scholarly journals Reduced Plasma Kallistatin Is Associated With the Severity of Coronary Artery Disease, and Kallistatin Treatment Attenuates Atherosclerotic Plaque Formation in Mice

2018 ◽  
Vol 7 (21) ◽  
Author(s):  
Yuyu Yao ◽  
Bing Li ◽  
Chang Liu ◽  
Cong Fu ◽  
Pengfei Li ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Atherosclerotic Plaque ◽  
Plaque Formation ◽  
Atherosclerotic Plaque Formation ◽  
Artery Disease

Reciprocal communication of perivascular epicardial adipose tissue and coronary atherogenesis

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Wildauer ◽  
S Honold ◽  
C Beyer ◽  
T Senoner ◽  
M Stuehlinger ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Atherosclerotic Plaque ◽  
Epicardial Adipose Tissue ◽  
Plaque Formation ◽  
Care Hospital ◽  
Atherosclerotic Plaque Formation ◽  
Artery Disease

Abstract Purpose Perivascular epicardial adipose tissue (PEAT) has been linked to underlying coronary artery disease (CAD) and proposed to modulate adjacent atherosclerotic plaque formation. In vitro and ex vivo studies support bilateral influence of adipose tissue and vessel wall. Therefore, we quantified PEAT volume and composition and its dynamics in a low coronary risk patient cohort with a semi-automate software in serial CT exams. Methods and materials We retrospectively included 120 patients (27% females) from a tertiary care hospital who underwent serial cardiac CT angiographies with a low cardiovascular risk profile. All coronary CTs were evaluated in a standardized approach: epicardial adipose tissue (EAT) volume and attenuation was quantified in total, in the atrioventricular (RCA, LCX) or interventricular (LAD) sulcus and in a 5mm radius for each coronary artery (PEAT). Coronary plaques were quantified using a semi-automated software and compared to progression, stability of regression between the two scans. The measurements were compared on a per-patient and per-vessel basis between plaque-naïve and diseased vessels. Results Of 120 patients (32% female), 59.2%) had atherosclerotic plaque formation. After 36 months mean follow-up, 22 (18.3%) showed a CAD regression plaques, 39 (32.5%) had stable coronary arteries and 49 (40.8%) progressive CAD. Total EAT volume decreased by −15.6±37.2 mm3 in the regressive group, increased by 2.7±30.6mm3 in the stable group and by 24.3±37.1mm3 in the progressive CAD group (p=0.003). Per-vessel analysis showed a significant decrease of perivascular EAT attenuation in patients with CAD regression (−3.8±7.6 HU) compared to CAD stable (1.2±9.1 HU) and CAD progressive patients (3.5±8.2 HU, p<0.0001). Mean sulcus EAT attenuation did not show a significant change at follow-up (p=0.135) Conclusion Epicardial adipose tissue volume is mutually changing with the progression or regression of coronary artery disease. Perivascular but not epicardial attenuation levels correlated to adjacent plaque and support a direct bilateral influence. Change per-vessel-basis (n=360) Funding Acknowledgement Type of funding source: None

Hypothyroidism in Otherwise Healthy Hypercholesterolemic Children

PEDIATRICS ◽  
1991 ◽  
Vol 88 (2) ◽  
pp. 332-334
Author(s):  
ARTHUR LAVIN ◽  
ALAN H. NAUSS
Keyword(s):  
United States ◽  
Coronary Artery Disease ◽  
The United States ◽  
Plaque Formation ◽  
Preventive Cardiology ◽  
Treatment Regimens ◽  
Atherosclerotic Plaque Formation ◽  
Symptomatic Coronary Artery Disease ◽  
Artery Disease ◽  
High Risk Screening

Atherosclerosis is the leading cause of death in the United States. Studies in adults have shown that intervention with combined diet and medication can reduce atherosclerotic plaque formation and, as a result, the incidence of symptomatic coronary artery disease.1-4 With a strong tradition of preventive medicine, the pediatric community has begun exploring the prevention of adult atherosclerosis through intervention in childhood. Although issues such as universal vs selective high-risk screening, ideal age for screening and intervention, and treatment regimens remain unresolved and controversial, many preventive cardiology clinics, as well as individual pediatricians, have been screening and treating children.5,6 As part of an initial evaluation of hypercholesterolemic children and prior to any intervention, it is important to determine whether other disease processes are contributing to the child's dyslipoproteinemia.

scholarly journals Interleukin-37: The Effect of Anti-Inflammatory Response in Human Coronary Artery Endothelial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Xianfeng Yan ◽  
Bin Xie ◽  
Guihai Wu ◽  
Jing Hu ◽  
Di Wang ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Inflammatory Response ◽  
Atherosclerotic Plaque ◽  
Inflammatory Responses ◽  
Plaque Formation ◽  
Human Coronary Artery ◽  
Atherosclerotic Plaque Formation

Interleukin-37 (IL-37) is unique in the IL-1 family since it broadly suppresses innate immunity and elevates in humans with inflammatory and autoimmune diseases. IL-37 shows definite groups and transcripts for human IL37 gene, but it is still not completely understood the effect and mechanisms of inflammatory response in endothelial cells. It is well accepted that endothelial dysfunction caused by inflammation is a key initiating event in atherosclerotic plaque formation, which leads to the occurrence and development of the cardiovascular adverse events in clinical since the inflammatory responses of endothelial cells could induce and enhance the deposition of extensive lipid and the formation of atherosclerotic plaque in the intima. Thus, it is essential to investigate the role and potential mechanisms in endothelial inflammatory response to prevent the formation and development of many cardiovascular diseases including atherosclerosis. So far, the recent studies have revealed that IL-37 is able to inhibit inflammatory response by suppressing the TLR2-NF-κB-ICAM-1 pathway intracellularly in human coronary artery endothelial cells (HCAECs). Further, the role of IL-37 may be related to the IL-18 pathway extracellularly and involved in the adhesion and transmigration of neutrophils in HCAECs.

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