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Almost the entire world, not only China, is currently experiencing the outbreak of a novel coronavirus that causes respiratory disease, severe pneumonia, and even death. The outbreak began in Wuhan, China, in December of 2019 and is currently still ongoing. This novel coronavirus is highly contagious and has resulted in a continuously increasing number of infections and deaths that have already surpassed the SARS-CoV outbreak that occurred in China between 2002 and 2003. It is now officially a pandemic, announced by WHO on the 11th of March. Currently, the 2019 novel coronavirus (SARS-CoV-2) can be identified by virus isolation or viral nucleic acid detection; however, false negatives associated with the nucleic acid detection provide a clinical challenge and thus make the imaging examination crucial. Imaging exams have been a main clinical diagnostic criteria for the 2019 novel coronavirus disease (COVID-19) in China. Imaging features of multiple patchy areas of ground glass opacity and consolidation predominately in the periphery of the lungs are characteristic manifestations on chest CT and extremely helpful in the early detection and diagnosis of this disease, which aids prompt diagnosis and the eventual control of this emerging global health emergency. Key Points • In December 2019, China, an outbreak of pneumonia caused by a novel, highly contagious coronavirus raised grave concerns and posed a huge threat to global public health. • Among the infected patients, characteristic findings on CT imaging include multiple, patchy, ground-glass opacity, crazy-paving pattern, and consolidation shadows, mainly distributed in the peripheral and subpleural areas of both lungs, which are very helpful for the frontline clinicians. • Imaging examination has become the indispensable means not only in the early detection and diagnosis but also in monitoring the clinical course, evaluating the disease severity, and may be presented as an important warning signal preceding the negative RT-PCR test results.

Background and aims Artery is subject to wall shear stress (WSS) and vessel structural stress (VSS) simultaneously. This study is designed to explore the role of VSS in development of atherosclerosis. Methods Silastic collars were deployed on the carotid to create two constrictions on 13 rabbits for a distinct mechanical environment at the constriction. MRI was performed to visualize arteries’ configuration. Animals with high fat (n = 9; Model-group) and normal diet (n = 4; Control-group) were sacrificed after 16 weeks. 3D fluid-structure interaction analysis was performed to quantify WSS and VSS simultaneously. Results Twenty plaques were found in Model-group and 3 in Control-group. In Model-group, 8 plaques located proximally to the first constriction (Region-1, close to the heart) and 7 distally to the second (Region-2, close to the head) and 5 plaques were found on the contralateral side of 3 rabbits. Plaques at Region-1 tended to be bigger than those at Region-2 and the macrophage density at these locations was comparable. Minimum time-averaged WSS (TAWSS) in Region-1 was significantly higher than that in Region-2, and both maximum oscillatory shear index (OSI) and particle relative residence time (RRT) were significantly lower. Peak and mean VSS in Region-1 were significantly higher than those in Region-2. Correlation analyses indicated that low TAWSS, high OSI and RRT were only associated with plaque in Region-2, while lesions in Region-1 were only associated with high VSS. Moreover, only VSS was associated with wall thickness of plaque-free regions in both regions. Conclusions VSS might contribute to the initialization and development of atherosclerosis solely or in combination with WSS.

This study aimed to assess the relationship between local mechanical stimuli and regional aortic tissue degeneration using fluid–structure interaction (FSI) analysis in patients with bicuspid aortic valve (BAV) disease. Nine patients underwent ascending aortic replacement were recruited. Tissues were collected to evaluate the pathology features in four regions, greater curvature (GC-region), posterior (P-region), anterior (A-region), and lesser curvature (LC-region). FSI analysis was performed to quantify vessel structural stress (VSS) and flow-induced parameters, including wall shear stress (WSS), oscillatory shear index (OSI), and particle relative residence time (RRT). The correlation between these biomechanical metrics and tissue degeneration was analyzed. Elastin in the medial layer and media thickness were thinnest and the gap between fibers was biggest in the GC-region, followed by the P-region and A-region, while the elastin and media thickness were thickest and the gap smallest in the LC-region. The collagen deposition followed a pattern with the biggest in the GC-region and least in the LC-region. There is a strong negative correlation between mean or peak VSS and elastin thickness in the arterial wall in the GC-region (r = -0.917; p = 0.001 and r = -0.899; p = 0.001), A-region (r = -0.748; p = 0.020 and r = -0.700; p = 0.036) and P-region (r = -0.773; p = 0.014 and r = -0.769; p = 0.015), and between mean VSS and fiber distance in the A-region (r = -0.702, p = 0.035). Moreover, strong negative correlation between mean or peak VSS and media thickness was also observed. No correlation was found between WSS, OSI, and RRT and aortic tissue degeneration in these four regions. These findings indicate that increased VSS correlated with local elastin degradation and aortic media degeneration, implying that it could be a potential biomechanical parameter for a refined risk stratification for patients with BAV.

Plaque rupture may be triggered by extreme stress/strain conditions. Inflammation is also implicated and can be imaged using novel imaging techniques. The impact of cap inflammation on plaque stress/strain and flow shear stress were investigated. A patient-specific MRI-PET/CT-based modeling approach was used to develop 3D fluid-structure interaction models and investigate the impact of inflammation on plaque stress/strain conditions for better plaque assessment. 18FDG-PET/CT and MRI data were acquired from 4 male patients (average age: 66) to assess plaque characteristics and inflammation. Material stiffness for the fibrous cap was adjusted lower to reflect cap weakening causing by inflammation. Setting stiffness ratio (SR) to be 1.0 (fibrous tissue) for baseline, results for SR=0.5, 0.25, and 0.1 were obtained. Thin cap and hypertension were also considered. Combining results from the 4 patients, mean cap stress from 729 cap nodes was lowered by 25.2% as SR went from 1.0 to 0.1. Mean cap strain value for SR=0.1 was 0.313, 114% higher than that from SR=1.0 model. The thin cap SR=0.1 model had 40% mean cap stress decrease and 81% cap strain increase compared with SR=1.0 model. The hypertension SR=0.1 model had 19.5% cap stress decrease and 98.6% cap strain increase compared with SR=1.0 model. Differences of flow shear stress with 4 different SR values were limited (

Intraplaque hemorrhage (IPH) and ulceration of carotid atherosclerotic plaques have been associated with vulnerability while calcification has been conventionally thought protective. However, studies suggested calcification size and location may increase plaque vulnerability. This study explored the association between calcium configurations and ulceration with IPH. One hundred thirty-seven consecutive symptomatic patients scheduled for carotid endarterectomy were recruited. CTA and CTP were performed prior to surgery. Plaque samples were collected for histology. According to the location, calcifications were categorized into superficial, deep and mixed types; according to the size and number, calcifications were classified as thick and thin, multiple and single. Seventy-one plaques had IPH (51.8%) and 83 had ulceration (60.6%). The appearance of IPH and ulceration was correlated (r = 0.49; p < 0.001). The incidence of multiple, superficial and thin calcifications was significantly higher in lesions with IPH and ulceration compared with those without. After adjusting factors including age, stenosis and ulceration, the presence of calcification [OR (95% CI), 3.0 (1.1-8.2), p = 0.035], multiple calcification [3.9 (1.4-10.9), p = 0.009] and superficial calcification [3.4 (1.1-10.8), p = 0.001] were all associated with IPH. ROC analysis showed that the AUC of superficial and multiple calcifications in detecting IPH was 0.63 and 0.66, respectively (p < 0.05). When the ulceration was combined, AUC increased significantly to 0.82 and 0.83, respectively. Results also showed that patients with lesions of both ulceration and IPH have significantly reduced brain perfusion in the area ipsilateral to the infarction. Superficial and multiple calcifications and ulceration were associated with carotid IPH, and they may be a surrogate for higher risk lesions. • CTA-defined superficial and multiple calcifications in carotid atherosclerotic plaques are independently associated with the presence of intraplaque hemorrhage. • The combination of superficial and multiple calcifications and ulceration is highly predictive of carotid intraplaque hemorrhage. • Patients with lesions of both ulceration and intraplaque hemorrhage have significantly reduced brain perfusion in the area ipsilateral to the infarction.

Stroke remains a major cause of death and disability worldwide, with approximately one-third of ischaemic strokes being a consequence of carotid atherosclerotic plaque rupture. Thus, diagnostic strategies that could identify those patients at highest risk of events are of critical importance.

This study aims to explore the relationship between plaque surface morphology and neovascularization using a high temporal and spatial resolution 4D contrast-enhanced MRI/MRA sequence. Twenty one patients with either recent symptoms or a carotid artery stenosis ≥40% were recruited in this study. Plaque surface morphology and luminal stenosis were determined from the arterial phase MRA images. Carotid neovascularization was evaluated by a previously validated pharmacokinetic (PK) modeling approach. K trans (transfer constant) and v p (partial plasma volume) were calculated in both the adventitia and plaque. Image acquisition and analysis was successfully performed in 28 arteries. Mean luminal stenosis was 44% (range 11–82%). Both adventitial and plaque K trans in ulcerated/irregular plaques were significantly higher than smooth plaques (0.079 ± 0.018 vs. 0.064 ± 0.011 min−1, p = 0.02; 0.065 ± 0.013 vs. 0.055 ± 0.010 min−1, p = 0.03, respectively). Positive correlations between adventitial K trans and v p against stenosis were observed (r = 0.44, p = 0.02; r = 0.55, p = 0.01, respectively). This study demonstrates the feasibility of using a single sequence to acquire both high resolution 4D CE-MRA and DCE-MRI to evaluate both plaque surface morphology and function. The results demonstrate significant relationships between lumen surface morphology and neovascularization.

BACKGROUND: Multiple overlapping uncovered stents (MOUS) system has shown potentials in managing complex aortic aneurysms with side branches involvement. It promotes the development of thrombus by modulating local flow pattern that reduces the wall tension, while maintaining patency of side branches. However the modulation of local hemodynamic parameters depends on various factors that have not been assessed comprehensively. METHODS: Aneurysm 3D geometry was reconstructed based on CT images. One-way fluid-structure interaction analysis was performed to quantify structural stress concentration in the wall, and changes of blood velocity, wall shear stress (WSS), oscillatory shear index (OSI), relative residence time (RRT) and pressure in the sac due to the stent deployment. RESULTS: High structural stress concentration due to stent deployment was found in the landing zone and it increased linearly with the number of stents deployed. The wall tension in the sac was unaffected by the stent deployment. Stress within the wall was insensitive to the different overlapping pattern. After one stent was deployed, the mean flow velocity in the sac reduced by 36.4%. The deployment of the 2nd stent further reduced the mean sac velocity by 10%. WSS decreased while both OSI and RRT increased after stent deployment, however pressure in the sac remained nearly unchanged. Except for the cases with complete stents struts alignment, different overlapping pattern had little effect on flow parameters. CONCLUSIONS: Mechanical parameters modulated by the MOUS are insensitive to different overlapping pattern suggesting that endovascular procedure can be performed with less attention to the overlapping pattern.

Background Gadolinium enhancement on high‐resolution magnetic resonance imaging ( MRI ) has been proposed as a marker of inflammation and instability in intracranial atherosclerotic plaque. We performed a systematic review and meta‐analysis to summarize the association between intracranial atherosclerotic plaque enhancement and acute ischemic stroke. Methods and Results We searched the medical literature to identify studies of patients undergoing intracranial vessel wall MRI for evaluation of intracranial atherosclerotic plaque. We recorded study data and assessed study quality, with disagreements in data extraction resolved by a third reader. A random‐effects odds ratio was used to assess whether, in any given patient, cerebral infarction was more likely in the vascular territory supplied by an artery with MRI ‐detected plaque enhancement as compared to territory supplied by an artery without enhancement. We calculated between‐study heterogeneity using the Cochrane Q test and publication bias using the Begg‐Mazumdar test. Eight articles published between 2011 and 2015 met inclusion criteria. These studies provided information about plaque enhancement characteristics from 295 arteries in 330 patients. We found a significant positive relationship between MRI enhancement and cerebral infarction in the same vascular territory, with a random effects odds ratio of 10.8 (95% CI 4.1–28.1, P P =0.14) or publication bias ( P =0.80) was present. Conclusions Intracranial plaque enhancement on high‐resolution vessel wall MRI is strongly associated with ischemic stroke. Evaluation for plaque enhancement on MRI may be a useful test to improve diagnostic yield in patients with ischemic strokes of undetermined etiology.

The mechanism underlying atherosclerotic ischemic events within the middle cerebral artery (MCA) is unclear. High structural stress induced by blood pressure might be a potential aetiology as plaque rupture occurs when such mechanical loading exceeds its material strength. To perform reliable analyses quantifying the mechanical loading within a plaque, the local blood pressure is needed. However, data on MCA blood pressure is currently lacking. In this study, the arterial pressure proximal to the stenotic site in the MCA was measured in 15 patients scheduled for intervention. The relationships between these local measurements and pre-intervention and intra-intervention non-invasive arm measurements were assessed. The impact of luminal stenosis on the local blood pressure was quantified. Compared with the pre-intervention arm measurement, the intra-intervention arm pressure decreased significantly by 23.9 ± 11.8 and 9.3 ± 14.7 % at diastole and systole, respectively. The pressure proximal to the stenosis was much lower than the pre-intervention arm measurement (diastole: 65.3 ± 15.7 vs 82.0 ± 9.7, p < 0.01; systole: 81.1 ± 15.9 vs 133.9 ± 18.7, p < 0.01; unit: mmHg). The systolic pressure in the MCA in patients with stenosis

Background— Although plaque rupture is responsible for most myocardial infarctions, few high-risk plaques identified by intracoronary imaging actually result in future major adverse cardiovascular events (MACE). Nonimaging markers of individual plaque behavior are therefore required. Rupture occurs when plaque structural stress (PSS) exceeds material strength. We therefore assessed whether PSS could predict future MACE in high-risk nonculprit lesions identified on virtual-histology intravascular ultrasound. Methods and Results— Baseline nonculprit lesion features associated with MACE during long-term follow-up (median: 1115 days) were determined in 170 patients undergoing 3-vessel virtual-histology intravascular ultrasound. MACE was associated with plaque burden ≥70% (hazard ratio: 8.6; 95% confidence interval, 2.5–30.6; P 2 (hazard ratio: 6.6; 95% confidence interval, 2.1–20.1; P =0.036), although absolute event rates for high-risk lesions remained P P =0.02). Furthermore, PSS improved the ability of virtual-histology intravascular ultrasound to predict MACE in plaques with plaque burden ≥70% (adjusted log-rank, P =0.003) and minimal luminal area ≤4 mm 2 ( P =0.002). Plaques responsible for MACE had larger superficial calcium inclusions, which acted to increase PSS ( P Conclusions— Baseline PSS is increased in plaques responsible for MACE and improves the ability of intracoronary imaging to predict events. Biomechanical modeling may complement plaque imaging for risk stratification of coronary nonculprit lesions.

BACKGROUND: Functional magnetic resonance (MR) imaging of atheroma using contrast media enables assessment of the systemic severity of atherosclerosis in different arterial beds. Whether black-blood imaging has similar ability remains widely unexplored. In this study, we evaluate whether black-blood imaging can differentiate carotid plaques of patients with and without coronary artery disease (CAD) in terms of morphological and biomechanical features of plaque vulnerability, thereby allowing assessment of the systemic severity nature of atherosclerosis in different arterial beds. METHODS: Forty-one patients with CAD and 59 patients without CAD underwent carotid black-blood MR imaging. Plaque components were segmented to identify large lipid core (LC), ruptured fibrous cap (FC), and plaque hemorrhage (PH). These segmented contours of plaque components were used to quantify maximum structural biomechanical stress. RESULTS: Patients with CAD and without CAD had comparable demographics and comorbidities. Both groups had comparable prevalence of morphological features of plaque vulnerability (FC rupture, 44% versus 41%, P = .90; PH, 58% versus 47%, P = .78; large LC, 32% versus 47%, P = .17), respectively. The maximum biomechanical stress was not significantly different for both groups (241versus 278 kPa, P = .14) respectively. CONCLUSIONS: Black-blood imaging does not appear to have the ability to differentiate between the morphological and biomechanical features of plaque vulnerability when comparing patients with and without symptomatic atherosclerotic disease in a distant arterial territory such as coronary artery.

SummaryCarotid atherosclerotic plaques are a major cause of ischaemic stroke. The biomechanical environment to which the arterial wall and plaque is subjected to plays an important role in the initiation, progression and rupture of carotid plaques. MRI is frequently used to characterize the morphology of a carotid plaque, but new developments in MRI enable more functional assessment of carotid plaques. In this review, MRI based biomechanical parameters are evaluated on their current status, clinical applicability, and future developments. Blood flow related biomechanical parameters, including endothelial wall shear stress and oscillatory shear index, have been shown to be related to plaque formation. Deriving these parameters directly from MRI flow measurements is feasible and has great potential for future carotid plaque development prediction. Blood pressure induced stresses in a plaque may exceed the tissue strength, potentially leading to plaque rupture. Multi-contrast MRI based stress calculations in combination with tissue strength assessment based on MRI inflammation imaging may provide a plaque stress-strength balance that can be used to assess the plaque rupture risk potential. Direct plaque strain analysis based on dynamic MRI is already able to identify local plaque displacement during the cardiac cycle. However, clinical evidence linking MRI strain to plaque vulnerability is still lacking. MRI based biomechanical parameters may lead to improved assessment of carotid plaque development and rupture risk. However, better MRI systems and faster sequences are required to improve the spatial and temporal resolution, as well as increase the image contrast and signal-to-noise ratio.

Atherosclerosis remains a major cause of morbidity and mortality worldwide, and a thorough understanding of the underlying pathophysiological mechanisms is crucial for the development of new therapeutic strategies. Although atherosclerosis is a systemic inflammatory disease, coronary atherosclerotic plaques are not uniformly distributed in the vascular tree. Experimental and clinical data highlight that biomechanical forces, including wall shear stress (WSS) and plaque structural stress (PSS), have an important role in the natural history of coronary atherosclerosis. Endothelial cell function is heavily influenced by changes in WSS, and longitudinal animal and human studies have shown that coronary regions with low WSS undergo increased plaque growth compared with high WSS regions. Local alterations in WSS might also promote transformation of stable to unstable plaque subtypes. Plaque rupture is determined by the balance between PSS and material strength, with plaque composition having a profound effect on PSS. Prospective clinical studies are required to ascertain whether integrating mechanical parameters with medical imaging can improve our ability to identify patients at highest risk of rapid disease progression or sudden cardiac events.

Background Atherosclerotic plaque is subjected to a repetitive deformation due to arterial pulsatility during each cardiac cycle and damage may be accumulated over a time period causing fibrous cap (FC) fatigue, which may ultimately lead to rupture. In this study, we investigate the fatigue process in human carotid plaques using in vivo carotid magnetic resonance (MR) imaging. Method Twenty seven patients with atherosclerotic carotid artery disease were included in this study. Multi-sequence, high-resolution MR imaging was performed to depict the plaque structure. Twenty patients were found with ruptured FC or ulceration and 7 without. Modified Paris law was used to govern crack propagation and the propagation direction was perpendicular to the maximum principal stress at the element node located at the vulnerable site. Results The predicted crack initiations from 20 patients with FC defect all matched with the locations of the in vivo observed FC defect. Crack length increased rapidly with numerical steps. The natural logarithm of fatigue life decreased linearly with the local FC thickness (R2 = 0.67). Plaques (n=7) without FC defect had a longer fatigue life compared with those with FC defect (p = 0.03). Conclusion Fatigue process seems to explain the development of cracks in FC, which ultimately lead to plaque rupture.

Background Carotid plaque rupture, characterized by ruptured fibrous cap (FC), is associated with subsequent cerebrovascular events. However, ruptured FC may heal following stroke and convey decreased risk of future events. This study aims to characterize the healing process of ruptured FC by assessing the lumen conditions, quantified by the lumen curvature and roughness, using in vivo carotid cardiovascular magnetic resonance (CMR). Methods Patients suffering from transient ischemic attack underwent high resolution carotid MR imaging within 72 hours of the acute cerebrovascular ischemic event. CMR imaging was repeated at 3 and 12 months in 26 patients, in whom FC rupture/erosion was observed on baseline images and subsequent cerebrovascular events were recorded during the follow-up period. Lumen curvature and roughness were quantified from carotid CMR images and changes in these values were monitored on follow-up imaging. Results Healing of ruptured plaque was observed in patients (23 out of 26) without any ischemic symptom recurrence as shown by the lumen surface becoming smoother during the follow-up period, characterized by decreasing maximum lumen curvature (p < 0.05), increasing minimum lumen curvature (p < 0.05) and decreasing lumen roughness (p < 0.05) during the one year follow-up period. Conclusions Carotid plaque healing can be assessed by quantification of the lumen curvature and roughness and the incidence of recurrent cerebrovascular events may be high in plaques that do not heal with time. The assessment of plaque healing may facilitate risk stratification of recent stroke patients on the basis of CMR results.

Background Studies using medical images have shown that intraplaque hemorrhage may accelerate plaque progression and may produce a stimulus for atherosclerosis development by increasing lipid core and plaque volume and creating new destabilizing factors. Image-based 3D computational models with fluid-structure interactions (FSI) will be used to perform plaque mechanical analysis and investigate possible associations between intraplaque hemorrhage and both plaque wall stress (PWS) and flow shear stress (FSS). Methods In vivo MRI data of carotid plaques from 5 patients with intraplaque hemorrhage confirmed by histology were acquired. 3D multi-component FSI models were constructed for each plaque to obtain mechanical stresses. Plaque Wall Stress (PWS) and Flow Shear Stress (FSS) were extracted from all nodal points on the lumen surface of each plaque for analysis. Results The mean PWS value from all hemorrhage nodes of the 5 plaques combined was higher than that from non-hemorrhage nodes (75.6 versus 68.1 kPa, P = 0.0003). The mean PWS values from hemorrhage nodes for each of the 5 plaques were all significantly higher (5 out of 5) than those from non-hemorrhage nodes (P < 0.05). The mean FSS value from all hemorrhage nodes of the 5 plaques combined was 30.4% higher than that from all non-hemorrhage nodes (15.0 versus 11.5 dyn/cm2, P = 0.0002). However, the mean flow shear stress values from individual cases showed mixed results: only one out of five plaques showed mean FSS value from hemorrhage nodes was higher than that from non-hemorrhage nodes; three out of five plaques showed that their mean FSS values from hemorrhage nodes were lower than those from non-hemorrhage nodes; and one plaque showed that the difference had no statistical significance. Conclusion The results of this study suggested that intraplaque hemorrhage nodes were associated with higher plaque wall stresses. Compared to flow shear stress, plaque wall stress has a better correlation with plaque component feature (hemorrhage) linked to plaque progression and vulnerability. With further validation, plaque stress analysis may provide additional stress indicators for image-based vulnerability assessment.

Background Autogenous vein grafting is widely used in regular bypassing procedures. Due to its mismatch with the host artery in both mechanical property and geometry, the graft often over expands under high arterial blood pressure and forms a step-depth where eddy flow develops, thus causing restenosis, fibrous graft wall, etc. External stents, such as sheaths being used to cuff the graft, have been introduced to eliminate these mismatches and increase the patency. Although histological and immunochemical studies have shown some positive effects of the external stent, the mechanical mismatch under the protection of an external stent remains poorly analyzed. Methods In this study, the jugular veins taken from hypercholesterolemic rabbits were transplanted into the carotid arteries, and non-woven polyglycolic acid (PGA) fabric was used to fabricate the external stents to study the effect of the biodegradable external stent. Eight weeks after the operation, the grafts were harvested to perform mechanical tests and histological examinations. An arc tangent function was suggested to describe the relationship between pressure and cross-sectional area to analyse the compliance of the graft. Results The results from the mechanical tests indicated that grafts either with or without external stents displayed large compliance in the low-pressure range and were almost inextensible in the high-pressure range. This was very different from the behavior of the arteries or veins in vivo. The data from histological tests showed that, with external stents, collagen fibers were more compact, whilst those in the graft without protection were looser and thicker. No elastic fiber was found in either kind of grafts. Furthermore, grafts without protection were over-expanded which resulted in much bigger cross-sectional areas. Conclusion The PGA external extent contributes little to the reduction of the mechanical mismatch between the graft and its host artery while remodeling develops. For the geometric mismatch, it reduces the cross-section area, therefore matching with the host artery much better. Although there are some positive effects, conclusively the PGA is not an ideal material for external stent.