Background: The augmentation index (AI) has been considered to reflect vascular property and predict a higher risk of coronary atherosclerosis. However, the association of augmentation index and coronary plaque morphology has not been fully elucidated.Optical coherence tomography (OCT) is a high-resolution imaging modality and allows us to analyze the plaque morphology in detail. In this study, we observed the coronary plaque morphology by OCT at the coronary culprit artery in patients with coronary artery disease (CAD) and evaluated the association of augmentation index and coronary plaque characteristics.. Methods: The measurement of AI by carotid ultrasound and OCT examinations were performed in 33 patients with CAD (stable angina pectoris (SAP): n=19, acute coronary syndrome (ACS): n=14). At the coronary culprit artery, plaque characterization (lipid or fibrous plaque) was analyzed. Futhermore, fibrous cap thickness, spotty calcification, thin cap fibroatheroma (TCFA), and plaque rupture ...
In the current study we assessed the longitudinal distribution of grayscale and IVUS-VH parameters among fibroatheromas in nonculprit coronary arteries, as well as the impact of vessel area and plaque burden on plaque rupture. The main findings are as follows: 1) there was a gradient of high-risk plaques (fibroatheromas of all types and plaque ruptures) from proximal to distal coronary segments, mainly in the LAD and LCX and least in the RCA; and 2) although proximal location was an independent predictor for plaque rupture, vessel area and plaque burden were better discriminants of plaque rupture versus nonruptured fibroatheromas rather than the distance from the ostium to the maximum NC site.. Previous autopsy, angiographic, IVUS, and optical coherence tomography studies elucidated that the majority of high-risk plaques including ruptured plaques accumulated in proximal segments of the coronary tree (5-8,15-17). Cheruvu et al. (5), Farb et al. (18), and Davies (19) have reported that most ...
The primary aim of this thesis was to quantify the collagenase concentrations in carotid plaques and to relate them to markers to plaque instability.;Recent studies have shown that strain therapy decreases cardiovascular risk, even in patients with normal cholesterol levels. A further aim of this thesis was to observe the effects of statins on clinical and biochemical indicators of plaque instability.;Atherosclerotic plaques were collected from 159 patients undergoing carotid endarterectomy. The presence and timing of carotid territory symptoms was ascertained. Pre-operative embolisation was recorded by transcranial Doppler. Each plaque was assessed for histological features of instability. Plaque MMP and cytokine concentrations was quantified using ELISA.;Significantly higher concentrations of active MMP-8 were observed in the plaques of symptomatic patients (p=0.0002), emboli-positive patients (p=0.0037) and in those plaques demonstrating histological evidence of rupture (p=0.0036). No ...
In the present study, we show that it is possible to identify genes that are differentially and reproducibly expressed in whole-mount advanced human atherosclerotic plaques by using the SSH procedure. In the present study, we describe the identification of several genes differentially expressed between advanced stable and ruptured atherosclerotic plaques. Our stable plaques are classified according to the morphological criteria of the AHA and are characterized by a thick fibrous cap, high smooth muscle cell/collagen content, and a small lipid core, but also comprise rupture-prone lesions, with a thin fibrous cap and a large lipid core, but with no signs of intraplaque hemorrhage or a healed fibrous cap. According to the classification scheme described by Virmani et al,5 our group of stable atherosclerotic plaques includes thin and thick fibrous cap atheromas and fibrocalcified plaques. Our group of ruptured plaques (type VI lesions according to the AHA classification) is defined by the presence ...
High density lipoprotein (HDL) has been proved to be a protective factor for coronary heart disease. Notably, HDL in atherosclerotic plaques can be nitrated (NO2-oxHDL) and chlorinated (Cl-oxHDL) by myeloperoxidase (MPO), likely compromising its cardiovascular protective effects. Here we determined the effects of NO2-oxHDL and Cl-oxHDL on SMC migration using wound healing and transwell assays, proliferation using MTT and BrdU assays, and apoptosis using Annexin-V assay in vitro, as well as on atherosclerotic plaque stability in vivo using a coratid artery collar implantation mice model. Our results showed that native HDL promoted SMC proliferation and migration, whereas NO2-oxHDL and Cl-oxHDL inhibited SMC migration and reduced capacity of stimulating SMC proliferation as well as migration, respectively. OxHDL had no significant influence on SMC apoptosis. In addition, we found that ERK1/2-phosphorylation was significantly lower when SMCs were incubated with NO2-oxHDL and Cl-oxHDL. Furthermore,
C-reactive protein (CRP) is a member of the pentraxin family and represents the most extensively studied proinflammatory molecule. In healthy individuals, only trace levels of CRP can be detected in the circulation. Under acute conditions, concentrations of CRP increase during the first 6 to 8 hours and can reach peak levels approaching 300 mg/L after approximately 48 hours.3 CRP is a robust clinical marker because of its analytical stability, shows reproducible results, and high-sensitivity assays with good precision are commercially available.. CRP is synthesized by hepatocytes and its production is under transcriptional control of several cytokines, with interleukin (IL)-6 being a primary stimulus. However, recent evidence has suggested that CRP may be also produced locally in vascular smooth muscle cells (SMCs) and macrophages of atherosclerotic lesions.4-5 A recent post-mortem study further confirmed a potential pathogenic role of CRP in atheromatous plaque vulnerability,6 demonstrating ...
Approach and Results-In the present study, we used a murine model of atherosclerosis (ApoE−/−) in conjunction with DKK3−/− and performed tandem stenosis of the carotid artery to evaluate atherosclerotic plaque development. We found that the absence of DKK3 leads to vulnerable atherosclerotic plaques, because of a reduced number of SMCs and reduced matrix protein deposition, as well as increased hemorrhage and macrophage infiltration. Further in vitro studies revealed that DKK3 can induce differentiation of Sca1+ vascular progenitors and fibroblasts into SMCs via activation of the TGF-β (transforming growth factor-β)/ATF6 and Wnt signaling pathways. Finally, we assessed the therapeutic potential of DKK3 in mouse and rabbit models and found that DKK3 altered the atherosclerotic plaque content via increasing SMC numbers and reducing vascular inflammation. ...
The goal of identifying high-risk plaques before they become disrupted (i.e., plaque rupture or intraplaque hemorrhage) leading to plaque progression and/or a new clinical event has preoccupied cardiologists for many years, with its promise that early and accurate identification of high-risk plaques would enable the development of pre-emptive therapeutic strategies to avert cardiac morbidity and mortality. The plaque morphology that underlies the majority of plaque disruption is the highly inflamed thin cap fibroatheroma (TCFA). Plaque disruption is a very complicated pathobiological and biomechanical process that is dependent on the nature and constituents of the plaque itself (1), as well as the external mechanical forces affecting that plaque. Rupture of the TCFAs fibrous cap occurs when plaque stress exceeds plaque strength, leading to abrupt superimposed intraplaque/intraluminal thrombus and a clinical acute coronary syndrome. In contrast, intraplaque hemorrhage, associated with subsequent ...
The rupture of atherosclerotic plaques is known to be associated with the stresses that act on or within the arterial wall. The extreme wall tensile stress is usually recognized as a primary trigger for the rupture of the plaque. The present study used one-way fluid-structure interaction simulation to investigate the impacts of fibrous cap thickness and lipid core volume to the wall tensile stress value and distributions on the fibrous cap. Von Mises stress was employed to represent the wall tensile stress (VWTS). A total of 13 carotid bifurcation cases were manipulated based on a base geometry in the study with varied combinations of fibrous cap thickness and lipid core volume in the plaque. Values of maximum VWTS and a stress value of VWTS_90, which represents the cut-off VWTS value of 90% in cumulative histogram of VWTS possessed at the computational nodes on the luminal surface of fibrous cap, were used to assess the risk of plaque rupture for each case. Both parameters are capable of ...
Vulnerable plaques, which are responsible for most acute ischemic events, are presently invisible to x-ray angiography. Their primary morphological features include a thin or ulcerated fibrous cap, a large necrotic core, superficial foam cells, and intraplaque hemorrhage. We present evidence that multimodal spectroscopy (MMS), a novel method that combines diffuse reflectance spectroscopy (DRS), intrinsic fluorescence spectroscopy (IFS), and Raman spectroscopy (RS), can detect these markers of plaque vulnerability. To test this concept, we perform an MMS feasibility study on 17 human carotid artery specimens. Following the acquisition of spectra, each specimen is histologically evaluated. Two parameters from DRS, hemoglobin concentration and a scattering parameter, are used to detect intraplaque hemorrhage and foam cells; an IFS parameter that relates to the amount of collagen in the topmost layers of the tissue is used to detect the presence of a thin fibrous cap; and an RS parameter related to ...
An elevated systemic inflammatory status is considered to be a riskfactor for future cardiovascular events. Multi Slice CT allows to assess and characterize coronary plaques and it is hypothesized that the presence of mixed and noncalcified plaques may be an indicator for plaque vulnerability. To date it is not clear whether there is an association between plaque composition determined by Dual Source CT and systemic biomarkers for inflammation and thrombogenity. In the present study we investigated 303 (102 female, 201 male, age 55 ± 9 years) consecutive patients with an intermediate likelihood for coronary artery disease, who underwent DSCT coronary angiography. The scan was performed on a Siemens Definiton Scanner (Forchheim, Germany) using a standard protocol. For analysis we divided the coronary tree in 15 segments according to the AHA-scheme and each segment was further divided in a proximal and a distal part. Each segment was then classified as containing no, noncalcified, mixed (20% ...
BackgroundCoronary atherothrombosis due to atherosclerotic plaque rupture or erosion is frequently associated with acute coronary syndromes (ACS). Significant efforts have been made to elucidate the pathophysiological mechanisms underlying acute coronary events. Materials and methodsThis narrative review is based on the material searched for and obtained via PubMed up to August 2014. The search terms we used were as follows: angiotensin, acute coronary syndromes, acute myocardial infarction in combination with atherosclerosis, vulnerability, clinical trial, ACE inhibitors, inflammation. ResultsAmong several regulatory components, the renin-angiotensin system (RAS) was shown as a key pathway modulating coronary atherosclerotic plaque vulnerability. Indeed, these molecules are involved in all stages of atherogenesis. Classically, the RAS is composed by a series of enzymatic reactions leading to the angiotensin (Ang) II generation and activity. However, the knowledge of RAS has expanded and ...
DESCRIPTION (provided by applicant): The overall goal of this project is to streamline the new advanced ultrasound imaging (USI) and magnetic resonance imaging (MRI) of carotid plaque for effective stroke risk tratification. Rupture of carotid plaque causes stroke posing threats to human life and long-term disability. Recent investigations have shown us that specific features of atherosclerotic plaques predispose them to plaque rupture, the proximate cause of clinical events. Magnetic resonance imaging (MRI) has been the gold standard for carotid plaque characterization. Latest ultrasound imaging (USI) technology makes it possible to contribute more to plaque characterization, yet it lacks of validation. The objective of this proposed effort is to extend the MRI high-risk plaque characterization technology and knowledge to validate the performance of USI plaque characterization and to compare and improve the performance of both MRI and USI with the information and knowledge from the other ...
Background: Optical coherence tomography (OCT) can detect detailed plaque features in native coronary arteries. Stent struts cause shadows that partially obscure the vessel wall, but plaque features can still be seen. We investigated the impact of stent artefact on plaque quantification and whether the plaque behind struts is associated with microvascular dysfunction. Methods: Patients retrospectively recruited from two centres, underwent OCT pre- and post-stenting on the same vessel segment. Lipid (LA) and calcium (CA) were measured as arcs. Macrophages, microchannels and cholesterol crystals were counted. Subsequently, we determined whether stented plaque features were associated with reduced TIMI flow grade in consecutive patients who underwent OCT post-stenting. Results: In 52 patients the lipid arc was similar pre- vs post-stent: median (55º [13º-93º] vs. 40º [18º-87°]; difference 1º [−7º to 16º], p = NS). Pre- and post-stent lipid were strongly correlated (r = 0.92, p , 0.001). ...
Atherosclerosis is recognized clinically as an arterial disease prominently involving the intima of medium- or large-sized arteries, including the aortic, carotid, coronary and cerebral arteries. Atherosclerotic lesions or plaques contain complex tissue matrix, including collagen, elastin, proteoglycans and extracellular and intracellular lipids with foamy macrophages and smooth muscle cells. In addition, inflammatory cellular components (e.g., T lymphocytes, macrophages, some basophils) also exist in the lesions. Disruption of atherosclerotic plaques appears to be the major cause of heart attacks and strokes. Although the risk of plaque rupture usually cannot be predicted, many postmortem examinations have revealed that this risk depends mainly on plaque composition (1,2). Most ruptured atherosclerotic plaques are characterized structurally by formation of a large, soft, lipid-rich, necrotic core covered by a thin fibrous cap densely infiltrated by macrophages. Inflammation is also a major ...
Recruitment of monocytes into atherosclerotic plaque has been shown to drive disease progression, and the presence of a higher number of macrophages has been associated with increased plaque vulnerability. Conversely, a reduction in plaque macrophage content has been associated with plaque stabilisation; however, it has not previously been described exactly how macrophages are removed from plaques, for example in the context of statin therapy.. Potteaux et al. aimed to elucidate this mechanism by use of the mouse Apoe-/- model, which has high levels of cholesterol and therefore spontaneously develops atherosclerotic lesions. However, in this case the authors re-introduced the apoE gene (by means of an adenoviral vector), and studied what happened to the mices atherosclerotic plaques subsequently.. Within two days of apoE complementation, plasma cholesterol levels had returned to normal levels, and HDL cholesterol levels had increased four fold, leading to a stabilisation of plaque area. At four ...
OBJECTIVES: The goal of this study was to determine whether a 3-T magnetic resonance imaging (MRI) protocol combining carotid atherosclerotic plaque and brain imaging can identify features of high-risk acutely symptomatic plaque that correlate with brain injury. BACKGROUND: It has previously been demonstrated that, in asymptomatic patients, MRI can identify features of carotid plaque that are associated with stroke, such as the presence of a large lipid core. We hypothesized that the early phase (|7 days) after a cerebrovascular event, when risk of recurrence is highest, may be associated with particular plaque characteristics that associate with cerebral injury. METHODS: Eighty-one patients (41 presenting acutely with transient ischemic attack [TIA] or minor stroke and 40 asymptomatic controls) underwent multicontrast carotid artery MRI on 2 separate occasions, each accompanied by diffusion-weighted imaging (DWI) and fluid-attenuated inversion recovery (FLAIR) imaging of the brain. RESULTS: Complex
There has been a great deal of research interest regarding the relationships among lipids, inflammation, and their effects on the arterial wall (11). Intravascular ultrasound has been used clinically as a representative imaging modality to evaluate the coronary arterial wall and plaque morphology, including quantification of plaque burden, but it is not possible to determine the thickness of the cap with this method, due to its poor resolution. In contrast, the high resolution of OCT makes it an ideal imaging modality for microstructural evaluation, such as determination of FCT (12,13), although this method is not suitable for evaluation of plaque burden due to its poor penetration depth. Therefore, assessment with a combination of both IVUS and OCT has the potential to allow detailed assessment of changes in plaque morphology.. The pathological features of the most common form of vulnerable plaque include a large lipid pool within the plaque, a thin fibrous cap, and macrophage accumulation ...
Mitochondria-associated ER membranes (MAMs) are crucial for lipid transport and synthesis, calcium exchange, and mitochondrial functions, and they also act as signaling platforms. These contact sites also play a critical role in the decision between autophagy and apoptosis with far reaching implications for cell fate. Vascular smooth muscle cell (VSMC) apoptosis accelerates atherogenesis and the progression of advanced lesions, leading to atherosclerotic plaque vulnerability and medial degeneration. Though the successful autophagy of damaged mitochondria promotes VSMC survival against pro-apoptotic atherogenic stressors, it is unknown whether MAMs are involved in VSMC mitophagy processes. Here, we investigated the role of the multifunctional MAM protein phosphofurin acidic cluster sorting protein 2 (PACS-2) in regulating VSMC survival following a challenge by atherogenic lipids. Using high-resolution confocal microscopy and proximity ligation assays, we found an increase in MAM contacts as in PACS-2
The investigators hypothesis is that local activation of the endogenous Lp-PLA2 plays an integral role in early atherosclerosis, and contributes to the mechanism of coronary endothelial dysfunction and to the structural and mechanical properties that characterize plaque vulnerability. Thus, our study will characterize prospectively the correlation between the functional and structural vascular wall properties, and the activity of the Lp-PLA2 pathway.. ...
Acute coronary syndromesâ€"unstable angina, myocardial infarction, and sudden cardiac deathâ€"are caused by acute disruption of an unstable coronary atheroma. Unstable plaques have three histologic characteristics: a large lipid core, many inflammatory cells, and a thin fibrous cap. Because the unstable plaque is not necessarily obstructive, it may cause no symptoms before rupture. The cellular processes that lead to the characteristic histologic features of unstable plaque have recently been identified. This new understanding of the cell biology of plaque instability suggests new therapeutic strategies: passivation of the endothelium, reduction of low-density lipoprotein (LDL) in the vessel wall by decreasing serum LDL levels or accelerating reverse cholesterol transport, inhibition of LDL oxidation, inhibition of inflammatory cytokine expression, and inhibition of thrombus formation. Although the morbidity and mortality resulting from acute coronary disease have been reduced by more than ...
Acute coronary syndromesâ€"unstable angina, myocardial infarction, and sudden cardiac deathâ€"are caused by acute disruption of an unstable coronary atheroma. Unstable plaques have three histologic characteristics: a large lipid core, many inflammatory cells, and a thin fibrous cap. Because the unstable plaque is not necessarily obstructive, it may cause no symptoms before rupture. The cellular processes that lead to the characteristic histologic features of unstable plaque have recently been identified. This new understanding of the cell biology of plaque instability suggests new therapeutic strategies: passivation of the endothelium, reduction of low-density lipoprotein (LDL) in the vessel wall by decreasing serum LDL levels or accelerating reverse cholesterol transport, inhibition of LDL oxidation, inhibition of inflammatory cytokine expression, and inhibition of thrombus formation. Although the morbidity and mortality resulting from acute coronary disease have been reduced by more than ...
Atherosclerosis is a chronic inflammatory disease, and developing therapies to promote its regression is an important clinical goal. We previously established that atherosclerosis regression is characterized by an overall decrease in plaque macrophages and enrichment in markers of alternatively activated M2 macrophages. We have now investigated the origin and functional requirement for M2 macrophages in regression in normolipidemic mice that received transplants of atherosclerotic aortic segments. We compared plaque regression in WT normolipidemic recipients and those deficient in chemokine receptors necessary to recruit inflammatory Ly6Chi (Ccr2-/- or Cx3cr1-/-) or patrolling Ly6Clo (Ccr5-/-) monocytes. Atherosclerotic plaques transplanted into WT or Ccr5-/- recipients showed reduced macrophage content and increased M2 markers consistent with plaque regression, whereas plaques transplanted into Ccr2-/- or Cx3cr1-/- recipients lacked this regression signature. The requirement of recipient Ly6Chi ...
Atherosclerosis is a chronic inflammatory disease, and developing therapies to promote its regression is an important clinical goal. We previously established that atherosclerosis regression is characterized by an overall decrease in plaque macrophages and enrichment in markers of alternatively activated M2 macrophages. We have now investigated the origin and functional requirement for M2 macrophages in regression in normolipidemic mice that received transplants of atherosclerotic aortic segments. We compared plaque regression in WT normolipidemic recipients and those deficient in chemokine receptors necessary to recruit inflammatory Ly6Chi (Ccr2-/- or Cx3cr1-/-) or patrolling Ly6Clo (Ccr5-/-) monocytes. Atherosclerotic plaques transplanted into WT or Ccr5-/- recipients showed reduced macrophage content and increased M2 markers consistent with plaque regression, whereas plaques transplanted into Ccr2-/- or Cx3cr1-/- recipients lacked this regression signature. The requirement of recipient Ly6Chi ...
Q: Dr. Pasterkamp, this year began with the publication of a very exciting study of yours in Arteriosclerosis Thrombosis and Vascular Biology. It points out the natural history of carotid artery plaques after an acute cerebral ischemia event providing support for current concepts as well as new aspects. What would point out as the key findings of the study?. A: For our research group there are several key findings. First, it confirms the outcome of previous studies and concepts that plaque remodeling can go in two directions. The mechanism of plaque destabilization has always been the main research domain for many cardiovascular investigators. But this study strengthens the idea that unstable plaques also stabilize after an event, which, in fact, is a normal response after an injury (like a rupture of cap). Secondly, it shows that cytokine expression in plaques can rapidly change over time independent of the amount of inflammatory cells. Many researchers use a limited number of human ...
Atherosclerotic plaques vulnerable for rupture are characterised by e.g., a large lipid pole, a high concentration of inflammatory cells and a thin fibrous cap. Recent research has showed that vulnerable plaques are structurally weaker and therefore more likely to rupture in response to physical forces; possible due to high local concentrations of macrophages and reactive oxygen species (ROS). It is well known that redox active iron catalyses production of ROS and that the presence of Fe(III) is linked to ROS production. The aim of this study was to investigate the distribution of Fe(III) in carotid plaques.. ...
Heart attack is when the blood flow to the heart is restricted causing the heart cells to die. The lack of blood flow is caused by a partial blockage to the a coronary artery causing the rupture of a vulnerable atherosclerotic plaque, an unstable collection of lipids and white blood cells in the wall of an artery. Cardiac Arrest is a heart condition where the heart does not
OBJECTIVE: The association of inflammatory cells and neovessels in atherosclerosis is considered a histological hallmark of high-risk active lesions. Therefore, the development and validation of noninvasive imaging techniques that allow for the detection of inflammation and neoangiogenesis in atherosclerosis would be of major clinical interest. Our aim was to test 2 techniques, black blood dynamic contrast enhanced MRI (DCE-MRI) and 18-fluorine-fluorodeoxyglucose (18F-FDG) PET, to quantify inflammation expressed as plaque neovessels content in a rabbit model of atherosclerosis. METHODS AND RESULTS: Atherosclerotic plaques were induced in the aorta of 10 rabbits by a combination of 2 endothelial abrasions and 4 months hyperlipidemic diet. Six rabbits underwent MRI during the injection of Gd-DTPA, whereas 4 rabbits were imaged after injection of 18F-FDG with PET. We found a positive correlation between neovessels count in atherosclerotic plaques and (1) Gd-DTPA uptake parameters evaluated by DCE-MRI (r=0
The atherosclerotic process in diabetic patients seems to be different compared to non-diabetics. Larger plaques, with higher necrotic core content, were confirmed in DM patients during postmortem studies [27]. These findings were confirmed in vivo by studies using IVUS in plaques from both stable and acute patients [28-30]. Studies assessing plaque phenotypes describe more-developed lesions in DM patients [31, 32]. We found accelerated progression in DM patients of both plaque burden and plaque risk profiles in our study. These findings are supported by the study published by Bayturan et al. [10] with data from 7 clinical trials involving 3437 patients, where the presence of diabetes was found as one of the predictors of plaque progression despite the achievement of very low levels of LDLc. The impact of the presence of diabetes on clinical events was tested in a study done by Kennedy et al. Lesions not causing ischemia (with fraction flow reserve , 0.8) led to clinical events in DM patients in ...
It has been supposed that the response to TGF-β1 within vascular lesions is an important aspect of atherosclerosis progression toward clinical expression in humans. In fact, atherosclerosis is considered a chronic inflammatory disease, and the balance between degradation and deposition of the extracellular matrix is thought to be important for the maintenance of plaque stability in humans.1 TGF-β is a growth factor that exerts many regulatory actions. These functions are best reflected in several antiinflammatory effects on vascular cells4 and in a strongly positive effect on extracellular matrix production.11. In the present study, we found that TGF-β mRNA levels are increased up to 3-fold in asymptomatic as compared with symptomatic plaques; TGF-β gene was transcriptionally active as demonstrated by the parallel increase in TGF-β1 protein expression at immunocytochemistry and Western blot analyses. Notably, enhanced TGF-β1 staining at immunohistochemistry and expression at Western blot ...
Create a coastal feel with our Ocean Front Wooden Shell Plaque! This sea-inspired plaque features a carved shell with a white-wash finish to complete the look!
In a new study performed in humans, researchers from Swedens Karolinska Institutet have determined the age of atherosclerotic plaques by taking advantage of
The mission of the Cardiovascular Diagnosis and Therapy is the rapid exchange of scientific information between clinicians and scientists worldwide. To reach this goal, the journal will focus on novel media.
Arterial plaques are evaluated by determining their deformation under the periodic pulsatile force of blood flow. A relationship between plaque deformation and rupture risk is established by measureme
Necrotic core formation in advanced atherosclerotic lesion, which is a collection of dead and necrotic macrophages surrounded by inflammatory cells, contributes...
JSC Isotope is an enterprise of Rosatom State Corporation working in the markets of isotope products, radiation devices, medical and general purpose equipment.
Plaque is a substance made up of fat, cholesterol and calcium that builds up in the coronary arteries that supply the heart with oxygen-rich blood,...
The primary objective is to compare the carotid plaque stability after placebo versus Omega-3 fatty acid treatment by assessing structural changes associated with plaque rupture and instability. The composite endpoint includes changes ...
Clearing plaque from the arteries is very difficult to accomplish, but it is possible to slow the rate of plaque build-up or possibly bring it to a halt, according to WebMD. This can be achieved by...
how do you test for plaque in the arteries? Ive seen a cardiologist for a mild mvp with regurg that is now worse and Im concerned about plaque since I have cholesterol of 262 and triglycrides of 233....
The phage produces two different plaque morphologies. The smaller plaques are about 1 mm in size and the larger plaques are 2-3x larger than the ...
When incubated at 37 degrees Celsius, plaques are slightly turbid and approximately 2.5 millimeters in diameter. The plaques can be seen after 24 hours incubation and do not change after 48 hours. When incubated at 30 degrees Celsius the plaque morphology does not change other then becoming slightly more turbid ...
Plaque is abnormal area within a blood vessel where large quantities of lipids accumulate forming a fatty mass of tissue that projects into the lumen ...
Im am really stuck what to write on kaydens plaque, we had something written down as thats how we felt but it was 2many words.. i didnt know if any1 had any ideas...
TY - JOUR. T1 - Ex Vivo Assessment of Various Histological Differentiation in Human Carotid Plaque with Near-infrared Spectroscopy Using Multiple Wavelengths. AU - Munemitsu, Toshihiro. AU - Ishii, Akira. AU - Okada, Eiji. AU - Chihara, Hideo. AU - Yoshida, Kazumichi. AU - Takahashi, Jun C.. AU - Takagi, Yasushi. AU - Miyamoto, Susumu. PY - 2019/5/15. Y1 - 2019/5/15. N2 - We previously reported that near-infrared hyperspectral imaging enabled the localization of atherosclerotic plaques from outside the vessels, but not the optical characteristics of each histological component. Therefore, the near-infrared spectrum of each component was collected from the sliced section of the human carotid plaque obtained with endarterectomy and the optical characteristics were confirmed in several wavelengths. Based on this information, we assessed the diagnostic accuracy for ex vivo chemogram in each plaque component created with near-infrared spectroscopy (NIRS), using multiple wavelengths. The chemogram ...
Figure 1. Multimodal approach to atherosclerosis imaging. A representative illustration of current and emerging atherosclerosis imaging modalities. Each modality offers unique measurements of disease severity. Together, this information can be used to determine anatomic and hemodynamic consequences of atherosclerosis, complimented by detail on plaque composition, overall disease burden, and current metabolic activity acting within an individual patient. A, X-ray angiography showing multiple right coronary artery atherosclerotic lesions (arrows) resulting in significant luminal narrowing; B, virtual histology intravascular ultrasound (VH-IVUS) demonstrating coronary plaque with high content of necrotic core (red), as well as dense calcium (white) and fibro-fatty regions (dark/light green); C, Computed tomographic (CT) angiography showing noncalcified plaque in the left anterior descending artery with positive remodeling (dashed line); D, single-photon emission computed tomography (SPECT) ...
Virtual histology intravascular ultrasound (VH-IVUS) is a clinically available technique for atherosclerosis plaque characterization. It, however, suffers from a poor longitudinal resolution due to electrocardiogram (ECG)-gated acquisition. This article presents an effective algorithm for IVUS image-based histology to overcome this limitation. After plaque area extraction within an input IVUS image, a textural analysis procedure consisting of feature extraction and classification steps is proposed. The pixels of the extracted plaque area excluding the shadow region were classified into one of the three plaque components of fibro-fatty (FF), calcification (CA) or necrotic core (NC) tissues. The average classification accuracy for pixel and region based validations is 75% and 87% respectively. Sensitivities (specificities) were 79% (85%) for CA, 81% (90%) for FF and 52% (82%) for NC. The kappa (k)50.61 and p value50.02 indicate good agreement of the proposed method withVHimages. Finally, the ...
To investigate the role of infrasound aortic pressure waves (IPW) in atherosclerotic plaque rupture. Atherosclerotic plaques have been simulated partly, in two dimensions, as being short or long Conical Intersections (CIS), that is to say ellip
Two potentially important findings were observed in the present study. Firstly, plasma concentrations of IL-18 are increased in patients with acute coronary syndromes with or without myocardial necrosis. Secondly, plasma concentrations of IL-18 correlate with the severity of myocardial dysfunction.. Although these findings are preliminary and need confirmation in a large multicentre study, we believe that they should be considered seriously for several reasons. IL-18 has the potential to promote both atherosclerotic plaque instability4 and systemic inflammatory responses through activation of monocytes/macrophages, lymphocytes, and endothelial cells. Indeed, we have recently showed that in vivo inhibition of IL-18 signalling greatly decreases plaque development and induces a switch to a stable plaque phenotype.7 In the human myocardium, IL-18 is upregulated following ischaemia and contributes to postischaemic myocardial dysfunction in vitro.5 IL-18 may aggravate the proinflammatory response ...
Background: Atherosclerosis is an important cause of stroke. Ultrasound offers the convenience of real-time and detailed assessment of carotid plaque features as well as arterial wall thickening and composition. Evaluation of these features is important for determining patients risk of suffering vascular events and also contributes to selecting the best treatment strategy.. Methods: Using ultrasound data analysis we have determined plaque features in the bifurcation and internal carotid artery (ICA), including: surface plaque irregularities, calcification, echogenicity (grey scale median-GSM) and other textural plaque features (Juxtaluminal black area, entropy, coarseness). In addition, intima media thickens (IMT) and its grey scale median (IM-GSM) was measured in common carotid artery (CCA). Using Cone Beam CT (CBCT) we have quantified calcification volume of the carotid plaques extracted after carotid endarterectomy procedure. For the meta-analysis we have used comprehensive meta-analysis ...