Lipid plaque burden in NSTE-ACS patients with or without COPD: insights from the SCAP Trial

2021 ◽  
Vol 69 (6) ◽  
Author(s):  
Rossella RUGGIERO ◽  
Alessandra SCOCCIA ◽  
Matteo SERENELLI ◽  
Andrea ERRIQUEZ ◽  
Giulia PASSARINI ◽  
...  
Keyword(s):  
Plaque Burden

Asymmetry of plaque burden in amyloid mouse models

2020 ◽  
Author(s):  
L Beyer ◽  
C Sacher ◽  
T Blume ◽  
J Sauerbeck ◽  
F Eckenweber ◽  
...  
Keyword(s):  
Mouse Models ◽  
Plaque Burden

The Role of Vascular Aging in Atherosclerotic Plaque Development and Vulnerability

2019 ◽  
Vol 25 (29) ◽  
pp. 3098-3111 ◽  
Author(s):  
Luca Liberale ◽  
Giovanni G. Camici
Keyword(s):  
Atherosclerotic Plaque ◽  
Molecular Mechanisms ◽  
Driving Forces ◽  
Plaque Burden ◽  
Vascular Aging ◽  
Age Related ◽  
Plaque Development ◽  
Increased Risk ◽  
The Impact ◽  
Over Time

Background: The ongoing demographical shift is leading to an unprecedented aging of the population. As a consequence, the prevalence of age-related diseases, such as atherosclerosis and its thrombotic complications is set to increase in the near future. Endothelial dysfunction and vascular stiffening characterize arterial aging and set the stage for the development of cardiovascular diseases. Atherosclerotic plaques evolve over time, the extent to which these changes might affect their stability and predispose to sudden complications remains to be determined. Recent advances in imaging technology will allow for longitudinal prospective studies following the progression of plaque burden aimed at better characterizing changes over time associated with plaque stability or rupture. Oxidative stress and inflammation, firmly established driving forces of age-related CV dysfunction, also play an important role in atherosclerotic plaque destabilization and rupture. Several genes involved in lifespan determination are known regulator of redox cellular balance and pre-clinical evidence underlines their pathophysiological roles in age-related cardiovascular dysfunction and atherosclerosis. Objective: The aim of this narrative review is to examine the impact of aging on arterial function and atherosclerotic plaque development. Furthermore, we report how molecular mechanisms of vascular aging might regulate age-related plaque modifications and how this may help to identify novel therapeutic targets to attenuate the increased risk of CV disease in elderly people.

scholarly journals Smooth muscle-specific HuR knockout induces defective autophagy and atherosclerosis

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Shanshan Liu ◽  
Xiuxin Jiang ◽  
Xiuru Cui ◽  
Jingjing Wang ◽  
Shangming Liu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cardiovascular Events ◽  
Rna Binding ◽  
Rna Binding Protein ◽  
Plaque Burden ◽  
Atherosclerotic Plaques ◽  
Ampk Activation ◽  
Homeostatic Regulation ◽  
Human Antigen R

AbstractHuman antigen R (HuR) is a widespread RNA-binding protein involved in homeostatic regulation and pathological processes in many diseases. Atherosclerosis is the leading cause of cardiovascular disease and acute cardiovascular events. However, the role of HuR in atherosclerosis remains unknown. In this study, mice with smooth muscle-specific HuR knockout (HuRSMKO) were generated to investigate the role of HuR in atherosclerosis. HuR expression was reduced in atherosclerotic plaques. As compared with controls, HuRSMKO mice showed increased plaque burden in the atherosclerotic model. Mechanically, HuR could bind to the mRNAs of adenosine 5′-monophosphate-activated protein kinase (AMPK) α1 and AMPKα2, thus increasing their stability and translation. HuR deficiency reduced p-AMPK and LC3II levels and increased p62 level, thereby resulting in defective autophagy. Finally, pharmacological AMPK activation induced autophagy and suppressed atherosclerosis in HuRSMKO mice. Our findings suggest that smooth muscle HuR has a protective effect against atherosclerosis by increasing AMPK-mediated autophagy.

scholarly journals Focal pericoronary adipose tissue attenuation is related to plaque presence, plaque type, and stenosis severity in coronary CTA

2021 ◽  
Author(s):  
Runlei Ma ◽  
Marly van Assen ◽  
Daan Ties ◽  
Gert Jan Pelgrim ◽  
Randy van Dijk ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Coronary Arteries ◽  
Plaque Burden ◽  
Severe Stenosis ◽  
Plaque Type ◽  
Plaque Development ◽  
Calcified Plaque ◽  
Stenosis Severity ◽  
Dual Source ◽  
Artery Disease

Abstract Objectives To investigate the association of pericoronary adipose tissue mean attenuation (PCATMA) with coronary artery disease (CAD) characteristics on coronary computed tomography angiography (CCTA). Methods We retrospectively investigated 165 symptomatic patients who underwent third-generation dual-source CCTA at 70kVp: 93 with and 72 without CAD (204 arteries with plaque, 291 without plaque). CCTA was evaluated for presence and characteristics of CAD per artery. PCATMA was measured proximally and across the most severe stenosis. Patient-level, proximal PCATMA was defined as the mean of the proximal PCATMA of the three main coronary arteries. Analyses were performed on patient and vessel level. Results Mean proximal PCATMA was −96.2 ± 7.1 HU and −95.6 ± 7.8HU for patients with and without CAD (p = 0.644). In arteries with plaque, proximal and lesion-specific PCATMA was similar (−96.1 ± 9.6 HU, −95.9 ± 11.2 HU, p = 0.608). Lesion-specific PCATMA of arteries with plaque (−94.7 HU) differed from proximal PCATMA of arteries without plaque (−97.2 HU, p = 0.015). Minimal stenosis showed higher lesion-specific PCATMA (−94.0 HU) than severe stenosis (−98.5 HU, p = 0.030). Lesion-specific PCATMA of non-calcified, mixed, and calcified plaque was −96.5 HU, −94.6 HU, and −89.9 HU (p = 0.004). Vessel-based total plaque, lipid-rich necrotic core, and calcified plaque burden showed a very weak to moderate correlation with proximal PCATMA. Conclusions Lesion-specific PCATMA was higher in arteries with plaque than proximal PCATMA in arteries without plaque. Lesion-specific PCATMA was higher in non-calcified and mixed plaques compared to calcified plaques, and in minimal stenosis compared to severe; proximal PCATMA did not show these relationships. This suggests that lesion-specific PCATMA is related to plaque development and vulnerability. Key Points • In symptomatic patients undergoing CCTA at 70 kVp, PCATMAwas higher in coronary arteries with plaque than those without plaque. • PCATMAwas higher for non-calcified and mixed plaques compared to calcified plaques, and for minimal stenosis compared to severe stenosis. • In contrast to PCATMAmeasurement of the proximal vessels, lesion-specific PCATMAshowed clear relationships with plaque presence and stenosis degree.

scholarly journals Procyanidin B2 Reduces Vascular Calcification through Inactivation of ERK1/2-RUNX2 Pathway

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 916
Author(s):  
Yingquan Liang ◽  
Guilan Chen ◽  
Feng Zhang ◽  
Xiaoxiao Yang ◽  
Yuanli Chen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Calcification ◽  
Aortic Root ◽  
Smooth Muscle Actin ◽  
Bone Morphogenetic Protein 2 ◽  
Plaque Burden ◽  
Runx2 Expression ◽  
Plaque Instability ◽  
Related Transcription Factor

Vascular calcification is strongly associated with atherosclerotic plaque burden and plaque instability. The activation of extracellular signal-regulated kinase 1/2 (ERK1/2) increases runt related transcription factor 2 (RUNX2) expression to promote vascular calcification. Procyanidin B2 (PB2), a potent antioxidant, can inhibit ERK1/2 activation in human aortic smooth muscle cells (HASMCs). However, the effects and involved mechanisms of PB2 on atherosclerotic calcification remain unknown. In current study, we fed apoE-deficient (apoE−/−) mice a high-fat diet (HFD) while treating the animals with PB2 for 18 weeks. At the end of the study, we collected blood and aorta samples to determine atherosclerosis and vascular calcification. We found PB2 treatment decreased lesions in en face aorta, thoracic, and abdominal aortas by 21.4, 24.6, and 33.5%, respectively, and reduced sinus lesions in the aortic root by 17.1%. PB2 also increased α-smooth muscle actin expression and collagen content in lesion areas. In the aortic root, PB2 reduced atherosclerotic calcification areas by 75.8%. In vitro, PB2 inhibited inorganic phosphate-induced osteogenesis in HASMCs and aortic rings. Mechanistically, the expression of bone morphogenetic protein 2 and RUNX2 were markedly downregulated by PB2 treatment. Additionally, PB2 inhibited ERK1/2 phosphorylation in the aortic root plaques of apoE−/− mice and calcified HASMCs. Reciprocally, the activation of ERK1/2 phosphorylation by C2-MEK1-mut or epidermal growth factor can partially restore the PB2-inhibited RUNX2 expression or HASMC calcification. In conclusion, our study demonstrates that PB2 inhibits vascular calcification through the inactivation of the ERK1/2-RUNX2 pathway. Our study also suggests that PB2 can be a potential option for vascular calcification treatment.

Impact of hinge motion on stent edge restenosis after new generation drug-eluting-stent implantation in RCA

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T Jimba ◽  
M Ikutomi ◽  
D Nishijyo ◽  
M Yamasaki ◽  
A Shindou ◽  
...  
Keyword(s):  
Stent Implantation ◽  
Biomechanical Properties ◽  
Plaque Burden ◽  
Drug Eluting Stent ◽  
Landing Zone ◽  
Binary Restenosis ◽  
Drug Eluting ◽  
New Generation ◽  
Hinge Angle

Abstract Background Edge restenosis still occurs after stent implantation, even by using new generation drug-eluting stents (DES) considered to have favorable biomechanical properties. Mechanical stress imposed on the stent edge are thought to be aggravated by hinge motion at a point between the stented and unstented segments, inducing chronic local inflammation and neointimal overgrowth. Purpose The aim of this study was to investigate the association between the development of edge restenosis and hinge motion in right coronary artery (RCA) where the excessive vessel movement is commonly observed. Methods Among consecutive 650 lesions in RCA where new generation DESs were implanted between 2009 and 2019, 427 serial lesions with sets of angiographies at baseline and follow-up (6–18 month) were included. In addition to conventional quantitative angiography analysis, hinge angle at stent edges was measured (Fig. 1). All the appropriate data for intravascular imaging were analyzed for both stent edges and reference segments. Results Binary restenosis occurred in 43 lesions, and 39 of them were referred to re-intervention. Fifty five percent of them were related to stent edges (15 at proximal and 9 at distal edges). Classical risk factors including diabetes and hemodialysis were more prevalent in the restenosis group (p<0.05). Hinge angle was statistically larger in edge restenosis group than body restenosis or no restenosis group (17.3° vs 11.6° vs 10.6°, p<0.001, Fig. 2). In per-edge analysis, hinge angle, dissection and residual plaque ratio were the independent predictors for binary restenosis (Table 1) with the optimal cut-off value of hinge angle 11.5°. The coexistence of excessive hinge angle and residual plaque burden had an amplified effect on the angiographic stenotic progression at stent edge (p for interaction <0.001) and the incidents of binary restenosis (16.7% vs 1.7% p<0.01, Figs. 3,4). Conclusion Substantial stress determined by angulation at the stent edge and its interaction with residual plaque can be considered as one of the plausible mechanisms for edge restenosis. For tortuous RCA lesions, it would be important to decide the stent-landing zone for minimizing hinge motion and optimize the future stent design. Funding Acknowledgement Type of funding source: None

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