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Journal of Internal Medicine Dec 2014Atherosclerosis is a silent chronic vascular pathology that is the cause of the majority of cardiovascular ischaemic events. The evolution of vascular disease involves a... (Review)
Review
Atherosclerosis is a silent chronic vascular pathology that is the cause of the majority of cardiovascular ischaemic events. The evolution of vascular disease involves a combination of endothelial dysfunction, extensive lipid deposition in the intima, exacerbated innate and adaptive immune responses, proliferation of vascular smooth muscle cells and remodelling of the extracellular matrix, resulting in the formation of an atherosclerotic plaque. High-risk plaques have a large acellular lipid-rich necrotic core with an overlying thin fibrous cap infiltrated by inflammatory cells and diffuse calcification. The formation of new fragile and leaky vessels that invade the expanding intima contributes to enlarge the necrotic core increasing the vulnerability of the plaque. In addition, biomechanical, haemodynamic and physical factors contribute to plaque destabilization. Upon erosion or rupture, these high-risk lipid-rich vulnerable plaques expose vascular structures or necrotic core components to the circulation, which causes the activation of tissue factor and the subsequent formation of a fibrin monolayer (coagulation cascade) and, concomitantly, the recruitment of circulating platelets and inflammatory cells. The interaction between exposed atherosclerotic plaque components, platelet receptors and coagulation factors eventually leads to platelet activation, aggregation and the subsequent formation of a superimposed thrombus (i.e. atherothrombosis) which may compromise the arterial lumen leading to the presentation of acute ischaemic syndromes. In this review, we will describe the progression of the atherosclerotic lesion along with the main morphological characteristics that predispose to plaque rupture, and discuss the multifaceted mechanisms that drive platelet activation and subsequent thrombus formation. Finally, we will consider the current scientific challenges and future research directions.
Topics: Atherosclerosis; Blood Coagulation; Endothelium, Vascular; Fibrinolysis; Humans; Necrosis; Plaque, Atherosclerotic; Rupture, Spontaneous; Thrombosis
PubMed: 25156650
DOI: 10.1111/joim.12296 -
The New England Journal of Medicine Aug 2020
Review
Topics: Acute Coronary Syndrome; Coronary Thrombosis; Humans; Inflammation; Plaque, Atherosclerotic; Rupture, Spontaneous; Tomography, Optical Coherence
PubMed: 32846063
DOI: 10.1056/NEJMra2000317 -
Redox Biology Aug 2017Atherosclerosis is a multifocal alteration of the vascular wall of medium and large arteries characterized by a local accumulation of cholesterol and non-resolving... (Review)
Review
Atherosclerosis is a multifocal alteration of the vascular wall of medium and large arteries characterized by a local accumulation of cholesterol and non-resolving inflammation. Atherothrombotic complications are the leading cause of disability and mortality in western countries. Neovascularization in atherosclerotic lesions plays a major role in plaque growth and instability. The angiogenic process is mediated by classical angiogenic factors and by additional factors specific to atherosclerotic angiogenesis. In addition to its role in plaque progression, neovascularization may take part in plaque destabilization and thromboembolic events. Anti-angiogenic agents are effective to reduce atherosclerosis progression in various animal models. However, clinical trials with anti-angiogenic drugs, mainly anti-VEGF/VEGFR, used in anti-cancer therapy show cardiovascular adverse effects, and require additional investigations.
Topics: Angiogenesis Inhibitors; Animals; Clinical Trials as Topic; Disease Progression; Humans; Neovascularization, Pathologic; Oxidative Stress; Plaque, Atherosclerotic
PubMed: 28212521
DOI: 10.1016/j.redox.2017.01.007 -
Journal of the American College of... Jun 2023
Topics: Humans; Plaque, Atherosclerotic; Atherosclerosis; Rupture, Spontaneous
PubMed: 37286251
DOI: 10.1016/j.jacc.2023.05.001 -
The New England Journal of Medicine Jan 2021
Topics: Atherosclerosis; Humans; Plaque, Atherosclerotic; Wound Healing
PubMed: 33471990
DOI: 10.1056/NEJMc2033613 -
Journal of the American Heart... Mar 2017
Review
Topics: Coronary Artery Disease; Coronary Vessels; Global Health; Humans; Morbidity; Plaque, Atherosclerotic
PubMed: 28314799
DOI: 10.1161/JAHA.117.005543 -
International Journal of Molecular... Mar 2021Atherosclerotic plaque is the pathophysiological basis of important and life-threatening diseases such as myocardial infarction. Although key aspects of the process of... (Review)
Review
Atherosclerotic plaque is the pathophysiological basis of important and life-threatening diseases such as myocardial infarction. Although key aspects of the process of atherosclerotic plaque development and progression such as local inflammation, LDL oxidation, macrophage activation, and necrotic core formation have already been discovered, many molecular mechanisms affecting this process are still to be revealed. This minireview aims to describe the current directions in research on atherogenesis and to summarize selected studies published in recent years-in particular, studies on novel cellular pathways, epigenetic regulations, the influence of hemodynamic parameters, as well as tissue and microorganism (microbiome) influence on atherosclerotic plaque development. Finally, some new and interesting ideas are proposed (immune cellular heterogeneity, non-coding RNAs, and immunometabolism) which will hopefully bring new discoveries in this area of investigation.
Topics: Animals; Atherosclerosis; Epigenesis, Genetic; Humans; Inflammation; Lipoproteins, LDL; Macrophage Activation; Plaque, Atherosclerotic
PubMed: 33805303
DOI: 10.3390/ijms22073513 -
Current Atherosclerosis Reports Oct 2020Inflammatory cytokines play a major role in atherosclerotic plaque progression. This review summarizes the rationale for personalized anti-inflammatory therapy. (Review)
Review
PURPOSE OF THE REVIEW
Inflammatory cytokines play a major role in atherosclerotic plaque progression. This review summarizes the rationale for personalized anti-inflammatory therapy.
RECENT FINDINGS
Systemic inflammatory parameters may be used to follow the clinical outcome in primary and secondary prevention. Medical therapy, both in patients with stable cardiovascular disease, or with acute events, may be tailored taking into consideration the level and course of systemic inflammatory mediators. There is significant space for improvement in primary prevention and in the treatment of patients who have suffered from severe cardiovascular events, paying attention to not only blood pressure and cholesterol levels but also including inflammatory parameters in our clinical analysis. The potential exists to alter the course of atherosclerosis with anti-inflammatory drugs. With increased understanding of the specific mechanisms that regulate the relationship between inflammation and atherosclerosis, new, more effective and specific anti-inflammatory treatment may become available.
Topics: Animals; Anti-Inflammatory Agents; Atherosclerosis; Cytokines; Disease Progression; Humans; Inflammation; Inflammation Mediators; Mice; Plaque, Atherosclerotic; Secondary Prevention; Treatment Outcome
PubMed: 33025148
DOI: 10.1007/s11883-020-00891-3 -
Current Atherosclerosis Reports Aug 2016Calcification of atherosclerotic lesions was long thought to be an age - related, passive process, but increasingly data has revealed that atherosclerotic calcification... (Review)
Review
Calcification of atherosclerotic lesions was long thought to be an age - related, passive process, but increasingly data has revealed that atherosclerotic calcification is a more active process, involving complex signaling pathways and bone-like genetic programs. Initially, imaging of atherosclerotic calcification was limited to gross assessment of calcium burden, which is associated with total atherosclerotic burden and risk of cardiovascular mortality and of all cause mortality. More recently, sophisticated molecular imaging studies of the various processes involved in calcification have begun to elucidate information about plaque calcium composition and consequent vulnerability to rupture, leading to hard cardiovascular events like myocardial infarction. As such, there has been renewed interest in imaging calcification to advance risk assessment accuracy in an evolving era of precision medicine. Here we summarize recent advances in our understanding of the biologic process of atherosclerotic calcification as well as some of the molecular imaging tools used to assess it.
Topics: Animals; Calcinosis; Humans; Molecular Imaging; Plaque, Atherosclerotic; Precision Medicine
PubMed: 27339750
DOI: 10.1007/s11883-016-0601-6 -
Journal of Ultrasound Sep 2022The aim of the proposed study was to conduct a feasibility study using a flat rectangular (2 × 10 mm) transducer operating at 4.0 MHz for creating thermal lesions...
PURPOSE
The aim of the proposed study was to conduct a feasibility study using a flat rectangular (2 × 10 mm) transducer operating at 4.0 MHz for creating thermal lesions in an arterial atherosclerotic plaque phantom. The proposed method can be used in the future for treating atherosclerotic plaques in human arteries.
MATERIALS AND METHODS
The flat rectangular transducer was firstly assessed in agar/silica evaporated milk phantom, polyacrylamide phantom and freshly excised turkeytissue phantom. Then, the same transducer was assessed in an arterial atherosclerotic plaque phantom which was created in the laboratory with a very low cost. The recipe of the atherosclerotic plaque phantom was 4% w/v agar, 1% w/v gypsum, 2% w/v butter and 93% water. The amount of plaque removal was evaluated visually and using an X-Ray system.
RESULTS
It was shown that the flat rectangular transducer can create thermal lesions on the agar/silica evaporated milk phantom, polyacrylamide phantom and in excised tissue. The size of the lesions matches the geometry of the transducer. Moreover, this transducer destroyed 27.1% of the atherosclerotic plaque phantom with 8 W acoustical power and 30 s duration.
CONCLUSIONS
This feasibility study demonstrated that atherosclerotic plaque can be destroyed using a very small flat rectangular (2 × 10 mm) transducer in a very small time interval of 30 s. In future clinical trials the transducer will be incorporated in a catheter which will be inserted intravascular (1-3 mm) wide and can be used to treat atherosclerotic plaques in the coronary arteries.
Topics: Agar; Coronary Vessels; Humans; Phantoms, Imaging; Plaque, Atherosclerotic; Silicon Dioxide
PubMed: 35098435
DOI: 10.1007/s40477-022-00658-3