Healthy Arteries Research Articles

Identification of Potential Targets Linked to the Cardiovascular/Alzheimer's Axis through Bioinformatics Approaches.

The identification of common targets in Alzheimer’s disease (AD) and cardiovascular disease (CVD) in recent years makes the study of the CVD/AD axis a research topic of great interest. Besides aging, other links between CVD and AD have been described, suggesting the existence of common molecular mechanisms. Our study aimed to identify common targets in the CVD/AD axis. For this purpose, genomic data from calcified and healthy femoral artery samples were used to identify differentially expressed genes (DEGs), which were used to generate a protein–protein interaction network, where a module related to AD was identified. This module was enriched with the functionally closest proteins and analyzed using different centrality algorithms to determine the main targets in the CVD/AD axis. Validation was performed by proteomic and data mining analyses. The proteins identified with an important role in both pathologies were apolipoprotein E and haptoglobin as DEGs, with a fold change about +2 and −2, in calcified femoral artery vs healthy artery, respectively, and clusterin and alpha-2-macroglobulin as close interactors that matched in our proteomic analysis. However, further studies are needed to elucidate the specific role of these proteins, and to evaluate its function as biomarkers or therapeutic targets.

Outcomes of cardiac CT investigations in patients from the Rapid Access Chest Pain clinic with consideration to additional CT modalities and individual risk factors

Abstract Funding Acknowledgements Type of funding sources: None. Coronary CT is a first line investigation according to NICE guidelines, yet there are still uncertainties in its ability to decrease adverse event rates. The high sensitivity and high negative predictive value of coronary CT only validates low to moderate pre-test probability of attaining significant CAD due to its low positive predictive value. Improving outcomes in coronary CT could avoid events and limit the use of invasive modalities such as invasive coronary angiography. Increased probability of MACE with presence of risk factors could also raise the merit of risk stratification utilization for better classification. This study provides insight into the effectiveness of CT as a first-line investigation for new onset angina referred to RACPC regardless of CAD probability and any further testing. Data differences on outcome probabilities in risk stratification utilization and different CT modalities, both coronary calcium scoring and coronary angiography, raised notion that the incremental value of these tools should not be overlooked. End-outcomes would compromise of MACE composites after a 6-month follow-up. We hypothesize that patients investigated with coronary CT as opposed to without, with presence or absence of functional testing, would grant better clinical outcomes. Data on 155 patients who registered in RACPC were identified and collected from Brunei Health Information Management Systems for a one-year period (August 2018- August 2019). Information on sociodemographic, risk factors, further diagnostic testing, CT reports and event follow-up at 6 months were extracted, subject to availability. Probability of CAD in patients were classified according to CCS and CTCA results. CAD was detected in 62 (40.0%) patients with non-obstructive or obstructive CAD in addition to low to high calcium scores. Over the 6-month follow-up period, MACE occurred in 8 patients in the CT group (6.3%) and 4 (13.8%) without CT. 126 (81.3%) patients with CT did not attain MACE (p = 0.19) and chances of getting CABG after adjustments with co- founding factors were significantly lower than without CT [HR = 2.654e-06; 95% CI = 2.204e-07-3.195e-05; p= <0.001]. A higher event probability was associated with a high CCS (41.1%) (p= <0.001) than abnormal CTCA (11.4%) (p = 0.018). MACE was also associated with multiple risk factors such as age (p= <0.001), hypertension (p = 0.001), diabetes (p= <0.001), high cholesterol(p = 0.027), and abnormal total cholesterol (0.010) and creatinine levels [serum creatinine, p= 0.017; creatinine clearance, p = 0.006]. Outcomes measured were not significantly better in those with cardiac CT however risk of coronary artery bypass graft was significantly lower. CCS is better than CTCA in event prospects but both possess promising prognostic values in healthy arteries. Multiple CAD risk factors associated with MACE were likely as a result of intense atherosclerosis, marking appeal for risk stratifications and preventive measures. Abstract Figure. Kaplan-Meier curves for MACE Abstract Figure. Multiple cox regression models

Immature Vascular Smooth Muscle Cells in Healthy Murine Arteries and Atherosclerotic Plaques: Localization and Activity.

The local development of atherosclerotic lesions may, at least partly, be associated with the specific cellular composition of atherosclerosis-prone regions. Previously, it was demonstrated that a small population of immature vascular smooth muscle cells (VSMCs) expressing both CD146 and neuron-glial antigen 2 is postnatally sustained in atherosclerosis-prone sites. We supposed that these cells may be involved in atherogenesis and can continuously respond to angiotensin II, which is an atherogenic factor. Using immunohistochemistry, flow cytometry, wound migration assay xCELLigence system, and calcium imaging, we studied the functional activities of immature VSMCs in vitro and in vivo. According to our data, these cells do not express nestin, CD105, and the leptin receptor. They are localized in atherosclerosis-prone regions, and their number increases with age, from 5.7% to 23%. Immature VSMCs do not migrate to low shear stress areas and atherosclerotic lesions. They also do not have any unique response to angiotensin II. Thus, despite the localization of immature VSMCs and the presence of the link between their number and age, our study did not support the hypothesis that immature VSMCs are directly involved in the formation of atherosclerotic lesions. Additional lineage tracing studies can clarify the fate of these cells during atherogenesis.

Tissue Clearing Approaches in Atherosclerosis.

Recent advances in cardiovascular research have led to a more comprehensive understanding of molecular mechanisms of atherosclerosis. It has become apparent that the disease involves three layers of the arterial wall: the intima, the media, and a connective tissue coat termed the adventitia. It is also now appreciated that arteries are surrounded by adipose and neuronal tissues. In addition, adjacent to and within the adventitia, arteries are embedded in a loose connective tissue containing blood vessels (vasa vasora) and lymph vessels, artery-draining lymph nodes and components of the peripheral nervous system, including periarterial nerves and ganglia. During atherogenesis, each of these tissues undergoes marked structural and cellular alterations. We propose that a better understanding of these cell-cell and cell-tissue interactions may considerably advance our understanding of cardiovascular disease pathogenesis. Methods to acquire subcellular optical access to the intact tissues surrounding healthy and diseased arteries are urgently needed to achieve these aims. Tissue clearing is a landmark next-generation, three-dimensional (3D) microscopy technique that allows to image large-scale hitherto inaccessible intact deep tissue compartments. It allows for detailed reconstructions of arteries by a combination of labelling, clearing, advanced microscopies and other imaging and data-analysis tools. Here, we describe two distinct tissue clearing protocols; solvent-based modified three-dimensional imaging of solvent-cleared organs (3DISCO) clearing and another using aqueous-based 2,2'-thiodiethanol (TDE) clearing, both of which complement each other.

Impact of stress and hypertension on the cerebrovasculature.

Both stress and hypertension (HTN) are considered major health problems that negatively impact the cerebral vasculature. In this article we summarize the possible relationship between stress and HTN. We conducted a systematic review of the literature using a database search of MEDLINE, PubMed, Scopus, and Web of Science. Psychological stress is known to be an important risk factor for essential hypertension. Acute stress can induce transient elevations of blood pressure in the context of the fight-or-flight response. With increased intensity and duration of a perceived harmful event, the normal physiological response is altered, resulting in a failure to return to the resting levels. These changes are responsible for the development of HTN. Genetic and behavioral factors are also very important for the pathogenesis of hypertension under chronic stress situation. In addition, HTN and chronic stress may lead to impaired auto-regulation, regional vascular remodeling, and breakdown of the blood brain barrier (BBB). The effects of both HTN and chronic stress on the cerebral blood vessels shows that both have common structural and functional effects including endothelial damage with subsequent increased wall thickness, vessel resistance, stiffness, arterial atherosclerosis, and altered hemodynamics. Most of the above mentioned vascular effects of stress were primarily reported in animal models. Further in-vivo standardization of pathological vascular indices and imaging modalities is warranted. Radiological quantification of these cerebrovascular changes is therefore essential for in depth understanding of the healthy and diseased cerebral arteries functions, identification and stratification of patients at risk of cardiovascular and neurological adverse events, enactment of preventive measures prior to the onset of systemic HTN, and the initiation of personalized medical management.

Circ-Sirt1 Decelerates Senescence by Inhibiting p53 Activation in Vascular Smooth Muscle Cells, Ameliorating Neointima Formation.

Vascular smooth muscle cell (VSMC) senescence is a major driver of neointimal formation. We have demonstrated that circ-Sirt1 derived from the SIRT1 gene suppressed VSMC inflammation and neointimal formation. However, the effect of circ-Sirt1 inhibiting inflammation on VSMC senescence during neointimal hyperplasia remains to be elucidated. Here, we showed that circ-Sirt1 was highly expressed in young and healthy arteries, which was decreased in aged arteries and neointima of humans and mice. Overexpression of circ-Sirt1 delayed Ang II-induced VSMC senescence in vitro and ameliorated neointimal hyperplasia in vivo. Mechanically, circ-Sirt1 inhibited p53 activity at the levels of transcription and post-translation modulation. In detail, circ-Sirt1, on the one hand, interacted with and held p53 to block its nuclear translocation, and on the other hand, promoted SIRT1-mediated p53 deacetylation and inactivation. In conclusion, our data suggest that circ-Sirt1 is a novel p53 repressor in response senescence-inducing stimuli, and targeting circ-Sirt1 may be a promising approach to ameliorating aging-related vascular disease.

Abstract 12771: HDAC Inhibition With Quisinostat Reduces Pulmonary Vascular Remodeling in Experimentally Induced Pulmonary Arterial Hypertension

Introduction: Histone deacetylases (HDACs) expression and activity are increased in pulmonary arterial hypertension (PAH). Although inhibiting HDACs has been promoted as a treatment for PAH, results from preclinical studies were equivocal and raised concerns regarding safety. Quisinostat is a “second generation” HDAC inhibitor, which is highly potent against HDAC1 and elicits a prolonged pharmacodynamic response. Hypothesis: Quisinostat may exert therapeutic effects in experimentally-induced PAH. Methods: HDAC1 expression was measured in lungs and microvascular endothelial cells (MVECs) from control donors and PAH patients. HDAC activity, proliferation and inflammation were measured after quisinostat treatment of PAH MVECs. Chronic quisinostat treatment was tested in three PAH rat models: the Sugen + hypoxia (SuHx), the Monocrotaline shunt flow (MF) and pulmonary artery banding (PAB) model. Results: HDAC1 expression is increased in lungs of PAH patients. Quisinostat decreased proliferation and mitigated inflammatory cytokine expression in MVECs. Conditioned medium from quisinostat treated PAH MVECs inhibited the growth of healthy pulmonary artery smooth muscle cells. In vivo , quisinostat treatment reduced right ventricular (RV) systolic pressure, RV afterload and total pulmonary resistance in SuHx rats. Further analysis by histology revealed that quisinostat reduced pulmonary vascular remodeling in both SuHx and MF rat models by reducing proliferation and perivascular inflammation. The PAB rat model demonstrated that quisinostat had no independent effect on RV function or remodeling. Conclusions: Quisinostat can partly reverse RV afterload and pulmonary vascular remodeling in established experimental PAH and may be a promising intervention for PAH.

Development of a Collagen Fibre Remodelling Rupture Risk Metric for Potentially Vulnerable Carotid Artery Atherosclerotic Plaques.

Atherosclerotic plaque rupture in carotid arteries can lead to stroke which is one of the leading causes of death or disability worldwide. The accumulation of atherosclerotic plaque in an artery changes the mechanical properties of the vessel. Whilst healthy arteries can continuously adapt to mechanical loads by remodelling their internal structure, particularly the load-bearing collagen fibres, diseased vessels may have limited remodelling capabilities. In this study, a local stress modulated remodelling algorithm is proposed to explore the mechanical response of arterial tissue to the remodelling of collagen fibres. This stress driven remodelling algorithm is used to predict the optimum distribution of fibres in healthy and diseased human carotid bifurcations obtained using Magnetic Resonance Imaging (MRI). In the models, healthy geometries were segmented into two layers: media and adventitia and diseased into four components: adventitia, media, plaque atheroma and lipid pool (when present in the MRI images). A novel meshing technique for hexahedral meshing of these geometries is also demonstrated. Using the remodelling algorithm, the optimum fibre patterns in various patient specific plaques are identified and the role that deviations from these fibre configurations in plaque vulnerability is shown. This study provides critical insights into the collagen fibre patterns required in carotid artery and plaque tissue to maintain plaque stability.

Trafficking of Mononuclear Phagocytes in Healthy Arteries and Atherosclerosis

Monocytes and macrophages play essential roles in all stages of atherosclerosis – from early precursor lesions to advanced stages of the disease. Intima-resident macrophages are among the first cells to be confronted with the influx and retention of apolipoprotein B-containing lipoproteins at the onset of hypercholesterolemia and atherosclerosis development. In this review, we outline the trafficking of monocytes and macrophages in and out of the healthy aorta, as well as the adaptation of their migratory behaviour during hypercholesterolemia. Furthermore, we discuss the functional and ontogenetic composition of the aortic pool of mononuclear phagocytes and its link to the atherosclerotic disease process. The development of mouse models of atherosclerosis regression in recent years, has enabled scientists to investigate the behaviour of monocytes and macrophages during the resolution of atherosclerosis. Herein, we describe the dynamics of these mononuclear phagocytes upon cessation of hypercholesterolemia and how they contribute to the restoration of tissue homeostasis. The aim of this review is to provide an insight into the trafficking, fate and disease-relevant dynamics of monocytes and macrophages during atherosclerosis, and to highlight remaining questions. We focus on the results of rodent studies, as analysis of cellular fates requires experimental manipulations that cannot be performed in humans but point out findings that could be replicated in human tissues. Understanding of the biology of macrophages in atherosclerosis provides an important basis for the development of therapeutic strategies to limit lesion formation and promote plaque regression.

Computer modeling of different shaped patches in classical carotid endarterectomy

Objective: to construct geometric models of carotid bifurcation and build a computer modeling for carotid endarterectomy (CEA) operations with patches of various configurations.Materials and methods. The method uses reconstructed models of a healthy blood vessel obtained from a preoperative computed tomography (CT) study of the affected blood vessel of a particular patient. Flow in the vessel is simulated by computational fluid dynamics using data from the patient's ultrasonic Doppler velocimetry and CT angiography. Risk factors are assessed by hemodynamic indices at the vessel wall associated with Wall Shear Stress (WSS).Results. We used the proposed method to study the hemodynamic results of 10 virtual CEA operations with patches of various shapes on a reconstructed healthy artery of a particular patient. The reason for patch implantation was to ensure that the vessel lumen is not narrowed as a result of the surgery, since closing the incision without a patch can reduce the vessel lumen circumference by 4–5 mm, which adversely affects blood flow. On the other hand, too wide a patch creates aneurysmorphic deformation of the internal carotid artery (ICA) mouth, which is not optimal due to formation of a large recirculation zone. In this case, it was found that the implanted patch width of about 3 mm provides an optimal hemodynamic outcome. Deviations from this median value, both upward and downward, impair hemodynamics. The absence of a patch gives the worst of the results considered.Conclusion: The proposed computer modeling technique is able to provide a personalized patch selection for classical CEA with low risk of restenosis in the long-term follow-up.

CFD Analysis on Effect of Angulation in A Healthy Abdominal Aorta-Renal Artery Junction

The recent developments in computational fluid dynamics (CFD) can be useful in observing the detailed haemodynamics in renal artery bifurcation for clinical evaluation and treatment. The present study focuses on haemodynamic behaviour of blood as it flows through the abdominal aorta-renal artery junction in an idealistic healthy artery with varying bifurcation angles to the abdominal aorta, i.e. from 30° to 90° with increments of 15°. This is to examine the effect of angulation on the junction and to determine whether arterial geometry plays a role in the prediction of atherosclerotic lesions. The three-dimensional models used in this study were generated using ANSYS WORKBENCH 19.0, and numerical simulation was done using FLUENT 19.0 solver. The blood flow is assumed to be Newtonian, incompressible and laminar. Haemodynamic parameters such as velocity, wall pressure and wall shear stress along with flow variation are compared among the different models. As the angulation increased, velocity and wall shear stress at the ostial region decreased by 14% and 52% respectively. Wall pressure at the same region saw an increase by 3%. Therefore, renal arteries with higher bifurcating angles to the abdominal aorta were observed to be more prone to the formation of atherosclerotic lesions. The present study is a precursor for future studies on renal artery with stenosis.

Matrix Stiffness Affects Glycocalyx Expression in Cultured Endothelial Cells.

Rationale: The endothelial cell glycocalyx (GCX) is a mechanosensor that plays a key role in protecting against vascular diseases. We have previously shown that age/disease mediated matrix stiffness inhibits the glycocalyx glycosaminoglycan heparan sulfate and its core protein Glypican 1 in human umbilical vein endothelial cells, rat fat pad endothelial cells and in a mouse model of age-mediated stiffness. Glypican 1 inhibition resulted in enhanced endothelial cell dysfunction. Endothelial cell culture typically occurs on stiff matrices such as plastic or glass. For the study of the endothelial GCX specifically it is important to culture cells on soft matrices to preserve GCX expression. To test the generality of this statement, we hypothesized that stiff matrices inhibit GCX expression and consequently endothelial cell function in additional cell types: bovine aortic endothelial cells, mouse aortic endothelial cell and mouse brain endothelial cells.Methods and Results: All cell types cultured on glass showed reduced GCX heparan sulfate expression compared to cells cultured on either soft polyacrylamide (PA) gels of a substrate stiffness of 2.5 kPa (mimicking the stiffness of young, healthy arteries) or on either stiff gels 10 kPa (mimicking the stiffness of old, diseased arteries). Specific cell types showed reduced expression of GCX protein Glypican 1 (4 of 5 cell types) and hyaluronic acid (2 of 5 cell types) on glass vs soft gels.Conclusion: Matrix stiffness affects GCX expression in endothelial cells. Therefore, the study of the endothelial glycocalyx on stiff matrices (glass/plastic) is not recommended for specific cell types.

Effect of Different Types of Stenosis on Generalized Power Law Model of Blood Flow in a Bifurcated Artery

This study is focus on generalized power law model of blood flow in a stenosed bifurcated artery under the effect of different types of stenosis. Stenosis can cause the narrowing of the artery that may reduce the flow of blood supply to the heart, and this may lead to the heart attacks. The geometry of the bifurcated artery with different classification of stenosis locations is considered in order to shows four possible morphologies formation of plaque from healthy artery to disease artery. The bifurcated artery is modelled as a two-dimensional rigid wall since the wall of a disease artery is reported to be less flexibility. Few assumptions are considered such as blood are incompressible, laminar, steady and characterized as the generalized power-law model. Simulation results are obtained using COMSOL Multiphysics 5.2, which is a software that based on the finite element method to solve this problem. Results concerning the effect of different locations of stenosis on generalized power law model of the blood flow characteristic such as streamlines pattern are discussed.

Nonbone Marrow CD34+ Cells Are Crucial for Endothelial Repair of Injured Artery.

[Figure: see text].

Image processing to delineate the boundaries of peripheral arterial walls

Abstract The analysis of the arterial wall properties is vital in the prediction of stroke events and arterial hypertension in humans. Numerous researchers have experimented with several approaches to model arterial vessels and to analyse their biomechanical behaviour for many years now. Our study is focussed on image processing of peripheral arterial cross sections to detect and isolate the distinct layers. These boundaries will enable the creation of FEM models for further analysis of arterial wall properties. In a clinical setting, it facilitates doctors to identify the optimum pressure that can be applied to the artery for the treatment of stenosis without damaging the morphology of the blood vessels. This paper aims at distinguishing the various layers of arterial walls from images by minimizing human intervention. Cross section images of arteries from various sources were collected[10][11]. The boundaries from the image were obtained using image processing techniques of MATLAB(R2021a). The approach identified was to convert the input RGB images to grayscale, thresholding and applying morphological operators to delineate the Intima, Media, and Adventitia. These regions of interests (ROI) were then superimposed to generate an image with differentiated boundaries and void of unnecessary noise and inhomogeneity. This approach gave us an insight of the differences in various methods of boundary detection and to infer the optimum approach for accurate demarcation of boundaries of the three layers of arterial walls. It paves a pathway for forward modelling and to perform detailed FEM analysis in in-vitro diagnostics. In a nutshell, it was observed that the edge detection procedure implemented could be used for healthy and stenotic arteries. Further studies must be conducted to test the efficiency across a wide range of images and hence generalise its usage. Upon satisfactory boundary detection, forward modelling could be performed using the identified geometric forms.

New in the etiology, pathogenesis, prevention and treatment of atherosclerosis. The two different types of cholesterol plaques have nothing to do with each other

The article is presented in the form of a review and analysis of the literature, which additionally helps to reveal the mechanisms of the pathogenesis of the development of atherosclerosis. This article provides a completely new understanding of the stages and sequence of atherosclerosis development. The modern vision is refuted, which states that all types of lesions in atherosclerosis are developed successively, one after another. The article sheds a light on a significant difference between type IV atherosclerotic lesions and between types V and VI atherosclerotic lesions. Type IV atherosclerotic lesions consists of one lipid core with molten extracellular lipid. Stretches the middle and outer layers of an artery from one side and protrudes beyond the anatomical artery dimensions over the years. In contrast, type V atherosclerotic lesions type is a long, concentric, soft, strong, elastic, yellow, uniform structure, in the form of a tube with a hole in the middle, located in the lumen, which is easily removed from the artery. This types V and VI atherosclerotic lesions - the author suggests calling “cylindrical cholesterol plaque”. Type V atherosclerotic lesions (cylindrical cholesterol plaque) has nothing to do with types I-V atherosclerotic lesions. There are many “coincidences” that make it impossible to see the difference between them. Type V atherosclerotic lesions (cylindrical cholesterol plaque) is an independent pathological structure that appears in a short period of time (few minutes) in the lumen of a healthy artery in case of artery spasm and appearance of a strong obstruction to blood flow. Low density lipoproteins are retained within the wall, in front of the site of arterial narrowing, and quickly create a CCP in the form of a hollow cylinder. All subsequent forms of types V and VI atherosclerotic lesions - concentric and eccentric, are the result of the destruction of the original concentric structure of the type V atherosclerotic lesions (cylindrical cholesterol plaque).

Mechanisms of vascular smooth muscle cell investment and phenotypic diversification in vascular diseases.

In contrast with the heart, the adult mammalian vasculature retains significant remodelling capacity, dysregulation of which is implicated in disease development. In particular, vascular smooth muscle cells (VSMCs) play major roles in the pathological vascular remodelling characteristic of atherosclerosis, restenosis, aneurysm and pulmonary arterial hypertension. Clonal lineage tracing revealed that the VSMC-contribution to disease results from the hyperproliferation of few pre-existing medial cells and suggested that VSMC-derived cells from the same clone can adopt diverse phenotypes. Studies harnessing the powerful combination of lineage tracing and single-cell transcriptomics have delineated the substantial diversity of VSMC-derived cells in vascular lesions, which are proposed to have both beneficial and detrimental effects on disease severity. Computational analyses further suggest that the pathway from contractile VSMCs in healthy arteries to phenotypically distinct lesional cells consists of multiple, potentially regulatable, steps. A better understanding of how individual steps are controlled could reveal effective therapeutic strategies to minimise VSMC functions that drive pathology whilst maintaining or enhancing their beneficial roles. Here we review current knowledge of VSMC plasticity and highlight important questions that should be addressed to understand how specific stages of VSMC investment and phenotypic diversification are controlled. Implications for developing therapeutic strategies in pathological vascular remodelling are discussed and we explore how cutting-edge approaches could be used to elucidate the molecular mechanisms underlying VSMC regulation.

Patient Specific Modelling of Blood Flow in Coronary ‎Artery

The performance of the heart is considerably affected by the blocks formed because of the deposition of ‎plaque inside the coronary artery. The blocks (stenosis) either in coronary artery or elsewhere force the ‎heart to work harder for pumping the oxygenated blood to the heart muscles and blood vessels. This ‎study analyses the flow through the stenosed coronary arteries via numerical modelling by using ANSYS ‎FLUENT software. Three real cases with different asymmetric stenosis levels (i.e., block level 33%, 66% ‎& 85%) are analysed by considering blood as a non-Newtonian fluid, and blood flow as pulsatile in ‎nature. As the flow regime falls in transition to turbulent region, the transition Shear Stress Transport ‎‎(SST) k-ω turbulence model is used to take care of the changeover stage from laminar to turbulent flow ‎and vice versa. The results show large variation both in Wall Shear Stress (WSS) and pressure drop near ‎the stenosis. Pressure drop becomes more significant at severe degrees of stenosis (66% and 85%) ‎compared to the mild case (33%). The study throws light on the critical distribution of shear stress and ‎pressure drop along the artery wall, which are considered as indicators of the commencement of heart ‎disease and further growth of stenosis. An indicator, viz., Fractional Flow Reserve (FFR), which relates ‎the percentage of stenosis to the pressure variations, can be used as an index to diagnose the severity of ‎stenosis. All the three cases with different stenotic levels were analysed under hyperaemic conditions and ‎found that even 45% stenosis case can go near to critical at hyperaemic flow conditions. The effect of ‎severity due to vessel constriction can be estimated by comparing the simulated pressure drop and WSS ‎before and after the stenosis, with the ones for a healthy artery. The present study developed a ‎methodology to calculate FFR value for unknown percentage of stenosis based on the simulated results ‎obtained from 33%, 66% and 85% stenosis. Thus, criticality of a patient with certain percentage stenosis ‎can also be evaluated. This simulation technique can be recommended as a non-invasive diagnostic tool ‎for the early detection of atherosclerosis‎‎.

Single cell sequencing reveals fibroblast heterogeneity in healthy and diseased vasculature

Background and Aims: Fibroblasts are present in healthy and diseased arteries. Their role in vascular dysfunction remains unclear, as current markers are unable to distinguish fibroblasts from other vascular cells. We used single-cell RNA-sequencing (SCS) to identify the adventitial fibroblast transcriptome and unravel heterogeneity.

Oxygen-sensitive Magnetic Resonance Imaging: A Noninvasive Step Forward for Diagnosing Vasculopathy in the Cardiac Allograft.

Oxygen-sensitive Magnetic Resonance Imaging: A Noninvasive Step Forward for Diagnosing Vasculopathy in the Cardiac Allograft.