Intracranial Atherosclerotic Burden and Cerebral Parenchymal Changes at 7T MRI in Patients With Transient Ischemic Attack or Ischemic Stroke.

Arjen Lindenholz,Theodoor D Witkamp,Anja G Van Der Kolk,Irene C Van Der Schaaf,Jeroen De Bresser,H Bart Van Der Worp,Jeroen Hendrikse

doi:10.3389/fneur.2021.637556

Abstract

The relevance of intracranial vessel wall lesions detected with MRI is not fully established. In this study (trial identification number: NTR2119; www.trialregister.nl), 7T MRI was used to investigate if a higher vessel wall lesion burden is associated with more cerebral parenchymal changes in patients with ischemic stroke or transient ischemic attack (TIA). MR images of 82 patients were assessed for the number of vessel wall lesions of the large intracranial arteries and for cerebral parenchymal changes, including the presence and number of cortical, small subcortical, and deep gray matter infarcts; lacunes of presumed vascular origin; cortical microinfarcts; and periventricular and deep white matter hyperintensities (WMHs). Regression analyses showed that a higher vessel wall lesion burden was associated with the presence of small subcortical infarcts, lacunes of presumed vascular origin, and deep gray matter infarcts (relative risk 1.18; 95% CI, 1.03–1.35) and presence of moderate-to-severe periventricular WMHs (1.21; 95% CI, 1.03–1.42), which are all manifestations of small vessel disease (SVD). The burden of enhancing vessel wall lesions was associated with the number of cortical microinfarcts only (1.48; 95% CI, 1.04–2.11). These results suggest an interrelationship between large vessel wall lesion burden and cerebral parenchymal manifestations often linked to SVD or, alternatively, that vascular changes occur in both large and small intracranial arteries simultaneously.

Highlights

Intracranial atherosclerosis (ICAS) is an important cause of ischemic stroke [1]
Between December 2009 and May 2018, patients presenting at our University hospital with TIA or ischemic stroke of the anterior circulation were eligible for inclusion in Abbreviations: ACA, anterior cerebral artery; CI, confidence interval; FLAIR, fluid-attenuated inversion recovery; ICA, internal carotid artery; ICAS, intracranial atherosclerosis; MCA, middle cerebral artery; MPIR-TSE, magnetization-prepared inversion-recovery turbo spin echo; SVD, small vessel disease; T, tesla; TIA, transient ischemic attack; TOAST, Trial of Org 10172 in Acute Stroke Treatment; WMH, white matter hyperintensity
An increased vessel wall lesion burden was associated with the presence of small subcortical infarcts, lacunes of presumed vascular origin, or deep gray matter infarcts, and with the presence of moderate-to-severe periventricular WMHs

Summary

Introduction

Intracranial atherosclerosis (ICAS) is an important cause of ischemic stroke [1]. Historically, ICAS has been evaluated by measuring the presence of intracranial stenosis using lumenographic techniques or by detecting vessel wall calcifications that generally reflect a more advanced stage of ICAS [2,3,4,5]. Over the last two decades, intracranial vessel wall MRI sequences have enabled in vivo visualization of the intracranial vessel wall itself [6,7,8]. Ex vivo studies applying intracranial vessel wall MRI to postmortem samples suggest that these changes represent vessel wall disease at an early stage to halfway on the developmental timeline of ICAS [13,14,15,16,17,18]. The parenchymal consequences of vessel wall changes presumably reflecting less advanced ICAS, are less clear, hampering interpretation of these changes in clinical practice

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