Plaque Structure Research Articles

Incresed inflammatory response in patients with the first myocardial infarction and nonsignificant stenosis of infarct-related artery

Atherosclerosis presents a serial of highly specific cellular and molecular responses, and could be described as inflammatory diseases. Accordingly, for development of acute myocardial infarction (AMI), structure and vulnerability of atherosclerotic plaque are more important than the extent of stenosis of infarct-related artery. Consequently, inflammation and atherosclerosis and its complications are in good correlation. C-reactive protein (CRP) as nonspecific inflammatory marker, has prognostic significance in coronary artery diseases. The aim of this study was to establish the correlation between inflammatory response expressed as levels of CRP and fibrinogen in serum and extent of coronary artery stenosis. Study included 35 patients with acute myocardial infarction, as the first manifestation of coronary artery disease, which were treated with thrombolytic therapy according to the guidelines. All the patient had a reperfusion. The patients with acute or chronic inflammatory diseases, an increased value of sedimentation, fibrinogen, CK > or = 190 U/L, early and late complications of AMI were excluded. CRP was measured on admission, after 24, 48 and 72 hrs, and 21 days latter, while fibriogen only on admission. All the patients underwent coronary angiography, and were divided into two groups: the group 1 (23 patients), with significant stenosis of infarct-related artery (stenosis > or = 75%), and the group 2 (13 patients) without significant stenosis (< 75%). Mean value of CRP serum level on admission in the group 1 was 4.4 mg/L, and in the group 2 7.2 mg/L (p < 0.001). The mean value of fibrinogen on admission in the group 1 was 2.7 g/L, and in the group 2 3.0 g/L (p < 0.001). The mean CRP value after 48 hrs in the group 1 was 21.7 mg/L, and in the group 2 42.4 mg/L. (p < 0.001). After three weeks, the mean CRP value was 4 mg/L in the group 1 and 5.5 mg/L in the group 2 (p < 0.001). There was no significant difference between the groups 1 and 2 related to gender, age, localization of AMI, CK, EF value, and risk factors for coronary artery disease. The patients with nonsignificant stenosis of infarct-related artery had increased inflammtory responses according to the CRP value, as a result of inflammatory process in atherosclerotic plaque and/or enhanced individual reactivity.

Loss of plakophilin 2 disrupts heart development in zebrafish

The desmosomal armadillo protein plakophilin 2 is the only plakophilin expressed in the heart, and mutations in the human plakophilin 2 gene result in arrhythmogenic right ventricular cardiomyopathy. To investigate loss of function, we knocked down plakophilin 2 by morpholino microinjection in zebrafish. This resulted in decreased heart rate, cardiac oedema, blood pooling, a failure of the heart to pattern correctly and a twisted tail. Co-injection of plakophilin 2 mRNA rescued the morphant phenotype, indicating the specificity of the knockdown. Desmosome numbers were decreased in morphant hearts and the plaque and midline structures of the desmosomes in the intercalated discs were disrupted when examined by electron microscopy. cmlc2 and vmhc expression at 48 hours post-fertilization (hpf) showed incomplete looping of the heart in morphant embryos by whole mount in situ hybridization, and bmp4 expression was expanded into the ventricle. The domain of expression of the heart marker nkx2.5 at 24 hpf was expanded. At the 18 somite stage, expression of the cardiogenic gene lefty2 was abolished in the left cardiac field, with concomitant increases in bmp4, spaw and lefty1 expression, likely resulting in the looping defects. These results indicate that plakophilin 2 has both structural and signalling roles in zebrafish heart development.

Comparative investigation of mechanical characteristics of stable and unstable carotid atherosclerotic plaques

The prognosis of patients with carotid atherosclerosis is determined by the factor of unstable atherosclerotic plaque. Change of longitudinal strain in junction place of healthy artery wall to plaque determined by local artery elasticity and leads to instability. Aim of the study: Comparative investigation of mechanical characteristics of the stable and unstable plaques in a carotid artery. Methods: In the main group (MGr) were studied 16 plaques with stenosis 7090%, and control group (CGr) 33 plaques with stenosis 25-45%. Carotid ultrasound examinations (PHILIPS iU22) were performed for estimated structure and stenosis of plaques. The ”healthy” wall stiffness (free from plaques -bhw) and plaques zone stiffness (in adventitia -badv and in plaques surface -bpl) were estimated using echo-tracking method by ALOKAa7 in B/M mode ultrasound imaging. Results: In the MGr majority of plaques had structure with hypoechogenic area (>50%) and calcification, third plaques had rough or ulcerated surface. In CGr dominated heterogeneous plaques with smooth surface. In both groups bhw was significantly lower, than badv (MGr: 8,95 3,14 vs 22,73 10,43, CGr: 9,43 2,64 vs 14,45 6,7, p<0,001), badv was significantly higher than bpl (MGr: 22,73 10,43 vs 7,7 5,04; CGr: 14,45 6,7 vs 11,69 6,84, p<0,001). Relative changes of plaques zone stiffness (100bpl 100/badv) was significantly higher in the MGr (51,28 24,17% vs 26,93 21,45%, pZ0,036). Conclusions: Our results confirm presence the significant gradient of stiffness in junction place of healthy artery wall to plaque. In group with unstable plaques this gradient was significantly higher, that allows considering the possibility of the unstable plaques criteria developing by echotracking method.

The Arctic amyloid-β precursor protein (AβPP) mutation results in distinct plaques and accumulation of N- and C-truncated Aβ

The Arctic (p. E693G) mutation in the amyloid-β precursor protein (AβPP) facilitates amyloid-β (Aβ) protofibril formation and generates clinical symptoms of Alzheimer's disease (AD). Here, molecular details of Aβ in post mortem brain were investigated with biochemical and morphological techniques. The basic structure of Arctic plaques resembled cotton wool plaques. However, they appeared ring-formed with Aβ42-specific antibodies, but were actually targetoid, since the periphery and center of many parenchymal Aβ deposits stained differently with mid-domain, N- and C-terminal Aβ antibodies. Aβ fibrils were similar in shape, albeit shorter than in sporadic AD brain, when examined by electron microscopy. Aβwild-type and Aβarctic codeposited and parenchymal deposits were highly enriched in both N- and C-terminally truncated Aβ. In contrast, cerebral amyloid angiopathy (CAA) contained a substantial amount of Aβ1-40. The absence of plaques with cores of fibrillary Aβ might be due to the scarcity of full-length Aβ, although other mechanisms could be involved. Our findings are discussed in relation to mechanisms and relevance of amyloid formation and to the clinical features of AD.

Complement system activation and endothelial dysfunction in patients with age‐related macular degeneration (AMD): possible relationship between AMD and atherosclerosis

Age-related macular degeneration (AMD) shares several pathological and epidemiological similarities with systemic atherosclerosis (AS). First, an association between AS and AMD is apparent from the analyses of the histological and biochemical structure of atherosclerotic plaques in the vascular walls and retinal drusen, the hallmark of AMD. Second, there is considerable evidence implicating endothelial dysfunction in the pathogenesis of both disorders, and cellular oxidative stress appears to be a common denominator underlying this process. Moreover, there are observations that the complement system (CS) triggering inflammatory response contributes to the onset and advancement of both diseases. The CS plays a role in the generation of drusen and neovascularization in AMD as well as in vascular endothelium activation, cell damage and ultimately atherosclerotic plaque formation in the course of systemic arteriosclerosis. It is widely recognized that both AMD and AS are not only related to local stimulation of the CS, but also result in its systemic activation. In addition, a specific Y402H polymorphism of the complement inhibitor factor H has been found to be associated with the incidence of both AMD and AS. Here, we propose a linking hypothesis between CS activation, endothelial dysfunction and the pathogenesis of two common and age-related pathological processes, AS and AMD. We also discuss the potential therapeutic value of pharmacological modulation of CS activation in these disorders.

209 Circulating cd28- lymphocytes are associated with cerebrovascular symptomatology, sex, and carotid plaque texture

209 Circulating cd28- lymphocytes are associated with cerebrovascular symptomatology, sex, and carotid plaque texture

&lt;em&gt;In vivo&lt;/em&gt; Near Infrared Fluorescence (NIRF) Intravascular Molecular Imaging of Inflammatory Plaque, a Multimodal Approach to Imaging of Atherosclerosis

The vascular response to injury is a well-orchestrated inflammatory response triggered by the accumulation of macrophages within the vessel wall leading to an accumulation of lipid-laden intra-luminal plaque, smooth muscle cell proliferation and progressive narrowing of the vessel lumen. The formation of such vulnerable plaques prone to rupture underlies the majority of cases of acute myocardial infarction. The complex molecular and cellular inflammatory cascade is orchestrated by the recruitment of T lymphocytes and macrophages and their paracrine effects on endothelial and smooth muscle cells.(1) Molecular imaging in atherosclerosis has evolved into an important clinical and research tool that allows in vivo visualization of inflammation and other biological processes. Several recent examples demonstrate the ability to detect high-risk plaques in patients, and assess the effects of pharmacotherapeutics in atherosclerosis.(4) While a number of molecular imaging approaches (in particular MRI and PET) can image biological aspects of large vessels such as the carotid arteries, scant options exist for imaging of coronary arteries.(2) The advent of high-resolution optical imaging strategies, in particular near-infrared fluorescence (NIRF), coupled with activatable fluorescent probes, have enhanced sensitivity and led to the development of new intravascular strategies to improve biological imaging of human coronary atherosclerosis. Near infrared fluorescence (NIRF) molecular imaging utilizes excitation light with a defined band width (650-900 nm) as a source of photons that, when delivered to an optical contrast agent or fluorescent probe, emits fluorescence in the NIR window that can be detected using an appropriate emission filter and a high sensitivity charge-coupled camera. As opposed to visible light, NIR light penetrates deeply into tissue, is markedly less attenuated by endogenous photon absorbers such as hemoglobin, lipid and water, and enables high target-to-background ratios due to reduced autofluorescence in the NIR window. Imaging within the NIR 'window' can substantially improve the potential for in vivo imaging.(2,5) Inflammatory cysteine proteases have been well studied using activatable NIRF probes(10), and play important roles in atherogenesis. Via degradation of the extracellular matrix, cysteine proteases contribute importantly to the progression and complications of atherosclerosis(8). In particular, the cysteine protease, cathepsin B, is highly expressed and colocalizes with macrophages in experimental murine, rabbit, and human atheromata.(3,6,7) In addition, cathepsin B activity in plaques can be sensed in vivo utilizing a previously described 1-D intravascular near-infrared fluorescence technology(6), in conjunction with an injectable nanosensor agent that consists of a poly-lysine polymer backbone derivatized with multiple NIR fluorochromes (VM110/Prosense750, ex/em 750/780nm, VisEn Medical, Woburn, MA) that results in strong intramolecular quenching at baseline.(10) Following targeted enzymatic cleavage by cysteine proteases such as cathepsin B (known to colocalize with plaque macrophages), the fluorochromes separate, resulting in substantial amplification of the NIRF signal. Intravascular detection of NIR fluorescence signal by the utilized novel 2D intravascular NIRF catheter now enables high-resolution, geometrically accurate in vivo detection of cathepsin B activity in inflamed plaque. In vivo molecular imaging of atherosclerosis using catheter-based 2D NIRF imaging, as opposed to a prior 1-D spectroscopic approach,(6) is a novel and promising tool that utilizes augmented protease activity in macrophage-rich plaque to detect vascular inflammation.(11,12) The following research protocol describes the use of an intravascular 2-dimensional NIRF catheter to image and characterize plaque structure utilizing key aspects of plaque biology. It is a translatable platform that when integrated with existing clinical imaging technologies including angiography and intravascular ultrasound (IVUS), offers a unique and novel integrated multimodal molecular imaging technique that distinguishes inflammatory atheromata, and allows detection of intravascular NIRF signals in human-sized coronary arteries.

Multimodal characterization of compositional, structural and functional features of human atherosclerotic plaques

Detection of atherosclerotic plaque vulnerability has critical clinical implications for avoiding sudden death in patients with high risk of plaque rupture. We report on multimodality imaging of ex-vivo human carotid plaque samples using a system that integrates fluorescence lifetime imaging (FLIM), ultrasonic backscatter microscopy (UBM), and photoacoustic imaging (PAI). Biochemical composition is differentiated with a high temporal resolution and sensitivity at the surface of the plaque by the FLIM subsystem. 3D microanatomy of the whole plaque is reconstructed by the UBM. Functional imaging associated with optical absorption contrast is evaluated from the PAI component. Simultaneous recordings of the optical, ultrasonic, and photoacoustic data present a wealth of complementary information concerning the plaque composition, structure, and function that are related to plaque vulnerability. This approach is expected to improve our ability to study atherosclerotic plaques. The multimodal system presented here can be translated into a catheter based intraluminal system for future clinical studies.

The diagnostic value of intracoronary optical coherence tomography

Optical coherence tomography (OCT) is a novel light-based imaging modality for application in the coronary circulation. Compared to conventional intravascular ultrasound, OCT has a ten-fold higher image resolution. This advantage has seen OCT successfully applied in the assessment of atherosclerotic plaque, stent apposition, and tissue coverage, heralding a new era in intravascular coronary imaging. The present article discusses the diagnostic value of OCT, both in cardiovascular research as well as in potential clinical application.The unparalleled high image resolution and strong contrast between the coronary lumen and the vessel wall structure enable fast and reliable image interpretation. OCT makes it possible to visualize the presence of atherosclerotic plaque in order to characterize the structure and extent of coronary plaque and to quantify lumen dimensions, as well as the extent of lumen narrowing, in unprecedented detail. Based on optical properties, OCT is able to distinguish different tissue types, such as fibrous, lipid-rich, necrotic, or calcified tissue. Furthermore, OCT is able to cover the visualization of a variety of features of atherosclerotic plaques that have been associated with rapid lesion progression and clinical events, such as thin cap fibroatheroma, fibrous cap thickness, dense macrophage infiltration, and thrombus formation. These unique features allow the use of OCT to assess patients with acute coronary syndrome and to study the dynamic nature of coronary atherosclerosis in vivo and over time. This permits new insights into plaque progression, regression, and rupture, as well as the study of effects of therapies aimed at modulating these developments.Today's OCT technology allows high detail resolution as well as fast and safe clinical image acquisition. These unique features have established OCT as the gold standard for the assessment of coronary stents. This technique makes it possible to study stent expansion, peri-procedural vessel trauma, and the interaction of the stent with the vessel wall down to the level of individual stent struts, both acutely as well as in the long term, where it is has proven extremely sensitive to the detection of even minor amounts of tissue coverage. These qualities render OCT indispensable to addressing vexing clinical questions such as the relationship of drug-eluting stent deployment, vascular healing, the true time course of endothelial stent coverage, and late stent thrombosis. This may also better guide the optimal duration of dual anti-platelet therapy that currently remains unclear and relatively empirical.In the future, OCT might emerge, parallel to its undisputed position in research, as the tool of choice in all clinical scenarios where angiography is limited by its nature as a two-dimensional luminogram.

In vivo MRI-based 3D Mechanical Stress–Strain Profiles of Carotid Plaques with Juxtaluminal Plaque Haemorrhage: An Exploratory Study for the Mechanism of Subsequent Cerebrovascular Events

Objectives Atherosclerotic plaque features, such as fibrous cap erosion, ulceration and rupture and presence of haemorrhage in carotid plaque are two important characteristics associated with subsequent cerebrovascular events and juxtaluminal haemorrhage/thrombus (JLH/T) indicates these two high-risk characteristics. This study aims to investigate the association between JLH/T and subsequent events in patients suffering from transient ischaemic attack (TIA). Three-dimensional mechanical analysis was employed to represent the critical mechanical stress (P-CStress) and stretch (P-CStretch) within the plaque. Methods Fifty TIA patients with mild-to-moderate carotid stenosis (30–69%) underwent high-resolution magnetic resonance imaging (MRI) within 72 h of the acute event and eight were excluded from the analysis due to various reasons. A total of 21 patients were found to have JLH/T in the carotid plaque and 21 did not (N-JLH/T). During a 2-year follow-up period, 11 (52.4%) patients in the JLH/T group experienced recurrent events and none in the N-JLH/T group. Three-dimensional plaque structure was reconstructed based on the in vivo MRI for the mechanical analysis. Results P-CStress of both groups was comparable (N-JLH/T: 174.45 ± 63.96 kPa vs. JLH/T: 212.60 ± 89.54 kPa; p = 0.120), but P-CStretch of JLH/T was significantly bigger than that of N-JLH/T (N-JLH/T: 1.21 ± 0.08 vs. JLH/T: 2.10 ± 0.53; p < 0.0001). Moreover, there were much bigger variations in stress and stretch of the JLH/T group during one cardiac cycle than in those of N-JLH/T group. Conclusions In vivo MRI-depicted JLH/T might be a high risk factor initiating recurrent events, as big deformation appearing around the rupture site might prevent healing and tear the haemorrhage/thrombus away from the host structure and prompt further thrombo-embolic events.

Vascular imaging with positron emission tomography

Atherosclerosis is an inflammatory disease that causes most myocardial infarctions, strokes and acute coronary syndromes. Despite the identification of multiple risk factors and widespread use of drug therapies, it still remains a global health concern with associated costs. Although angiography is established as the gold standard means of detecting coronary artery stenosis, it does not image the vessel wall itself, reporting only on its consequences such as luminal narrowing and obstruction. MRI and computed tomography provide more information about the plaque structure, but recently positron emission tomography (PET) imaging using [(18) F]-fluorodeoxyglucose (FDG) has been advocated as a means of measuring arterial inflammation. This results from the ability of FDG-PET to highlight areas of high glucose metabolism, a feature of macrophages within atherosclerosis, particularly in high-risk plaques. It is suggested that the degree of FDG accumulation in the vessel wall reflects underlying inflammation levels and that tracking any changes in FDG uptake over time or with drug therapy might be a way of getting an early efficacy readout for novel anti-atherosclerotic drugs. Early reports also demonstrate that FDG uptake is correlated with the number of cardiovascular risk factors and possibly even the risk of future cardiovascular events. This review will outline the evidence base, shortcomings and emerging applications for FDG-PET in vascular imaging. Alternative PET tracers and other candidate imaging modalities for measuring vascular inflammation will also be discussed.

The three-dimensional molecular structure of the desmosomal plaque

The cytoplasmic surface of intercellular junctions is a complex network of molecular interactions that link the extracellular region of the desmosomal cadherins with the cytoskeletal intermediate filaments. Although 3D structures of the major plaque components are known, the overall architecture remains unknown. We used cryoelectron tomography of vitreous sections from human epidermis to record 3D images of desmosomes in vivo and in situ at molecular resolution. Our results show that the architecture of the cytoplasmic surface of the desmosome is a 2D interconnected quasiperiodic lattice, with a similar spatial organization to the extracellular side. Subtomogram averaging of the plaque region reveals two distinct layers of the desmosomal plaque: a low-density layer closer to the membrane and a high-density layer further away from the membrane. When combined with a heuristic, allowing simultaneous constrained fitting of the high-resolution structures of the major plaque proteins (desmoplakin, plakophilin, and plakoglobin), it reveals their mutual molecular interactions and explains their stoichiometry. The arrangement suggests that alternate plakoglobin-desmoplakin complexes create a template on which desmosomal cadherins cluster before they stabilize extracellularly by binding at their N-terminal tips. Plakophilins are added as a molecular reinforcement to fill the gap between the formed plaque complexes and the plasma membrane.

Mapping elasticity moduli of atherosclerotic plaque in situ via atomic force microscopy

Several studies have suggested that evolving mechanical stresses and strains drive atherosclerotic plaque development and vulnerability. Especially, stress distribution in the plaque fibrous capsule is an important determinant for the risk of vulnerable plaque rupture. Knowledge of the stiffness of atherosclerotic plaque components is therefore of critical importance. In this work, force mapping experiments using atomic force microscopy (AFM) were conducted in apolipoprotein E-deficient (ApoE(-/-)) mouse, which represents the most widely used experimental model for studying mechanisms underlying the development of atherosclerotic lesions. To obtain the elastic material properties of fibrous caps and lipidic cores of atherosclerotic plaques, serial cross-sections of aortic arch lesions were probed at different sites. Atherosclerotic plaque sub-structures were subdivided into cellular fibrotic, hypocellular fibrotic and lipidic rich areas according to histological staining. Hertz's contact mechanics were used to determine elasticity (Young's) moduli that were related to the underlying histological plaque structure. Cellular fibrotic regions exhibit a mean Young modulus of 10.4±5.7kPa. Hypocellular fibrous caps were almost six-times stiffer, with average modulus value of 59.4±47.4kPa, locally rising up to ∼250kPa. Lipid rich areas exhibit a rather large range of Young's moduli, with average value of 5.5±3.5kPa. Such precise quantification of plaque stiffness heterogeneity will allow investigators to have prospectively a better monitoring of atherosclerotic disease evolution, including arterial wall remodeling and plaque rupture, in response to mechanical constraints imposed by vascular shear stress and blood pressure.

Color doppler ultrasonography and multislice computer tomography angiography in carotid plaque detection and characterization

Cerebrovascular diseases are the third leading cause of mortality in the world, following malignant and cardiovascular diseases. Therefore, their timely and precise diagnostics is of great importance. The aim of this study was to compare duplex scan Color Doppler ultrasonography (CDU) with multislice computed tomography angiography (MSCTA) in detection of morphological and functional disorders at extracranial level of carotid arteries. The study included 75 patients with 150 carotid arteries examined in the period from January 2008 to April 2009. The patients were firstly examined by CDU, then MSCTA, followed by the surgery of extracranial segment of carotid arteries. In 10 patients, the obtained material was referred for histopathological (HP) examination. We used both CDU and MSCT in the analysis of: plaque surface, plaque structure, degree of stenosis, and the presence of in-traplaque hemorrhage. The results obtained by CDU and MSCTA were first compared between themselves, and then to intraoperative findings. Retrospective analysis showed that MSCTA is more sensitive than CDU in assessment of plaque surface (for smooth plaques CDU 89%: MSCTA 97%; for plaques with irregular surface CDU 75% : MSCTA 87%; for ulcerations CDU 54%: MSCTA 87%). Regarding determination of plaque structure (mixed plaque CDU 66% : MSCTA 70%; correlation with HP findings CDU 94% : MSCTA 96%) and localization (CDU 63%: MSCTA 65%), and in terms of sensitivity and specificity, both methods showed almost the same results. Also, there is no statistical difference between these two methods for the degree of stenosis (CDU 96%: MSCTA 98%). Atherosclerotic disease of extracranial part of carotid arteries primarily affects population of middle-aged and elderly, showing more associated risk factors. Sensitivity and specificity of CDU and MSCTA regarding plaque composition, the degree of stenosis and plaque localization are almost the same. These results and the fact that there are no adverse effects (high radiation dose) compared to MSCTA indicate that CDU should be the initial method in diagnostic algorythm for carotid arteries.

9F-10 動脈狭窄モデルにおける流れと変形のプラーク部構成による影響(OS-1(2) 循環器系のバイオメカニクスと医療機器設計(4))

9F-10 動脈狭窄モデルにおける流れと変形のプラーク部構成による影響(OS-1(2) 循環器系のバイオメカニクスと医療機器設計(4))

NARRATIVES OF INSCRIPTIONS ON MEMORIAL PLATES OF JEWS, RUSSIANS, LATVIANS AND LATGALIANS: MEMORY CULTURE DISCOURSE

NARRATIVES OF INSCRIPTIONS ON MEMORIAL PLATES OF JEWS, RUSSIANS, LATVIANS AND LATGALIANS: MEMORY CULTURE DISCOURSE

Comparative in vivo analysis of the atherosclerotic plaque targeting properties of eight human monoclonal antibodies

ObjectiveThe selective in vivo localization of antibody derivatives in atherosclerotic plaques may open novel diagnostic and therapeutic applications. Here, we present a comparative in vivo localization analysis of eight radioiodinated human monoclonal antibodies in apolipoprotein E-deficient (ApoE−/−) mice. MethodsAnimals were fed with a cholesterol-rich diet, followed by harvesting of the aorta 24h after intravenous antibody injection and investigated by autoradiographic analysis. Localization of F8 antibody on atherosclerotic plaque structures was further studied in three-color fluorescence microscopy. ResultsThe study revealed that the F8 antibody, specific to the alternatively spliced EDA domain of fibronectin, exhibited the highest plaque-targeting potential among the antibodies analyzed in this study, with an ability to preferentially localize to all plaques within the aorta. Targeting results were confirmed by injection of fluorescein-labeled F8 antibody, followed by three-color fluorescence microscopy analysis. ConclusionThese findings open novel biomolecular avenues for the in vivo imaging of atherosclerotic plaques and for pharmacodelivery applications, since F8 had previously been reported by our group to strongly stain atherosclerotic plaques in human carotid arteries.

Preliminary study on evaluation of neovascularization within carotid soft plaques with contrast-enhanced three dimensional ultrasonography

Objective To investigate the clinical value of contrast-enhanced three-dimensional ultrasound in assessing neovascularization within carotid soft plaques. Methods Thirty-six cases with 42 soft plaques were examined with contrast-enhanced two dimensional ultrasound and contrast-enhanced three dimensional ultrasound. Soft plaques were divided into four grades according to distribution and shape of contrast media:grade Ⅰ (there was no enhancement in plaque) , grade Ⅱ (plaque was enhanced with sparse spots pattern or enhanced in small range locally), grade Ⅲ (plaque was enhanced with sparse spots and short-line pattern ),grade Ⅳ (plaque was enhanced with line and grid pattern). Results The results of contrast-enhanced two-dimensional ultrasound were as followed: 4.8% grade Ⅰ , 35.7% grade Ⅱ , 52.4% grade Ⅲ and 7.1% grade Ⅳ. The results of contrast-enhanced three-dimensional ultrasound were as followed:9.5% grade Ⅱ , 47.6% grade Ⅲ and 42.9% grade Ⅳ. Conclusions Spatial distribution of neovascularization within carotid soft plaques could be reflected comprehensively by contrast-enhanced three dimensional ultrasound, and it might be a new mothod to investigate spatial structure and microvascular perfusion of soft plaques furtherly. Key words: Ultrasonography, three-dimensional; Microbubbles; Carotid stenosis; Plaques

Image Retrieval and Classification of Carotid Plaque Ultrasound Images

The extraction of multiple features from high-resolution ultrasound images of atherosclerotic carotid plaques, characterizing the plaque morphology and structure can be used for the classification and retrieval of similar plaques and the identification of individuals with asymptomatic carotid stenosis at risk of stroke. The objective of this work was to de- velop an automated image retrieval and classification system for the retrieval of similar carotid plaque ultrasound images, which will assist the physician in making his diagnostic decision based on similar previous cases. The neural self- organizing map (SOM) and the statistical K-nearest neighbor (KNN) classifiers were used for the retrieval and the classi- fication of the carotid plaques into symptomatic or asymptomatic. Twenty different feature sets including texture, shape, morphological, histogram and correlogram features were extracted from the carotid plaque images and the classification results were further combined in order to improve the success rate. The results on a dataset of 274 carotid plaque ultra- sound images show that image retrieval and classification for carotid plaque image are feasible and that features like multi-region histogram or texture can be used successfully for the identification of cases with similar symptoms output.

Biomechanical structural stresses of atherosclerotic plaques

Atherosclerotic plaques may rupture without warning, causing fatal clinical events such as myocardial infarction and stroke. Degree of stenosis, which is the current criterion for assessment of atherosclerotic disease severity, has been observed to have poor correlation with plaque vulnerability. Under physiological conditions, plaque undertakes mechanical loadings due to blood pressure and flow. From the material view point, rupture possibly occurs when the extra loading exceeds the material strength of the plaque. Therefore, morphological and mechanical features should be considered in an integrated way for a more accurate assessment of plaque vulnerability and for identification of the at-risk patient. Biomechanical stress analysis is a technique that allows such comprehensive assessment. This article focuses on the mechanical stresses in the plaque structure, which are believed to be of greater magnitude than the associated wall shear stress and are thought to be more closely associated with plaque rupture. We discuss the basic mechanics that govern plaque behavior, the material properties of atherosclerotic tissues and the studies investigating the association between high biomechanical stresses and plaque rupture. Parameter studies investigating the effect of morphologic factors on the critical biomechanical stresses and limitations of current simulation models are also reviewed.