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Background Immediate and accurate detection of intracranial hemorrhages (ICHs) is essential to provide a good clinical outcome for patients with ICH. Artificial intelligence has the potential to provide this, but the assessment of these methods needs to be investigated in depth. This study aimed to assess the ability of Canon's AUTOStroke Solution ICH detection algorithm to accurately identify patients both with and without ICHs present. Methods Data from 200 ICH and 102 non-ICH patients who presented with stroke-like symptoms between August 2016 and December 2019 were collected retrospectively. Patients with ICH had at least one of the following hemorrhage types: intraparenchymal (n = 181), intraventricular (n = 45), subdural (n = 13), or subarachnoid (n = 19). Noncontrast computed tomography scans were analyzed for each patient using Canon's AUTOStroke Solution ICH algorithm to determine which slices contained hemorrhage. The algorithm's ability to detect ICHs was assessed using sensitivity, specificity, positive predictive value, and negative predictive value. Percentages of cases correctly identified as ICH positive and negative were additionally calculated. Results Automated analysis demonstrated the following metrics for identifying hemorrhage slices within all 200 patients with ICH (95% confidence intervals): sensitivity = 0.93 ± 0.03, specificity = 0.93 ± 0.01, positive predictive value = 0.85 ± 0.02, and negative predictive value = 0.98 ± 0.01. A total of 95% (245 of 258) of ICH volumes were correctly triaged, whereas 88.2% (90 of 102) of non-ICH cases were correctly classified as ICH negative. Conclusions Canon's AUTOStroke Solution ICH detection algorithm was able to accurately detect intraparenchymal, intraventricular, subdural, and subarachnoid hemorrhages in addition to accurately determine when an ICH was not present. Having this automated ICH detection method could drastically improve treatment times for patients with ICH.

Computed tomography perfusion (CTP) is crucial for acute ischemic stroke (AIS) patient diagnosis. To improve infarct prediction, enhanced image processing and automated parameter selection have been implemented in Vital Images’ new CTP+ software. We compared CTP+ with its previous version, commercially available software (RAPID and Sphere), and follow-up diffusion-weighted imaging (DWI). Data from 191 AIS patients between March 2019 and January 2020 was retrospectively collected and allocated into endovascular intervention ( n = 81) and conservative treatment ( n = 110) cohorts. Intervention patients were treated for large vessel occlusion, underwent mechanical thrombectomy, and achieved successful reperfusion of thrombolysis in cerebral infarction 2b/2c/3. Conservative treatment patients suffered large or small vessel occlusion and did not receive intravenous thrombolysis or mechanical thrombectomy. Infarct and penumbra were assessed using intervention and conservative treatment patients, respectively. Infarct and penumbra volumes were segmented from CTP+ and compared with 24-h DWI along with RAPID, Sphere, and Vitrea. Mean infarct differences (95% confidence intervals) and Spearman correlation coefficients (SCCs) between DWI and each CTP software product for intervention patients are: CTP+ = (5.8 ± 5.9 ml, 0.62), RAPID = (10.0 ± 5.2 ml, 0.73), Sphere = (3.0 ± 6.0 ml, 0.56), Vitrea = (7.2 ± 4.9 ml, 0.66). For conservative treatment patients, mean infarct differences and SCCs are: CTP+ = (–8.0 ± 5.4 ml, 0.64), RAPID = (–25.6 ± 11.5 ml, 0.60), Sphere = (–25.6 ± 8.0 ml, 0.66), Vitrea = (1.3 ± 4.0 ml, 0.72). CTP+ performed similarly to RAPID and Sphere in addition to its semi-automated predecessor, Vitrea, when assessing intervention patient infarct volumes. For conservative treatment patients, CTP+ outperformed RAPID and Sphere in assessing penumbra. Semi-automated Vitrea remains the most accurate in assessing penumbra, but CTP+ provides an improved workflow from its predecessor.

BackgroundCT perfusion (CTP) infarct and penumbra estimations determine the eligibility of patients with acute ischemic stroke (AIS) for endovascular intervention. This study aimed to determine volumetric and spatial agreement of predicted RAPID, Vitrea, and Sphere CTP infarct with follow-up fluid attenuation inversion recovery (FLAIR) MRI infarct.Methods108 consecutive patients with AIS and large vessel occlusion were included in the study between April 2019 and January 2020 . Patients were divided into two groups: endovascular intervention (n=58) and conservative treatment (n=50). Intervention patients were treated with mechanical thrombectomy and achieved successful reperfusion (Thrombolysis in Cerebral Infarction 2b/2 c/3) while patients in the conservative treatment group did not receive mechanical thrombectomy or intravenous thrombolysis. Intervention and conservative treatment patients were included to assess infarct and penumbra estimations, respectively. It was assumed that in all patients treated conservatively, penumbra converted to infarct. CTP infarct and penumbra volumes were segmented from RAPID, Vitrea, and Sphere to assess volumetric and spatial agreement with follow-up FLAIR MRI.ResultsMean infarct differences (95% CIs) between each CTP software and FLAIR MRI for each cohort were: intervention cohort: RAPID=9.0±7.7 mL, Sphere=−0.2±8.7 mL, Vitrea=−7.9±8.9 mL; conservative treatment cohort: RAPID=−31.9±21.6 mL, Sphere=−26.8±17.4 mL, Vitrea=−15.3±13.7 mL. Overlap and Dice coefficients for predicted infarct were (overlap, Dice): intervention cohort: RAPID=(0.57, 0.44), Sphere=(0.68, 0.60), Vitrea=(0.70, 0.60); conservative treatment cohort: RAPID=(0.71, 0.56), Sphere=(0.73, 0.60), Vitrea=(0.72, 0.64).ConclusionsSphere proved the most accurate in patients who had intervention infarct assessment as Vitrea and RAPID overestimated and underestimated infarct, respectively. Vitrea proved the most accurate in penumbra assessment for patients treated conservatively although all software overestimated penumbra.

OBJECTIVE. The objective of this study was to compare image quality and clinically significant lesion detection on deep learning reconstruction (DLR) and iterative reconstruction (IR) images of submillisievert chest and abdominopelvic CT. MATERIALS AND METHODS. Our prospective multiinstitutional study included 59 adult patients (33 women, 26 men; mean age ± SD, 65 ± 12 years old; mean body mass index [weight in kilograms divided by the square of height in meters] = 27 ± 5) who underwent routine chest (n = 22; 16 women, six men) and abdominopelvic (n = 37; 17 women, 20 men) CT on a 640-MDCT scanner (Aquilion ONE, Canon Medical Systems). All patients gave written informed consent for the acquisition of low-dose (LD) CT (LDCT) after a clinically indicated standard-dose (SD) CT (SDCT). The SDCT series (120 kVp, 164-644 mA) were reconstructed with interactive reconstruction (IR) (adaptive iterative dose reduction [AIDR] 3D, Canon Medical Systems), and the LDCT (100 kVp, 120 kVp; 30-50 mA) were reconstructed with filtered back-projection (FBP), IR (AIDR 3D and forward-projected model-based iterative reconstruction solution [FIRST], Canon Medical Systems), and deep learning reconstruction (DLR) (Advanced Intelligent Clear-IQ Engine [AiCE], Canon Medical Systems). Four subspecialty-trained radiologists first read all LD image sets and then compared them side-by-side with SD AIDR 3D images in an independent, randomized, and blinded fashion. Subspecialty radiologists assessed image quality of LDCT images on a 3-point scale (1 = unacceptable, 2 = suboptimal, 3 = optimal). Descriptive statistics were obtained, and the Wilcoxon sign rank test was performed. RESULTS. Mean volume CT dose index and dose-length product for LDCT (2.1 ± 0.8 mGy, 49 ± 13mGy·cm) were lower than those for SDCT (13 ± 4.4 mGy, 567 ± 249 mGy·cm) (p < 0.0001). All 31 clinically significant abdominal lesions were seen on SD AIDR 3D and LD DLR images. Twenty-five, 18, and seven lesions were detected on LD AIDR 3D, LD FIRST, and LD FBP images, respectively. All 39 pulmonary nodules detected on SD AIDR 3D images were also noted on LD DLR images. LD DLR images were deemed acceptable for interpretation in 97% (35/37) of abdominal and 95-100% (21-22/22) of chest LDCT studies (p = 0.2-0.99). The LD FIRST, LD AIDR 3D, and LD FBP images had inferior image quality compared with SD AIDR 3D images (p < 0.0001). CONCLUSION. At submillisievert chest and abdominopelvic CT doses, DLR enables image quality and lesion detection superior to commercial IR and FBP images.

BACKGROUND AND PURPOSE: Brain CTP is used to estimate infarct and penumbra volumes to determine endovascular treatment eligibility for patients with acute ischemic stroke. We aimed to assess the accuracy of a Bayesian CTP algorithm in determining penumbra and final infarct volumes. MATERIALS AND METHODS: Data were retrospectively collected for 105 patients with acute ischemic stroke (55 patients with successful recanalization [TICI 2b/2c/3] and large-vessel occlusions and 50 patients without interventions). Final infarct volumes were calculated using DWI and FLAIR 24 hours following CTP imaging. RAPID and the Vitrea Bayesian CTP algorithm (with 3 different settings) predicted infarct and penumbra volumes for comparison with final infarct volumes to assess software performance. Vitrea settings used different combinations of perfusion maps (MTT, TTP, CBV, CBF, delay time) for infarct and penumbra quantification. Patients with and without interventions were included for assessment of predicted infarct and penumbra volumes, respectively. RESULTS: RAPID and Vitrea default setting had the most accurate final infarct volume prediction in patients with interventions ([Spearman correlation coefficient, mean infarct difference] default versus FLAIR: [0.77, 4.1 mL], default versus DWI: [0.72, 4.7 mL], RAPID versus FLAIR: [0.75, 7.5 mL], RAPID versus DWI: [0.75, 6.9 mL]). Default Vitrea and RAPID were the most and least accurate in determining final infarct volume for patients without an intervention, respectively (default versus FLAIR: [0.76, –0.4 mL], default versus DWI: [0.71, –2.6 mL], RAPID versus FLAIR: [0.68, −49.3 mL], RAPID versus DWI: [0.65, –51.5 mL]). CONCLUSIONS: Compared with RAPID, the Vitrea default setting was noninferior for patients with interventions and superior in penumbra estimation for patients without interventions as indicated by mean infarct differences and correlations with final infarct volumes.

BACKGROUND AND PURPOSE: Ulceration in carotid plaque is a risk indicator for ischemic stroke. Our aim was to compare plaque ulcer detection by standard TOF and CE-MRA techniques and to identify factors that influence its detection. MATERIALS AND METHODS: Carotid MR imaging scans were acquired on 2066 participants in the ARIC study. We studied the 600 thickest plaques. TOF-MRA, CE-MRA, and black-blood MR images were analyzed together to define ulcer presence (plaque surface niche ≥2 mm in depth). Sixty ulcerated arteries were detected. These arteries were randomly assigned, along with 40 nonulcerated plaques from the remaining 540, for evaluation of ulcer presence by 2 neuroradiologists. Associations between ulcer detection and ulcer characteristics, including orientation, location, and size, were determined and explored by CFD modeling. RESULTS: One CE-MRA and 3 TOF-MRAs were noninterpretable and excluded. Of 71 ulcers in 56 arteries, readers detected an average of 39 (55%) on both TOF-MRA and CE-MRA, 26.5 (37.5%) only on CE-MRA, and 1 (1.5%) only on TOF-MRA, missing 4.5 (6%) ulcers by both methods. Ulcer detection by TOF-MRA was associated with its orientation (distally pointing versus perpendicular: OR = 5.57 [95% CI, 1.08–28.65]; proximally pointing versus perpendicular: OR = 0.21 [95% CI, 0.14–0.29]); location relative to point of maximum stenosis (distal versus isolevel: OR = 5.17 [95% CI, 2.10–12.70]); and neck-to-depth ratio (OR = 1.96 [95% CI, 1.11–3.45]) after controlling for stenosis and ulcer volume. CONCLUSIONS: CE-MRA detects more ulcers than TOF-MRA in carotid plaques. Missed ulcers on TOF-MRA are influenced by ulcer orientation, location relative to point of maximum stenosis, and neck-to-depth ratio.

Background and Purpose— Hemodynamic insults at arterial bifurcations are hypothesized to play a key role in intracranial aneurysm formation. This study investigates aneurysm-initiating vascular responses at the rabbit basilar terminus subsequent to common carotid artery ligation. Methods— Nine adult female New Zealand white rabbits were subjected to sham, unilateral, or bilateral common carotid artery ligation to produce varying degrees of compensatory basilar artery flow increase. Basilar artery flow velocity and geometry were monitored by transcranial Doppler and rotational angiography, respectively, for 12 weeks after surgery. Bifurcation tissues were harvested at 12 weeks and examined histologically. From the histological sections, we quantified the destructive structural changes at the basilar terminus and correlated them with the basilar artery flow rate increase. Results— Subsequent to common carotid artery ligation, basilar artery flow rate increased by 105% to 900% at the maximum. All common carotid artery-ligated rabbits presented nascent aneurysm formation characterized by a bulge with thinned media and absent internal elastic lamina near the basilar terminus. We defined a nascent aneurysm index based on a multiplicative combination of the local destructive remodeling lengths measured at the nascent aneurysm. The nascent aneurysm index strongly correlated with the increase in basilar artery flow rate with R 2 =0.91. Conclusion— Without other known predisposition, flow increase alone at the basilar bifurcation can lead to a nascent aneurysm. This nascent aneurysm formation is dose-dependent on basilar artery flow increase.

Background and Purpose— Arterial bifurcation apices are common sites for cerebral aneurysms, raising the possibility that the unique hemodynamic conditions associated with flow dividers predispose the apical vessel wall to aneurysm formation. This study sought to identify the specific hemodynamic insults that lead to maladaptive vascular remodeling associated with aneurysm development and to identify early remodeling events at the tissue and cellular levels. Methods— We surgically created new branch points in the carotid vasculature of 6 female adult dogs. In vivo angiographic imaging and computational fluid dynamics simulations revealed the detailed hemodynamic microenvironment for each bifurcation, which were then spatially correlated with histologic features showing specific tissue responses. Results— We observed 2 distinct patterns of vessel wall remodeling: (1) hyperplasia that formed an intimal pad at the bifurcation apex and (2) destructive remodeling in the adjacent region of flow acceleration that resembled the initiation of an intracranial aneurysm, characterized by disruption of the internal elastic lamina, loss of medial smooth muscle cells, reduced proliferation of smooth muscle cells, and loss of fibronectin. Conclusions— Strong localization of aneurysm-type remodeling to the region of accelerating flow suggests that a combination of high wall shear stress and a high gradient in wall shear stress represents a “dangerous” hemodynamic condition that predisposes the apical vessel wall to aneurysm formation.

Geometric indices defined on intracranial aneurysms have been widely used in rupture risk assessment and surgical planning. However, most indices employed in clinical settings are currently evaluated based on two-dimensional images that inevitably fail to capture the three-dimensional nature of complex aneurysmal shapes. In addition, since measurements are performed manually, they can suffer from poor inter and intra operator repeatability. The purpose of the current work is to introduce objective and robust techniques for the 3D characterization of intracranial aneurysms, while preserving a close connection to the way aneurysms are currently characterized in clinical settings. Techniques for automatically identifying the neck plane, key aneurysm dimensions, shape factors, and orientations relative to the parent vessel are demonstrated in a population of 15 sidewall and 15 terminal aneurysms whose surface has been obtained by two trained operators using both level-set segmentation and thresholding, the latter reflecting typical clinical practice. Automatically-identified neck planes are shown to be in concordance with those manually positioned by an expert neurosurgeon, and automatically-derived geometric indices are shown to be largely insensitive to segmentation method or operator. By capturing the 3D nature of aneurysmal sacs and by minimizing observer variability, our approach allows large retrospective and prospective studies on aneurysm geometric risk factors to be performed using routinely acquired clinical images.

While it is widely appreciated that volumetric blood flow rate (VFR) dynamics change with age, there has been no detailed characterization of the typical shape of carotid bifurcation VFR waveforms of older adults. Toward this end, retrospectively gated phase contrast magnetic resonance imaging was used to measure time-resolved VFR waveforms proximal and distal to the carotid bifurcations of 94 older adults (age 68 +/- 8 years) with little or no carotid artery disease, recruited from the BLSA cohort of the VALIDATE study of factors in vascular aging. Timings and amplitudes of well-defined feature points from these waveforms were extracted automatically and averaged to produce representative common, internal and external carotid artery (CCA, ICA and ECA) waveform shapes. Relative to young adults, waveforms from older adults were found to exhibit a significantly augmented secondary peak during late systole, resulting in significantly higher resistance index (RI) and flow augmentation index (FAI). Cycle-averaged VFR at the CCA, ICA and ECA were 389 +/- 74, 245 +/- 61 and 125 +/- 49 mL min(-1), respectively, reflecting a significant cycle-averaged outflow deficit of 5%, which peaked at around 10% during systole. A small but significant mean delay of 13 ms between arrivals of ICA versus CCA/ECA peak VFR suggested differential compliance of these vessels. Sex and age differences in waveform shape were also noted. The characteristic waveforms presented here may serve as a convenient baseline for studies of VFR waveform dynamics or as suitable boundary conditions for models of blood flow in the carotid arteries of older adults.

Approximately 80% to 90% of intracranial aneurysms (IA) are saccular or berry pouches formed at or near bifurcation apices or on the outer curvature of curved vessels in regions of complex hemodynamics (42). IA formation is proposed to result from maladaptive vascular responses to elevated hemodynamic stress at these locations (24, 26, 37). However, the specific causative hemodynamic microenvironments responsible for the biological changes that underlie aneurysm-initiating remodeling have not been elucidated. Recently, we surgically created a Y-shaped bifurcation from 2 native common carotid arteries (CCAs) in dogs (28) and examined how a naive vessel responded to impinging flow at a bifurcation apex from time zero. We found that the periapical wall underwent destructive remodeling characteristic of IA initiation, including degradation of the internal elastic lamina, loss of smooth muscle cells (SMCs) and endothelial cells (ECs), and reduced cell proliferation (29). Using high-resolution in vivo image-based computational fluid dynamics (CFD) to quantify the impinging flow environment and its spatial association with the observed histological changes, we demonstrated that morphological and cellular aneurysmal changes were localized in a flow acceleration region characterized by high wall shear stress (WSS) and high WSS gradient (WSSG) (28, 29). These observations suggest that the aneurysm-initiating remodeling results from maladaptation of the periapical arterial wall to high WSS and high WSSG hemodynamic insult and that this hemodynamic microenvironment constitutes a “danger zone” prone to aneurysm initiation. The current study examines whether the maladaptive remodeling in response to high WSS and high WSSG hemodynamics induces significant molecular up- or down-regulation of specific markers associated with IAs, such as endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS), nitrotyrosine, and matrix metalloproteinase (MMP)-2 and -9 (1, 3, 13, 19, 23, 39). Additionally, we sought to localize these findings to their specific hemodynamic environments.

Hemodynamic forces play critical roles in vascular pathologies such as atherosclerosis, aneurysms, and stenosis. However, detailed relationships between the specific in vivo hemodynamic microenvironment and vascular responses leading to the triggering or exacerbation of pathological remodeling of the vessel remain elusive. We have developed a hemodynamics-biology co-mapping technique that enables in situ correlation between the in vivo blood flow field and vascular changes secondary to hemodynamic insult. The hemodynamics profile is obtained from computational fluid dynamics simulation within the vascular geometry reconstructed from three-dimensional in vivo images, whereas the vascular response is obtained from histology or immunohistochemistry on harvested vascular tissue. The hemodynamics field is virtually sectioned in the histological slicing planes and digitally co-mapped with the histological images, thereby enabling correlation of the specific local vascular responses with the inciting hemodynamic stresses. We demonstrate application of this technique to rabbit basilar terminus subjected to elevated flow. Morphological changes at the basilar terminus 5 days after the flow increase were co-mapped with the initial wall shear stress and wall shear stress gradient distributions, from which localization of destructive remodeling in a specific hemodynamic zone was noticed. This method paves the way for further investigations to determine the connection between in vivo mechanical stimuli and biological responses, such as initiation of aneurysmal remodeling.

Pathological extremes in cerebrovascular remodeling may contribute to basilar artery (BA) dolichoectasia and fusiform aneurysm development. Factors regulating cerebrovascular remodeling are poorly understood. To better understand hemodynamic influences on cerebrovascular remodeling, we examined BA remodeling following common carotid artery (CCA) ligation in an animal model.Rabbits were subjected to sham surgery (3 animals), unilateral CCA ligation (3 animals), or bilateral CCA ligation (5 animals). Transcranial Doppler ultrasonography and rotational angiography were used to compute BA flow, diameter, wall shear stress (WSS), and a tortuosity index on Days 0, 1, 4, 7, 14, 28, 56, and 84. Basilar artery tissues were stained and analyzed at Day 84. Statistical analysis was performed using orthogonal contrast analysis, repeated measures analysis of variance, or mixed regression analysis of repeated measures. Statistical significance was defined as a probability value0.05.Basilar artery flow and diameter increased significantly after the procedure in both ligation groups, but only the bilateral CCA ligation group demonstrated significant differences between groups. Wall shear stress significantly increased only in animals in the bilateral CCA ligation group and returned to baseline by Day 28, with 52% of WSS correction occurring by Day 7. Only the bilateral CCA ligation group developed significant BA tortuosity, occurring within 7 days postligation. Unlike the animals in the sham and unilateral CCA ligation groups, the animals in the bilateral CCA ligation group had histological staining results showing a substantial internal elastic lamina fragmentation.Increased BA flow results in adaptive BA remodeling until WSS returns to physiological baseline levels. Morphological changes occur rapidly following flow alteration and do not require chronic insult to affect substantial and significant structural transformation. Additionally, it appears that there exists a flow-increase threshold that, when surpassed, results in significant tortuosity.

Since the early 1970s, studies of arterial bifurcation morphology have suggested linkage between hemodynamic stresses and vascular remodeling (2, 16). It is generally accepted that blood flow patterns and hemodynamic stresses associated with such morphology contribute to the development of vascular pathologies (4, 5, 11). Cerebral aneurysms are preferentially located near arterial bifurcations or along the outer curvature of arteries on or near the Circle of Willis (10, 15). The local hemodynamics at such sites are complex, presenting impinging flow, regions of high wall shear stress (WSS), gradients in wall shear stress (WSSG), combinations of both, as well as “disturbed flow” (1, 8, 18). Yet, these relationships between hemodynamic conditions at an arterial bifurcation and pathological vascular remodeling leading to aneurysms are not well understood. Recent developments in computational fluid dynamics (CFD) enable detailed characterization of three-dimensional (3-D) flow fields in arteries of humans and larger animals (6). Thus, angiographic imaging and CFD can provide detailed flow fields from which measured hemodynamics can be correlated spatially and temporally with specific tissue responses in local microenvironments. Such hemodynamic-vascular response correlations constitute a model system for studying disease mechanisms that are mediated by altered hemodynamics. In this study, we present a new method for correlating morphological changes in the vascular wall with the local hemodynamics in a surgically created arterial bifurcation in dogs. To study how arterial tissue adapts to the complex hemodynamic environment of impinging flow, we created the bifurcation from native arterial segments and studied how the morphology of the vascular wall changed in response to altered hemodynamics. The major benefit of using a created bifurcation is to establish a cause and effect relationship between the altered hemodynamics (specifically, the flow impingement normally associated with a bifurcation) and remodeling of the vascular wall at the cellular level. Here, the naive vessel wall had never before been exposed to the type of impingement flow. New morphology that develops after the bifurcation has been created can thus be attributed to hemodynamic insult resulting from manipulated exposure of the naive vessel wall to impinging flow. Our observations provide insight into how complex hemodynamic conditions near the apex of an arterial bifurcation (including flow impingement, WSS and spatial variations, or gradients, of WSS) could affect vascular remodeling processes, including those that go awry. The changes observed have important implications concerning the fundamental mechanisms of aneurysm initiation.