated with a high ICAC grade. After adjustment for age and other risk factors, only acute SVI was associated with a high ICAC grade (P = 0.002). Although age emerged as the most important determinant of ischemic cerebral changes, there were rather complex interactions among multiple risk factors with different infarct types. A high ICAC grade demonstrated a correlation with acute SVI in our patients independent of these risk factors.