scholarly journals Features of atherosclerosis in carotid and coronary arteries

2021 ◽  
pp. 44-53
Author(s):  
E. V. Konstantinova ◽  
A. A. Bogdanova ◽  
A. A. Sagatelyan ◽  
A. I. Kovaikin ◽  
E. S. Pershina ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Circulatory System ◽  
Coronary Vessels ◽  
Mortality And Morbidity ◽  
Plaque Instability ◽  
Effective Interventions ◽  
Inflammatory Processes ◽  
Unstable Plaques ◽  
Plaque Destabilization

Atherothrombosis is a leading cause of myocardial infarction and ischemic atherothrombotic stroke. It represents a stage of atherosclerosis which is a pathologic process throughout the circulatory system. However, atherosclerosis has specific development characteristics in  different vascular beds. Multiple factors contribute to atherosclerosis formation and progression such as genetic factors, vessel hemodynamics, and vessel anatomy. A better understanding of differences in vessels would improve prevention and treatment of atherosclerosis and its complication. In this article we review features of atherosclerosis in carotid and coronary vessels. We discuss specific conditions of local hemodynamics in the areas of bifurcation which promote atherosclerotic plaque progression, and review characteristics of unstable plaques in carotid and coronary vessels. We analyze immunologic and inflammatory processes, extracellular matrix degradation and remodeling, cellular apoptosis and autophagy occurring during atherosclerotic plaque destabilization as well as the possibility of diffuse plaque instability in systemic atherosclerosis. We review association and interaction of  atherosclerotic processes in  coronary and carotid arteries, and its significance for a patient. Improvement in understanding of atherosclerosis pathogenesis can lead to advances in atherosclerosis prevention. Timely and effective interventions would promote prevention of myocardial infarction and ischemic stroke which is highly important taking into account high mortality and morbidity rates.

scholarly journals Carotid atherosclerotic plaque instability in patients with acute myocardial infarction

2002 ◽  
Vol 39 ◽  
pp. 308 ◽  
Author(s):  
Andrea Rossi ◽  
Lorenzo Franceschini ◽  
Massimiliano Fusaro ◽  
Giorgio Golia ◽  
Piero Zardini
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Carotid Atherosclerotic Plaque ◽  
Plaque Instability

scholarly journals Mast cells are increased in the media of coronary lesions in patients with myocardial infarction and may favor atherosclerotic plaque instability

2017 ◽  
Vol 69 (3) ◽  
pp. 548-554 ◽  
Author(s):  
Koba Kupreishvili ◽  
Wessel W. Fuijkschot ◽  
Alexander B.A. Vonk ◽  
Yvo M. Smulders ◽  
Wim Stooker ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Mast Cells ◽  
Atherosclerotic Plaque ◽  
Plaque Instability ◽  
The Media ◽  
Coronary Lesions

P4610Gut microbiome and atherosclerotic plaque instability: does choline consumption in red meat influence plaque stability?

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y.-C Chen ◽  
V Doma ◽  
R Reimark ◽  
Y.-L Ying ◽  
K Peter
Keyword(s):  
Atherosclerotic Plaque ◽  
High Fat Diet ◽  
Red Meat ◽  
T Test ◽  
Plaque Burden ◽  
High Fat ◽  
Plaque Instability ◽  
Choline Group ◽  
Choline Intake ◽  
Unstable Plaques

Abstract Background Myocardial infarction is the major cause of deaths worldwide. Gut bacteria can process choline as abundant in red meat and subsequently converted by flavin containing monooxygenase in the liver to trimethylamin-N-oxide (TMAO) metabolite, which is strongly associated with cardiovascular events. Aim To investigate the gut microbiome and its association with atherosclerotic plaque instability. Methods Forty-eight Apolipoprotein E deficient mice were randomly divided into two groups and two time points, fed with a high fat diet (containing either 0.4% choline or 3% choline) at 12 weeks of age, for 7 weeks or for 14 weeks. All mice underwent Tandem Stenosis (TS) surgery to induce the development of unstable plaques. Stool samples were collected directly from the colon. Measurements of gut microbes were performed by AGRF diversity profiling. After bacterial genomic DNA isolation, 16S rRNA were sequenced by targeting 27F-519R (V1-V3) and 341F-806R (V3-V4) on the Illumina MiSeq platform. Vessel segments of TS were histologically processed and plaque composition of lipid, collagen, and intraplaque hemorrhage (marker of unstable plaques) were performed by a series of chemical staining and immunohistochemistry. Results Monocytes and granulocytes in mouse blood were significantly increased in the high choline group (p<0.05, unpaired t-test) after 7 weeks of high fat diet (21% fat, 0.15% Cholesterol, 3% Choline). Profiling of gut microbiota showed that Fimicutes were down regulated in the high choline group (p<0.05, unpaired t-test). Within Phylum Fimicutes, only Clostridia (class) Clostridiales (order) were significantly downregulated. Interestingly, histological analysis of TS segments showed that TER-119 (intraplaque haemorrhage marker) and CD42c (platelet marker) were significantly increased in the high choline group, indicating atherosclerotic plaques are more unstable and prone to rupture (p<0.05, unpaired t-test). Nevertheless, CD68 (Foam cells) in plaques, and total atherosclerotic plaque burden in the aortic sinus and aortic arch were not affected by the elevated levels of choline consumption. Conclusion Choline intake increases circulating monocytes and granulocyte numbers in the blood but not in the atherosclerotic plaque itself. Whereas the total plaque burden is not changed by an increased choline intake, the reduction of Fimicutes, Clostridia and Clostridiales seems to contribute to atherosclerotic plaque instability. Acknowledgement/Funding Heart Foundation 2018 Future Leader Fellowship (2018 FLF) ID: 102068 Chen

Atherosclerotic plaque instability in carotid arteries: miR-200c as a promising biomarker

2018 ◽  
Vol 132 (22) ◽  
pp. 2423-2436 ◽  
Author(s):  
Alessandra Magenta ◽  
Sara Sileno ◽  
Marco D’Agostino ◽  
Francesca Persiani ◽  
Sara Beji ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Atherosclerotic Plaque ◽  
Early Recognition ◽  
Monocyte Chemoattractant Protein 1 ◽  
Carotid Plaques ◽  
Plaque Instability ◽  
Atherosclerosis Progression ◽  
E Box ◽  
Unstable Plaques ◽  
Endothelial Nitric Oxide

Early recognition of vulnerable carotid plaques could help in identifying patients at high stroke risk, who may benefit from earlier revascularisation. Nowadays, different biomarkers of plaque instability have been unravelled, among these miRNAs are promising tools for the diagnosis and treatment of atherosclerosis. Inflammation, reactive oxygen species (ROS) and endothelial dysfunction play a key role in unstable plaques genesis. We showed that miR-200c induces endothelial dysfunction, ROS production and a positive mechanism among miR-200c and miR-33a/b, two miRNAs involved in atherosclerosis progression. The goal of the present study was to determine whether miR-200c could be an atherosclerosis biomarker. Carotid plaques of patients that underwent carotid endarterectomy (CEA) were assayed for miR-200c expression. miR-200c was up-regulated in carotid plaques (n=22) and its expression was higher in unstable (n=12) compared with stable (n=10) plaques. miR-200c positively correlated with instability biomarkers (i.e. monocyte chemoattractant protein-1, cicloxigenase-2 (COX2), interleukin 6 (IL6), metalloproteinase (MMP) 1 (MMP1), 9 (MMP9)) and miR-33a/b. Moreover, miR-200c negatively correlated with stability biomarkers (i.e. zinc finger E-box binding homoeobox 1 (ZEB1), endothelial nitric oxide (NO) synthase (eNOS), forkhead boxO1 (FOXO1) and Sirtuin1 (SIRT1)) (stable plaques = 15, unstable plaques = 15). Circulating miR-200c was up-regulated before CEA in 24 patients, correlated with miR-33a/b and decreased 1 day after CEA. Interestingly, 1 month after CEA, circulating miR-200c is low in patients with stable plaques (n=11) and increased to control levels, in patients with unstable plaques (n=13). Further studies are needed to establish whether miR-200c represents a circulating biomarker of plaque instability. Our results show that miR-200c is an atherosclerotic plaque progression biomarker and suggest that it may be clinically useful to identify patients at high embolic risk.

scholarly journals The Risk of Carotid Plaque Instability in Patients with Metabolic Syndrome: It is Higher in Women with Hypertriglyceridemia

2021 ◽  
Author(s):  
Francesca Servadei ◽  
Lucia Anemona ◽  
Marina Cardellini ◽  
Manuel Scimeca ◽  
Manuela Montanaro ◽  
...  
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Carotid Plaque ◽  
Cerebrovascular Diseases ◽  
Plaque Instability ◽  
Female Patients ◽  
Asymptomatic Patients ◽  
Increased Risk ◽  
Unstable Plaques ◽  
Plaque Destabilization

Abstract Background: Metabolic syndrome certainly favors growth of carotid plaque; however, it is uncertain if it determines plaque destabilization. Furthermore, it is likely that only some components of metabolic syndrome are associated with increased risk of plaque destabilization. Therefore, we evaluated the effect of different elements of metabolic syndrome, individually and in association, on carotid plaques destabilization. Methods: A total of 186 carotid endarterectomies from symptomatic and asymptomatic patients were histologically analysed and correlated with major cardiovascular risk factors. Results: Metabolic syndrome, regardless of the cluster of its components, is not associated with a significant increase in risk of plaque destabilization, rather with the presence of stable plaques. The incidence of unstable plaques in patients with metabolic syndrome is quite low (43.9%), when compared with that seen in the presence of some risk factors, but significantly increases in the subgroup of female patients with hypertriglyceridemia, showing an odds ratio of 3.01 (CI 95% 0.25 - 36.30). Conclusions: Our data may help to identify patients with real increased risk of acute cerebrovascular diseases and may support the hypothesis that the control of hypertriglyceridemia should be a key point on prevention of carotid atherosclerotic plaque destabilization, especially in post-menopausal female patients. Keywords: Metabolic syndrome, carotid, histology, hypertriglyceridemia , post-menopause.

Carotid atherosclerotic plaque instability in patients with acute myocardial infarction

2006 ◽  
Vol 111 (2) ◽  
pp. 263-266 ◽  
Author(s):  
Andrea Rossi ◽  
Lorenzo Franceschini ◽  
Massimilano Fusaro ◽  
Mariantonietta Cicoira ◽  
Alejandra Amado Eleas ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Carotid Atherosclerotic Plaque ◽  
Plaque Instability

Comprehensive analysis of dysregulated genes associated with atherosclerotic plaque destabilization

2021 ◽  
pp. 153537022110332
Author(s):  
Cheng Qian ◽  
Yuling Jing ◽  
Meng Xia ◽  
Qiang Ye
Keyword(s):  
Myocardial Infarction ◽  
Differentially Expressed Genes ◽  
Atherosclerotic Plaque ◽  
Cardiovascular Events ◽  
Expression Patterns ◽  
Rank Aggregation ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
Atherosclerotic Cardiovascular Disease ◽  
Plaque Destabilization

Atherosclerotic plaque destabilization is a dominating cause of acute cardiovascular events such as myocardial infarction and stroke. This study aims to identify genetic biomarkers related to atherosclerotic plaque destabilization using bioinformatics. Three transcriptome datasets of human carotid atherosclerotic plaque samples were downloaded from ArrayExpress and Gene Expression Omnibus databases, including E-MATB-2055, E-TABM-190, and GSE120521. With Robust Rank Aggregation analysis, we documented 46 differentially expressed genes between stable and unstable/ruptured plaques. Functional enrichment analysis using DAVID tool demonstrated that these genes were mainly related to biological functions such as extracellular matrix disassembly, collagen catabolic process, response to mechanical stimulus, and PPAR signaling pathway. A protein–protein interaction network for the differentially expressed genes was constructed, and eight pivotal genes ( ITGAM, MMP9, PLAUR, CCR1, CD163, CD36, ADAM8, and IL1RN) were obtained from the network with a connective degree > 5. The expression patterns of these hub differentially expressed genes could be verified in atherosclerotic plaque samples with intraplaque hemorrhage. Using gene set variation analysis, the eight genes were integrated to generate an atherosclerotic plaque destabilization score, which showed a high performance in not only discriminating individuals with myocardial infarction from those with stable coronary illness, but also in predicting future acute cardiovascular events in atherosclerotic patients. In conclusion, the findings of this study will enhance our knowledge on the pathological mechanisms involved in atherosclerotic plaque destabilization, and provide potential gene biomarkers for risk stratification of patients with atherosclerotic cardiovascular disease.

An electron microscopic study of the intra-myocardial lesions in cases of acute myocardial infarction

1978 ◽  
Vol 36 (2) ◽  
pp. 484-485
Author(s):  
Masahiro Ono ◽  
Kaoru Aihara ◽  
Gompachi Yajima
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Vessels ◽  
Vascular Wall ◽  
Vascular Changes ◽  
Electron Microscopic ◽  
Main Trunk ◽  
Mechanical Destruction ◽  
Transmission Electron ◽  
Myocardial Lesions

The pathogenesis of the arteriosclerosis in the acute myocardial infarction is the matter of the extensive survey with the transmission electron microscopy in experimental and clinical materials. In the previous communication,the authors have clarified that the two types of the coronary vascular changes could exist. The first category is the case in which we had failed to observe no occlusive changes of the coronary vessels which eventually form the myocardial infarction. The next category is the case in which occlusive -thrombotic changes are observed in which the myocardial infarction will be taken placed as the final event. The authors incline to designate the former category as the non-occlusive-non thrombotic lesions. The most important findings in both cases are the “mechanical destruction of the vascular wall and imbibition of the serous component” which are most frequently observed at the proximal portion of the coronary main trunk.

Optical coherent tomography for the diagnostic of non-obstructive coronary artery myocardial infarction

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
I Leonova ◽  
S Boldueva ◽  
V Feoktistova ◽  
D Evdokimov
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Coronary Artery ◽  
Coronary Angiography ◽  
Atherosclerotic Plaque ◽  
St Elevation ◽  
Spontaneous Dissection

Abstract Funding Acknowledgements Type of funding sources: None. The widespread use of coronary angiography (CAG) in patients with acute coronary syndrome led to the understanding that in some patients myocardial infarction (MI) occurs against angiographically unchanged or slightly modified coronary arteries (CA). In such cases, the so-called "type 2 IM" is diagnosed in some patients, however, to determine the true cause of MI, a modern method of investigation such as optical coherence tomography (OCT) is needed to visualize the intima of the CA and detect a minimal atherosclerotic process.  The purpose of the study was to establish the etiology of MI without obstructive coronary artery disease (MINOCA) using OCT. Materials and methods 160 conclusions of the OCT were analyzed. In 9 (6%) cases, the study was conducted in patients who underwent proven MI (mean age 43,1 ± 13,2, 8 males, 1 female) who had no hemodynamically significant CA stenosis according to CAG data. Results in 2 cases (22%) patients had ST-elevation MI, thrombotic occlusion of the CA (in one case, thrombaspiration was performed). In both patients, spontaneous dissection of the intima of the unmodified CA was detected in the OCT. The remaining 7 patients had non-ST-elevation MI, and in 2 cases, a diagnosis of type 2 MI was established: in both patients, the atherosclerotic plaque was visualized, narrowing the lumen of the CA less than 50%, in one case MI developed against a background of the hypertensive crisis, in another - against a background of spasm of CA. In the remaining 5 patients, OCT revealed subintimal atheromatous, with elements of local dissection of the intima. Thus, in 78% of patients atherosclerosis of CA of different severity (from the subintimal deposition of lipids to the development of atherosclerotic plaque, narrowing the clearance of the SC by less than 50%) was diagnosed. In the analysis of risk factors for coronary heart disease (CHD), 57% of patients with atheromatous CA had more than 2 risk factors for CHD: 3 (42%) smoked, 5 (71%) - obesity, 4 (57% ) - had arterial hypertension, 3 (42%) had dyslipidemia, 1 (14%) had type 2 diabetes. In the group of patients with spontaneous intima dissection of the CA, 1 patient (woman) did not have CHD risk factors, the 2-nd suffered from obesity and hypertension. For all patients a lifestyle correction was recommended; statins, antiplatelets were prescribed, patients with spontaneous dissection of CA had the recommendation of examination in the medical-genetic center. Conclusion Based on the results of the study, in most cases, the cause of IMBOC development was an atherosclerotic lesion of the coronary arteries, which is not always visualized with standard coronary angiography. Basically, the patients were young and middle-aged. Most patients had different risk factors for coronary heart disease.

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