“…It is likely that the different ICAC patterns require different prevention strategies as different risk factors have been identified. This is a rapidly evolving field with many questions still to be answered [22].…”
“…It is likely that the different ICAC patterns require different prevention strategies as different risk factors have been identified. This is a rapidly evolving field with many questions still to be answered [22].…”
“…Furthermore, medial ICAC predominately affects the internal elastic lamina adjacent to smooth muscle cells of the medial vascular layer leading to loss of arterial elasticity and compliance [1,2,22]. Such stiffening of the arterial wall is associated with an increase in pulse wave velocity and pulse pressure [23,24]. Consequently, this may impair regulation of collateral blood flow [25,26] thereby reducing the beneficial effect of collaterals predominately in patients with medial ICAC.…”
Background and aims: Distinct subtypes of intracranial carotid artery calcification (ICAC) have been found (i.e., medial and intimal), which may differentially be associated with the formation of collaterals. We investigated the association of ICAC subtype with collateral status in patients undergoing endovascular thrombectomy (EVT) for ischemic stroke. We further investigated whether ICAC subtype modified the association between collateral status and functional outcome. Methods: We used data from 2701 patients with ischemic stroke undergoing EVT. Presence and subtype of ICAC were assessed on baseline non-contrast CT. Collateral status was assessed on baseline CT angiography using a visual scale from 0 (absent) to 3 (good). We investigated the association of ICAC subtype with collateral status using ordinal and binary logistic regression. Next, we assessed whether ICAC subtype modified the association between collateral status and functional outcome (modified Rankin Scale, 0-6). Results: Compared to patients without ICAC, we found no association of intimal or medial ICAC with collateral status (ordinal variable). When collateral grades were dichotomized (3 versus 0-2), we found that intimal ICAC was significantly associated with good collaterals in comparison to patients without ICAC (aOR, 1.41 [95% CI:1.06-1.89]) or with medial ICAC (aOR,). The association between higher collateral grade and better functional outcome was significantly modified by ICAC subtype (p for interaction = 0.01). Conclusions: Patients with intimal ICAC are more likely to have good collaterals and benefit more from an extensive collateral circulation in terms of functional outcome after EVT.
“…Intracranial ICAC (ICAC) is an expression of intracranial atherosclerosis and a common incidental finding on non-contrast computed tomography of the head (CT) [ 3 ]. Its prevalence ranges from 46 to 82% in the general adult population to almost 100% in individuals older than 90 years [ 4 ]. The most common sites of calcification are the cavernous carotid and the carotid siphon where the severity of calcification is associated with the presence of small vessel disease and white matter lesions [ 5 – 8 ], both of which have been shown to adversely affect cognition in older adults [ 9 ].…”
Background
Intracranial internal carotid artery (ICA) calcification is a common incidental finding in non-contrast head CT. We evaluated the predictive value of ICAC (ICAC) for future risk of cognitive decline and compared the results with conventional imaging biomarkers of dementia.
Methods
In a retrospective observational cohort, we included 230 participants with a PET-CT scan within 18 months of a baseline clinical assessment and longitudinal imaging assessments. Intracranial ICAC was quantified on baseline CT scans using the Agatson calcium score, and the association between baseline ICA calcium scores and the risk of conversion from a CDR of zero in baseline to a persistent CDR > 0 at any follow-up visit, as well as longitudinal changes in cognitive scores, were evaluated through linear and mixed regression models. We also evaluated the association of conventional imaging biomarkers of dementia with longitudinal changes in cognitive scores and a potential indirect effect of ICAC on cognition through these biomarkers.
Results
Baseline ICA calcium score could not distinguish participants who converted to CDR > 0. ICA calcium score was also unable to predict longitudinal changes in cognitive scores, imaging biomarkers of small vessel disease such as white matter hyperintensities (WMH) volume, or AD such as hippocampal volume, AD cortical signature thickness, and amyloid burden. Severity of intracranial ICAC increased with age and in men. Higher WMH volume and amyloid burden as well as lower hippocampal volume and AD cortical signature thickness at baseline predicted lower Mini-Mental State Exam scores at longitudinal follow-up. Baseline ICAC was indirectly associated with longitudinal cognitive decline, fully mediated through WMH volume.
Conclusions
In elderly and preclinical AD populations, atherosclerosis of large intracranial vessels as demonstrated through ICAC is not directly associated with a future risk of cognitive impairment, or progression of imaging biomarkers of AD or small vessel disease.
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