Hemodynamic significance of intracranial atherosclerotic disease and ipsilateral imaging markers of cerebral small vessel disease.

INTRODUCTION: Cerebral small vessel disease (CSVD) commonly exists in patients with symptomatic intracranial atherosclerotic disease (sICAD). We aimed to investigate the associations of hemodynamic features of sICAD lesions with imaging markers and overall burden of CSVD. PATIENTS AND METHODS: Patients with anterior-circulation sICAD (50%-99% stenosis) were analyzed in this cross-sectional study. Hemodynamic features of a sICAD lesion were quantified by translesional pressure ratio (PR = Pressurepost-stenotic/Pressurepre-stenotic) and wall shear stress ratio (WSSR = WSSstenotic-throat/WSSpre-stenotic) via CT angiography-based computational fluid dynamics modeling. PR ⩽median was defined as low ("abnormal") PR, and WSSR ⩾ fourth quartile as high ("abnormal") WSSR. For primary analyses, white matter hyperintensities (WMHs), lacunes, and cortical microinfarcts (CMIs) were assessed in MRI and summed up as overall CSVD burden, respectively in ipsilateral and contralateral hemispheres to sICAD. Enlarged perivascular spaces (EPVSs) and cerebral microbleeds (CMBs) were assessed for secondary analyses. RESULTS: Among 112 sICAD patients, there were more severe WMHs, more lacunes and CMIs, and more severe overall CSVD burden ipsilaterally than contralaterally (all p < 0.05). Abnormal PR and WSSR (vs normal PR and WSSR) was significantly associated with moderate-to-severe WMHs (adjusted odds ratio = 10.12, p = 0.018), CMI presence (5.25, p = 0.003), and moderate-to-severe CSVD burden (12.55; p = 0.033), ipsilaterally, respectively independent of contralateral WMHs, CMI(s), and CSVD burden. EPVSs and CMBs were comparable between the two hemispheres, with no association found with the hemodynamic metrics. DISCUSSION AND CONCLUSION: There are more severe WMHs and CMI(s) in the hemisphere ipsilateral than contralateral to sICAD. The hemodynamic significance of sICAD lesions was independently associated with severities of WMHs and CMI(s) ipsilaterally.

Intracranial atherosclerosis: From anatomy to pathophysiology.

Background Intracranial atherosclerotic stenosis is an important etiology subtype of ischemic stroke. Stenosis severity was thought to be the main reference index for clinical treatment and research. However, stenosis could not reflect the ischemia risk completely, instead the hemodynamic state across the lesion, the extent of collateral circulation, and perfusion impairment downstream the stenosis are more important. Aims We write this review aimed to summarize novel angiographic methods applied in the evaluation of functional severity of ICAS, and commented on their limitations and prospects in future research. Summary of review The main methods to estimate cerebral blood flow including fractional flow assessed by signal intensity ratio, computational fluid dynamics analysis or pressure wire, quantitative magnetic resonance angiography. Fractional flow as a series cerebral hemodynamic parameters may reflect the status of collateral circulation and cerebral blood flow. But the accuracy of the methods was not validated. The method to calculate fractional flow reserve in cardiovascular disease cannot duplicate in cerebrovascular disease. Fractional flow measurement by floating a pressure guidewire across the intracranial stenosis was technically feasible and safe. In the future researches, a non-invasive method should be established to identify high-risk intracranial lesions and may help in decision-making. Conclusions The relationship between stenosis and cerebral blood flow was individualized. Cerebral hemodynamic criteria should be used to screen patients to endovascular treatment, which will optimize the diagnosis and treatment strategies for patients with symptomatic intracranial artery stenosis.

Plasma DNA as a prognostic marker for stroke patients with negative neuroimaging within the first 24 h of symptom onset.

Modern neuroimaging safely and reliably diagnoses stroke and provides information for outcome prediction. However, some patients with clinical stroke have no detectable abnormality on neuroimaging and other patients are not fit for such investigations. Therefore, we evaluated the potential of plasma DNA and serum S100 protein concentrations to predict post-stroke mortality and morbidity in patients with negative neuroimaging results. Patients with stroke-like symptoms but negative neuroimaging results were recruited. Both plasma and serum were collected from each patient for plasma DNA and serum S100 analysis. The primary outcome measures were 6-month mortality and morbidity using the post-stroke modified Rankin score (mRS). Forty-four patients were recruited to the study. Seventeen (39%) patients were classified as post-stroke mRS grades 3-6. The median plasma DNA concentration of this group of patients was significantly higher than that of patients with post-stroke mRS grades 0-2. Median serum S100 protein concentrations did not show significant differences between the two groups. Plasma DNA concentrations > 800 kilogenome-equivalent/l have a sensitivity of 42% and a specificity of 100% for predicting 6-month post-stroke mRS (grades 0-2), with an area under the receiver operator characteristic (ROC) curve of 0.742. By comparison, serum S100 protein concentrations > 0.09 microg/l have a sensitivity of 48% and specificity of 75% for predicting 6-month post-stroke mRS (grades 0-2), and the area under the curve is 0.542. Plasma DNA concentration predicts post-stroke morbidity and mortality in patients with negative neuroimaging, and may be more effective than S100 protein measurement.