Editorial for “Cerebrovascular Reactivity Timing and Stroke Risk in Patients With Intracranial Stenosis”

Abstract

It is a widely acknowledged clinical challenge that for patients with symptomatic atherosclerotic and nonatherosclerotic intracranial steno-occlusive disease, the rates of high 2-year ischemic stroke occurrence are considerable. In response to this challenging issue, researchers are motivated to utilize new noninvasive brain imaging technologies in the pursuit of possible markers for predicting infarct. Specifically, patients with intracranial atherosclerotic arterial disease (ICAD) and patients with nonatherosclerotic arterial stenosis (i.e. moyamoya vasculopathy) often display different etiologies. However, both ICAD and moyamoya would give rise to intracranial steno-occlusion, reduced cerebral perfusion pressure (CPP), and in many cases tissue-level hemometabolic impairment. The CPP reduction will cause compensatory increases in microvascular cerebral blood volume (CBV) for the maintenance of CBF. The CBV increase will accordingly result in the decrease of cerebrovascular reserve capacity (i.e. the ability of arterioles to increase CBV). Together, evaluation of cerebrovascular reactivity and reserve capacity can be critical to infarct risk prediction. Prior literature has provided evidence that cerebrovascular reactivity (CVR)-weighted or cerebral blood flow (CBF)weighted magnetic resonance imaging (MRI) can in vivo assess compensatory hemometabolic parameters and these metrics might be important clinical indicators of diseases. Published studies have emphasized the importance of identifying markers of recurrent stroke risk in atherosclerotic patients. Also, recent findings point to that impaired collateral flow might be considered as potential risk factor, and stroke risk has been demonstrated to be related to angiography and perfusion have been followed. However, by far, it remains unknown whether prognosis (namely, the identification of brain parenchyma that may progress to infarct) can be indicated by and even strongly correlated with aberrations in parameters such as CVR and associated temporal changes in CVR. Particularly, it is not clear that how tissue-level hemodynamic impairment and compensation may differ in intracranial patients and time-independent metrics CVR have not yet been studied as markers of recurrent infarct risk. Motivated by this challenge, Juttukonda et al conducted a prospective longitudinal study, aiming to provide initial evidence on whether CBF and CVR metrics may have relevance for infarct prediction. In this issue of JMRI, the article by Juttukonda et al advances our knowledge about the relevance between CBF/CVR and infarct, which may provide biomarkers of 1– 2-year infarct risk. They used 3.0 T MRI to scan adult participants (age = 18–85 years) with symptomatic intracranial atherosclerotic disease (ICAD; N = 26) or moyamoya disease (N = 43) stenosis >50% of a major intracranial artery. The authors initially scanned the participants within 45 days of stroke and then obtained follow-up imaging for new infarct assessment at a target time of 1.5 years. Based on these data, they investigated whether tissue-level hemodynamic patterns present within 45 days of stroke or transient ischemic attacks (TIA) can predict new infarct development during the next 1–2 years. We found that lengthened CVRdelay (in atherosclerotic patients) and reduced CVRmax (in nonatherosclerotic patients) may help distinguish brain parenchyma at particularly high risk for new recurrent infarcts in patients with symptomatic intracranial atherosclerotic disease. While Juttukonda et al have been a significant contribution to this field, future studies should involve large sample size and more consistent imaging parameters to validate these findings. Also, other confounding factors that may contribute to the observed new infarcts require further investigations to be clarified.