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Vulnerable plaque

Ammara Usman, Umar Sadat, Zhongzhao Teng, Martin J Graves, Jonathan R Boyle, Kevin Varty, Paul D Hayes, Jonathan H Gillard
BACKGROUND: Functional magnetic resonance (MR) imaging of atheroma using contrast media enables assessment of the systemic severity of atherosclerosis in different arterial beds. Whether black-blood imaging has similar ability remains widely unexplored. In this study, we evaluate whether black-blood imaging can differentiate carotid plaques of patients with and without coronary artery disease (CAD) in terms of morphological and biomechanical features of plaque vulnerability, thereby allowing assessment of the systemic severity nature of atherosclerosis in different arterial beds...
October 17, 2016: Journal of Stroke and Cerebrovascular Diseases: the Official Journal of National Stroke Association
Gerard Pasterkamp, Hester M den Ruijter, Peter Libby
The concept of the 'vulnerable plaque' originated from pathological observations in patients who died from acute coronary syndrome. This recognition spawned a generation of research that led to greater understanding of how complicated atherosclerotic plaques form and precipitate thrombotic events. In current practice, an increasing number of patients who survive their first event present with non-ST-segment elevation myocardial infarction (NSTEMI) rather than myocardial infarction (MI) with ST-segment elevation (STEMI)...
October 20, 2016: Nature Reviews. Cardiology
Giovanni Cimmino, Francesco S Loffredo, Alberto Morello, Saverio D Elia, Raffaele De Palma, Plinio Cirillo, Paolo Golino
In the last twenty years, our comprehension of the molecular mechanisms involved in formation, progression and complication of atherosclerotic plaque has advanced significantly and the main role of inflammation and immunity in this phenomenon is now largely accepted. Accumulating evidence highlight the crucial role of different inflammatory and immune cells, such as monocytes and T-lymphocytes, in the pathophysiology of atherosclerotic lesion, particularly in contributing to its complications, such as rupture or ulceration...
October 13, 2016: Current Cardiology Reviews
Junichiro Hashimoto
Arterial structure and function change progressively with advancing age. Owing to long-lasting repetitive stretch with intermittent cardiac contraction, elastic fibers in the tunica media of large arteries gradually degenerate and are replaced by collagenous fibers. Such medial degeneration causes elastic arteries to stiffen and dilate. However, the speed of the vascular aging varies considerably among individuals; a discrepancy often exists between the chronological age of an individual and the biological age of his or her arteries...
September 2016: Journal of Hypertension
Girish Dwivedi, Yingwei Liu, Shrankhala Tewari, Joao Inacio, Matthieu Pelletier-Galarneau, Benjamin J W Chow
BACKGROUND: Coronary computed tomography (CT) angiography (CCTA) has the ability to detect, characterize, and quantify atherosclerotic plaques. The aim of our study was to evaluate the prognostic power of CCTA-quantified plaque subtypes. MATERIALS AND METHODS: A total of 36 patients with adverse events and 36 Morise score-matched patients who remained event free on follow-up were identified. Using CCTA images, plaque subtype volumes in the major epicardial arteries were analyzed using predetermined attenuation ranges in Hounsfield units (HU): 1 to 30 HU (low attenuating), 31 to 70 HU (intermediate attenuating), 71 to 150 HU (high attenuating), and mean coronary lumen+2 SD to 1000 HU (calcified)...
November 2016: Journal of Thoracic Imaging
D A Bangasser, H Dong, J Carroll, Z Plona, H Ding, L Rodriguez, C McKennan, J G Csernansky, S H Seeholzer, R J Valentino
Several neuropsychiatric and neurodegenerative disorders share stress as a risk factor and are more prevalent in women than in men. Corticotropin-releasing factor (CRF) orchestrates the stress response, and excessive CRF is thought to contribute to the pathophysiology of these diseases. We previously found that the CRF1 receptor (CRF1) is sex biased whereby coupling to its GTP-binding protein, Gs, is greater in females, whereas β-arrestin-2 coupling is greater in males. This study used a phosphoproteomic approach in CRF-overexpressing (CRF-OE) mice to test the proof of principle that when CRF is in excess, sex-biased CRF1 coupling translates into divergent cell signaling that is expressed as different brain phosphoprotein profiles...
October 18, 2016: Molecular Psychiatry
Taizen Nakase, Tatsuya Ishikawa, Hajime Miyata
Fragility of atheromatous plaque in the internal carotid artery can be a risk of brain infarction. The activation of macrophages by oxidative stress and the vulnerability of vascular endothelial cells have been reported to participate in the fragility of atheromatous plaque. Therefore, from the view point of prevention of brain infarction, we investigated the pathological factors which may influence the stabilization of atheromatous plaque. Patients undertaking carotid endoarterectomy (CEA) were continuously screened...
October 13, 2016: Neuropathology: Official Journal of the Japanese Society of Neuropathology
Edward B Thorp
No abstract text is available yet for this article.
October 14, 2016: Circulation Research
Mark W Kennedy, Enrico Fabris, Alexander J Ijsselmuiden, Holger Nef, Sebastian Reith, Javier Escaned, Fernando Alfonso, Niels van Royen, Wojtek Wojakowski, Adam Witkowski, Ciro Indolfi, Jan Paul Ottervanger, Harry Suryapranata, Elvin Kedhi
BACKGROUND: Fractional flow reserve (FFR) is a widely used tool for the identification of ischaemia-generating stenoses and to guide decisions on coronary revascularisation. However, the safety of FFR-based decisions in high-risk subsets, such as patients with Diabetes Mellitus (DM) or vulnerable stenoses presenting thin-cap fibro-atheroma (TCFA), is unknown. This study will examine the impact of optical coherence tomography (OCT) plaque morphological assessment and the identification of TCFA, in combination with FFR to better predict clinical outcomes in DM patients...
October 10, 2016: Cardiovascular Diabetology
Tian-Hui An, Quan-Wei He, Yuan-Peng Xia, Sheng-Cai Chen, Suraj Baral, Ling Mao, Hui-Juan Jin, Ya-Nan Li, Meng-Die Wang, Jian-Guo Chen, Ling-Qiang Zhu, Bo Hu
Atherosclerotic plaque vulnerability is the major cause for acute stroke and could be regulated by macrophage polarization. MicroRNA-181b (miR-181b) was involved in macrophage differential. Here, we explore whether miR-181b could regulate atherosclerotic plaque vulnerability by modulating macrophage polarization and the underline mechanisms. In acute stroke patients with atherosclerotic plaque, we found that the serum level of miR-181b was decreased. Eight-week apolipoprotein E knockout (ApoE(-/-)) mice were randomly divided into three groups (N = 10): mice fed with normal saline (Ctrl), mice fed with high-fat diet, and tail vein injection with miRNA agomir negative control (AG-NC)/miR-181b agomir (181b-AG, a synthetic miR-181b agonist)...
October 8, 2016: Molecular Neurobiology
Eduardo Pozo, Pilar Agudo-Quilez, Antonio Rojas-González, Teresa Alvarado, María José Olivera, Luis Jesús Jiménez-Borreguero, Fernando Alfonso
Myocardial infarction and sudden cardiac death are frequently the first manifestation of coronary artery disease. For this reason, screening of asymptomatic coronary atherosclerosis has become an attractive field of research in cardiovascular medicine. Necropsy studies have described histopathological changes associated with the development of acute coronary events. In this regard, thin-cap fibroatheroma has been identified as the main vulnerable coronary plaque feature. Hence, many imaging techniques, such as coronary computed tomography, cardiac magnetic resonance or positron emission tomography, have tried to detect noninvasively these histomorphological characteristics with different approaches...
September 26, 2016: World Journal of Cardiology
Maria D Radu, Kyohei Yamaji, Hector M García-García, Serge Zaugg, Masanori Taniwaki, Konstantinos C Koskinas, Patrick W Serruys, Stephan Windecker, Jouke Dijkstra, Lorenz Räber
AIMS: The minimum fibrous cap thickness (FCT) is considered a major criterion of coronary plaque vulnerability according to autopsy studies. We aimed to assess the reproducibility in the measurement of the optical coherence tomography (OCT)-detected minimum FCT and the agreement in the classification of thin-cap fibroatheroma (TCFA), by a software-based semi-automatic method compared with the manual method. METHODS AND RESULTS: A total of 50 frames with fibroatheromas (FA) were randomly selected from the Integrated Biomarker Imaging Study-4 (IBIS-4)...
October 10, 2016: EuroIntervention
Carol C Mitchell, James H Stein, Thomas D Cook, Shahriar Salamat, Xiao Wang, Tomy Varghese, Daren C Jackson, Carolina Sandoval Garcia, Stephanie M Wilbrand, Robert J Dempsey
Inflammation and angiogenesis play major roles in carotid plaque vulnerability. The purpose of this study was to determine whether gray-scale features of carotid plaques are associated with histologic markers for inflammation. Thirty-eight individuals completed a dedicated research carotid ultrasound exam before carotid endarterectomy. Gray-scale analysis was performed on plaque images to measure plaque echogenicity (gray-scale median [GSM] pixel brightness), plaque area, presence of discrete white areas (DWAs) and the percent of black area near the lumen on any one component of the plaque...
October 5, 2016: Ultrasound in Medicine & Biology
J C van den Born, R Mencke, S Conroy, C J Zeebregts, H van Goor, J L Hillebrands
Atherosclerotic plaques are classically divided into stable and vulnerable plaques. Vulnerable plaques are prone to rupture with a risk for infarction. High intraplaque microvessel density predisposes to plaque vulnerability. Hydrogen sulfide (H2S) is a proangiogenic gasotransmitter which is endogenously produced by cystathionine γ-lyase (CSE), and is believed to have vasculoprotective effects. However, due to its proangiogenic effects, H2S may result in pathological angiogenesis in atherosclerotic plaques, thereby increasing plaque vulnerability...
October 6, 2016: Scientific Reports
Karine Bertoldi, Laura Reck Cechinel, Bruna Schallenberger, Louisiana Meireles, Carla Basso, Gisele Agustini Lovatel, Lisiane Bernardi, Marcelo Lazzaron Lamers, Ionara Rodrigues Siqueira
A growing body of evidence has demonstrated amyloid plaques in aged brain; however, little attention has been given to amyloid precursor protein (APP) processing machinery during the healthy aging process. The amyloidogenic and non-amyloidogenic pathways, represented respectively by β- and α-secretases (BACE and TACE), are responsible for APP cleavage. Our working hypothesis is that the normal aging process could imbalance amyloidogenic and non-amyloidogenic pathways specifically BACE and TACE activities...
October 1, 2016: Behavioural Brain Research
Vjekoslav Tomulić, David Gobić, Davorka Lulić, David Židan, Luka Zaputović
Adhesion molecules play an important role in inflammation, atherosclerosis and coronary artery disease (CAD). These molecules are expressed on the surface of dysfunctional endothelial cells, causing inflammatory cells from the circulation to adhere and migrate through the endothelium. Their expression is upregulated in acute coronary syndrome (ACS) and after percutaneous coronary intervention (PCI). The contact between stent struts and endothelium upregulates endothelial cell gene expression, endothelial cell activation and inflammation...
October 2016: Medical Hypotheses
Hendrik H G Hansen, Gert Jan de Borst, Michiel L Bots, Frans L Moll, Gerard Pasterkamp, Chris L de Korte
BACKGROUND AND PURPOSE: Carotid plaque rupture is a major cause of stroke. Key issue for risk stratification is early identification of rupture-prone plaques. A noninvasive technique, compound ultrasound strain imaging, was developed providing high-resolution radial deformation/strain images of atherosclerotic plaques. This study aims at in vivo validation of compound ultrasound strain imaging in patients by relating the measured strains to typical features of vulnerable plaques derived from histology after carotid endarterectomy...
September 29, 2016: Stroke; a Journal of Cerebral Circulation
Luca Liberale, Franco Dallegri, Fabrizio Montecucco, Federico Carbone
Macrophages are highly heterogeneous and plastic cells. They were shown to play a critical role in all stages of atherogenesis, from the initiation to the necrotic core formation and plaque rupture. Lesional macrophages primarily derive from blood monocyte, but local macrophage proliferation as well as differentiation from smooth muscle cells have also been described. Within atherosclerotic plaques, macrophages rapidly respond to changes in the microenvironment, shifting between pro- (M1) or anti-inflammatory (M2) functional phenotypes...
September 29, 2016: Thrombosis and Haemostasis
Chunbao Liu, Xiao Zhang, Yiling Song, Yichun Wang, Fengzhen Zhang, Yingying Zhang, Yongxue Zhang, Xiaoli Lan
BACKGROUND AND AIMS: Early detection and evaluation of vulnerable atherosclerotic plaque are important for risk stratification and timely intervention, and vascular cell adhesion molecule 1 (VCAM1) assists in adhesion and recruitment of inflammatory cells to vulnerable lesions. We labeled a single-chain variable fragment (scFv) of VCAM1 with (99m)technetium ((99m)Tc) and fluorescent markers to investigate its potential utility in detecting vulnerable plaques in animal models of atherosclerosis...
September 13, 2016: Atherosclerosis
X Yang, C Yao, T Tian, X Li, H Yan, J Wu, H Li, L Pei, D Liu, Q Tian, L-Q Zhu, Y Lu
The entorhinal cortex (EC) is one of the most vulnerable brain regions that is attacked during the early stage of Alzheimer's disease (AD). Here, we report that the synaptic terminals of pyramidal neurons in the EC layer II (ECIIPN) directly innervate CA1 parvalbumin (PV) neurons (CA1PV) and are selectively degenerated in AD mice, which exhibit amyloid-β plaques similar to those observed in AD patients. A loss of ECIIPN-CA1PV synapses disables the excitatory and inhibitory balance in the CA1 circuit and impairs spatial learning and memory...
September 27, 2016: Molecular Psychiatry
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