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Published on: April 23, 2021
Hypertension, intracranial arteriosclerosis, and structural brain changes in patients with TIA or ischemic stroke
Xi Li1,2,3,4, Bernhard P Berghout1,4, Gijs van Rooijen3,4
1Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands.
Insights
Intracranial carotid artery calcification (ICAC) partially explains how hypertension leads to brain atrophy and white matter lesions in stroke patients. Internal elastic lamina (IEL) calcification, not intimal calcification, plays a key role.
Area of Science:
- Neurology
- Radiology
- Vascular Medicine
Background:
- Hypertension is a significant risk factor for structural brain changes like atrophy and cerebral small vessel disease.
- Intracranial arteriosclerosis is a potential mechanism linking hypertension to these brain alterations.
- Intracranial carotid artery calcification (ICAC) serves as a proxy for intracranial arteriosclerosis.
Purpose of the Study:
- To investigate if ICAC mediates the association between hypertension and structural brain changes in patients with TIA or ischemic stroke.
- To determine the role of different ICAC subtypes (intimal and internal elastic lamina - IEL) in this association.
Main Methods:
- A registry study included 968 patients with TIA or ischemic stroke.
- Non-contrast CT (NCCT) and CT-angiography (CTA) were used to assess ICAC presence, volume, and subtypes (intimal vs. IEL).
- Structural brain changes (atrophy, white matter lesions, lacunes) were evaluated using NCCT, and mediation analysis was performed.
Main Results:
- ICAC was prevalent in 67.8% of patients.
- ICAC presence partially explained the link between hypertension and periventricular white matter lesions (7.1%), deep white matter lesions (3.6%), and lacunes (17.6%).
- Hypertension was associated with increased atrophy mediated by ICAC (OR: 1.02). IEL calcification, specifically, mediated the association with periventricular WML (16.8%) and atrophy (OR: 1.12).
Conclusions:
- ICAC partially mediates the relationship between hypertension and structural brain changes, including atrophy and white matter lesions.
- While intimal calcification is common, IEL calcification is more significant in explaining hypertension's impact on brain structure.
- These findings highlight the importance of assessing ICAC in hypertensive patients at risk for stroke.
Introduction:
Hypertension is a major risk factor of structural brain changes, including atrophy and cerebral small vessel disease. Intracranial arteriosclerosis could be an underlying mechanism between hypertension and structural brain changes. This study investigated whether intracranial carotid artery calcification (ICAC), as a proxy for intracranial arteriosclerosis, explains the association between hypertension and structural brain changes in patients with TIA or ischemic stroke.
Patients And Methods:
About 968 patients (mean age 62.7 years) with TIA or ischemic stroke from a registry who underwent non-contrast CT (NCCT) and CT-angiography (CTA) were included in this study. Presence and volume (mm3) of ICAC were assessed on CTA. Subtypes of ICAC were assessed on NCCT, where ICAC was categorized into intimal and internal elastic lamina (IEL) type calcification. Structural brain changes, indicated by atrophy, periventricular and deep white matter lesions (WML), and lacunes were assessed on NCCT. Mediation analysis was performed using ICAC, ICAC volume, and ICAC subtypes as mediators.
Results:
ICAC was prevalent in 67.8% of patients, with 52.6% of them exhibiting intimal calcification, and 26.5% exhibiting IEL calcification. Atrophy, periventricular WML, deep WML, and lacunes were present in 48.1%, 56.4%, 43.0% and 17.1% of patients respectively. The presence of ICAC explained 7.1% of the association of hypertension with periventricular WML, 3.6% with deep WML, and 17.6% with lacunes. Hypertension was associated with increased atrophy through ICAC (OR: 1.02, 95% CI: 1.00-1.05). In subgroup analyses, IEL calcification partly explained the association between hypertension and periventricular WML (16.8%), and atrophy (OR: 1.12, 95% CI: 1.02-1.27). Intimal calcification did not explain any association.
Conclusion:
ICAC partially explained the association between hypertension and atrophy, periventricular and deep WML, and lacunes. Although intimal calcification was more prevalent in ischemic stroke patients, IEL calcification takes the leading role in explaining the association between hypertension and structural brain changes.
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