scholarly journals Migration of ApoA1+ Macrophage Phenotypes from Pericoronary Adipose Tissue to Coronary Plaque: A Possible Mechanism for Suppression of Human Coronary Atherosclerosis

2020 ◽  
Vol 4 (1) ◽  
pp. 012-020
Author(s):  
Nobuyuki Hiruta ◽  
Yasumi Uchida ◽  
Ei Shimoyama ◽  
Tsuyoshi Tabata
Keyword(s):  
Adipose Tissue ◽  
Coronary Atherosclerosis ◽  
Coronary Plaque ◽  
Macrophage Phenotypes

scholarly journals Different Expression of Mitochondrial and Endoplasmic Reticulum Stress Genes in Epicardial Adipose Tissue Depends on Coronary Atherosclerosis

2021 ◽  
Vol 22 (9) ◽  
pp. 4538
Author(s):  
Helena Kratochvílová ◽  
Miloš Mráz ◽  
Barbora J. Kasperová ◽  
Daniel Hlaváček ◽  
Jakub Mahrík ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endoplasmic Reticulum ◽  
Adipose Tissue ◽  
Cardiac Surgery ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Mrna Expression ◽  
Coronary Atherosclerosis ◽  
Stress Genes ◽  
Valvular Surgery

The aim of our study was to analyze mitochondrial and endoplasmic reticulum (ER) gene expression profiles in subcutaneous (SAT) and epicardial (EAT) adipose tissue, skeletal muscle, and myocardium in patients with and without CAD undergoing elective cardiac surgery. Thirty-eight patients, 27 with (CAD group) and 11 without CAD (noCAD group), undergoing coronary artery bypass grafting and/or valvular surgery were included in the study. EAT, SAT, intercostal skeletal muscle, and right atrium tissue and blood samples were collected at the start and end of surgery; mRNA expression of selected mitochondrial and ER stress genes was assessed using qRT-PCR. The presence of CAD was associated with decreased mRNA expression of most of the investigated mitochondrial respiratory chain genes in EAT, while no such changes were seen in SAT or other tissues. In contrast, the expression of ER stress genes did not differ between the CAD and noCAD groups in almost any tissue. Cardiac surgery further augmented mitochondrial dysfunction in EAT. In our study, CAD was associated with decreased expression of mitochondrial, but not endoplasmic reticulum stress genes in EAT. These changes may contribute to the acceleration of coronary atherosclerosis.

Coronary plaque instability is associated with inflammatory activity of visceral adipose tissue and carotid artery: a prospective pilot F-18 FDG PET/CT study

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Pahk ◽  
H.W Kwon ◽  
J.S Eo ◽  
H.S Seo ◽  
S Kim
Keyword(s):  
Adipose Tissue ◽  
Carotid Artery ◽  
Systemic Inflammation ◽  
Fdg Pet ◽  
Coronary Plaque ◽  
Inflammatory Activity ◽  
Plaque Instability ◽  
Pet Ct ◽  
Fdg Pet Ct ◽  
Visceral Adipose

Abstract Background Dysfunctional Visceral adipose tissue (VAT) secretes pro-inflammatory cytokines and promotes inflammatory cell infiltration into VAT thereby boosting insulin resistance and systemic inflammation which eventually lead to increased risk of cardiovascular disease (CVD). F-18 FDG PET/CT is well known to reflect the inflammatory activity of classically activated (M1) macrophage. Purpose We hypothesized that F-18 FDG PET/CT could reflect the inflammatory activity of dysfunctional VAT and carotid artery which were associated with coronary plaque instability. Methods A total of 90 participants were enrolled in this prospective study. F-18 FDG PET/CT was performed in 32 participants with acute myocardial infarction (AMI) within a week of disease onset, 33 participants with stable coronary artery disease (CAD), and 25 control subjects. Maximum standardized uptake value (SUVmax) was calculated in VAT, subcutaneous adipose tissue (SAT), spleen, and bone marrow (BM). Target-to-background ratio (TBR) was calculated in right carotid artery and right jugular vein. Results The SUVmax of VAT and the TBR of right carotid artery were highest in patients with AMI, intermediate in patient with stable CAD, and lowest in control subjects. Systemic inflammation surrogate markers such as high-sensitivity C-reactive protein, spleen SUVmax were also showed similar pattern like the SUVmax of VAT and the TBR of right carotid artery. Furthermore, multiple linear regression analysis showed that the SUVmax of VAT and spleen SUVmax were independently associated with the TBR of right carotid artery. Conclusions F-18 FDG PET/CT could reflect the synchronized systemic inflammation in VAT and carotid artery which could affect the coronary artery instability. Furthermore, our findings offer clinical insights into risk stratification, monitoring of therapy, and physiological changes in the development of CAD. Funding Acknowledgement Type of funding source: None

Abstract P193: Increased High Density Lipoprotein Cholesterol:ApolipoproteinA1 Ratio is Associated with Less Progression of Coronary Atherosclerosis in Statin-Treated Patients

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Preethi Mani ◽  
Kiyoko Uno ◽  
Julie Thornton ◽  
Stephen Nicholls
Keyword(s):  
Coronary Atherosclerosis ◽  
Coronary Plaque ◽  
Cholesterol Content ◽  
Favorable Effect ◽  
Plaque Burden ◽  
P Value ◽  
Plaque Progression ◽  
Coronary Syndrome ◽  
Hdl Function ◽  
Atheroma Volume

Background HDL cholesterol (HDL-C) and apolipoprotein AI (apoAI) levels are inversely related to adverse cardiovascular outcome. Associations between these HDL related measures and their ratio with coronary plaque progression have not been studied. It has been proposed that increasing HDL particle cholesterol content impairs HDL function, but impact on disease progression is unknown. We hypothesize that all HDL related measures are inversely associated with coronary plaque progression. Methods Retrospective analysis was performed of 1528 statin treated patients with angiographic CAD who had serial evaluation of atheroma burden with intravascular ultrasound. Relationships between achieved levels of HDL related measures with clinical characteristics and changes in plaque burden were determined. Results Strong correlation between HDL-C and apoAI (r=0.73, p<0.0001) was noted. Patients with highest levels of HDL-C:apoAI were more likely to be female, black, and have lower BMI and less likely to be smokers or have previous revascularization (all p<0.001) or acute coronary syndrome (p=0.013). HDL-C, apoAI, and HDL-C:apoAI demonstrated negative correlation with change in total atheroma volume (p<0.01). For HDL-C:apoAI and HDL-C, increasing tertiles of achieved levels were associated with a linear benefit in slowing progression. For apoAI, a nonlinear association was seen, with similar benefit on progression in the middle and upper tertiles ( Table ). There was no statistical interaction for heterogeneity between HDL-C:apoAI and atheroma burden based on achieved levels of HDL-C (p=0.581). Change in IVUS Measures By Tertiles of Achieved HDL-related Parameters Percent Atheroma Volume Parameter T1 T2 T3 P Value HDL-C 0.58±0.27 0.26±0.27 0.11±0.27 0.012 ApoAI 0.28±0.26 −0.04±0.26 −0.08±0.26 0.10 HDL-C:ApoAI 0.22±0.27 0.13±0.27 −0.27±0.27 0.021 Total Atheroma Volume Parameter T1 T2 T3 P Value HDL-C −2.46±2.21 −4.18±2.20 −5.31±2.20 0.035 ApoAI −4.94±2.13 −6.30±2.13 −7.40±2.13 0.135 HDL-C:ApoAI −4.59±2.25 −6.38±2.24 −8.07±2.26 0.022 Conclusions Increase in all HDL related measures was associated with less progression of coronary atherosclerosis. Association of higher HDL-C:ApoAI with favorable effect on plaque progression at all levels of HDL-C suggests intact HDL functionality of larger cholesterol rich particles. Interventions that increase HDL particle cholesterol content, such as CETP inhibitors, may thus have beneficial effect at the artery wall.

Abstract 2511: Impact of Olmesartan on Progression of Coronary Atherosclerosis; - A Serial Volumetric IVUS Analysis from the OLIVUS Trial -

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Atsushi Hirohata ◽  
Hirosuke Yamaji ◽  
Masaaki Murakami ◽  
Eiki Hirose ◽  
Keisuke Ohkawa ◽  
...  
Keyword(s):  
Angina Pectoris ◽  
Stable Angina ◽  
Coronary Atherosclerosis ◽  
Coronary Plaque ◽  
Stable Angina Pectoris ◽  
Plaque Volume ◽  
Receptor Blocking ◽  
Percent Change ◽  
Angiotension Ii

Prior intravascular ultrasound (IVUS) trials suggest slowing of coronary plaque progression with some medicines but have not shown convincing evidence of regression using angiotension-II receptor blocking agents (ARB). A prospective, double-blind, randomized, multicenter trial (Impact of OLmesartan on progression of coronary atherosclerosis; evaluation by IntraVascular UltraSound [OLIVUS]) was performed in 247 stable angina pectoris patients with native coronary artery lesions. When these patients underwent percutaneous coronary intervention for culprit lesions, IVUS was performed in their non-culprit vessels (without angiographically documented coronary stenosis [<50%]). Patients were randomly assigned to receive 20 mg of Olmesartan or control, and treated with a combination of β-blockers, calcium channel blockers, diuretics, nitrates, glycemic control agents and/or statins per physician’s guidance. Patients already on ACE inhibitors or other ARBs were excluded. Serial IVUS examinations (baseline and 14-months follow-up) were performed to assess coronary plaque volume. Volumetric IVUS analyses (mean measured length:41.2 ± 8.7mm) included lumen (LV), plaque (PV), vessel volume (VV), percent plaque volume (% PV), percent change in total PV (PCPV) and percent change in % PV (PC%PV). At baseline, patient characteristics and all IVUS parameters were identical between the two groups. However, follow-up IVUS showed significantly decreased PCPV and PC%PV in the Olmesartan group, despite similar blood pressure (table ). In addition, multivariate analysis identified Olmesartan administration as one of the factors that decreased plaque volume (β-coefficient −0.29 (95%CI, −0.7 to 0.4), p<0.01). These observations suggest a positive role in potential plaque regression through the administration of Olmesartan, an angiotension-II receptor blocking agent, for patients with stable angina pectoris.

Abstract 11885: Differential Contributions of Abdominal Visceral Fat and Epicardial Fat to Coronary Atherosclerosis in Non-Obese Japanese Patients

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Ken Harada ◽  
Takashi Kataoka ◽  
Masahiro Takeshita ◽  
Kazuhiro Harada ◽  
Ayako Kunimura ◽  
...  
Keyword(s):  
Visceral Fat ◽  
Coronary Atherosclerosis ◽  
Japanese Patients ◽  
Coronary Plaque ◽  
Epicardial Fat ◽  
Systemic Effects ◽  
Visceral Fat Area ◽  
Coronary Syndrome ◽  
Abdominal Visceral Fat ◽  
Noncalcified Plaque

Introduction: Epicardial fat is a source of adipocytokines that have both paracrine and systemic effects and is implicated in coronary atherosclerosis. The relation between epicardial fat volume (EFV) and circulating adipocytokine levels has remained unknown, however. Objectives: We assessed the relation between EFV and both plasma adipocytokine concentrations and coronary atherosclerotic plaque. Methods: Consecutive Japanese patients suspected of having coronary artery disease (n = 216) were examined. Individuals with acute coronary syndrome or with inadequate CT imaging were excluded. A total of 164 patients (65 ± 10 years; 70% men; BMI, 23.8 ± 3.6 kg/m2) was enrolled. Plasma levels of adiponectin, interleukin-6 (IL-6), plasminogen activator inhibitor-1 (PAI-1), and vascular endothelial growth factor (VEGF) were measured. The characteristics of coronary plaque, abdominal visceral fat area, and EFV were determined by 64-slice CT. Results: EFV was greater in subjects with noncalcified plaque than in those with no plaque or with calcified plaque (126 ± 39 vs. 98 ± 34 and 97 ± 45 mL, respectively; P = 0.010). EFV was significantly correlated with BMI, plasma triglyceride concentration, and the triglyceride/HDL-cholesterol ratio (r = 0.51, 0.19, and 0.20, respectively) but not with plasma adipocytokine levels, whereas plasma adiponectin and IL-6 levels were significantly correlated (r = -0.49 and 0.20, respectively) with visceral fat area, in patients with coronary plaque. Conclusions: Patients with noncalcified plaque had increased EFV but their plasma adipocytokine levels had not increased. Adipocytokines in plasma may be derived mainly from abdominal visceral fat, whereas epicardial fat may promote coronary atherosclerosis directly through a paracrine mechanism rather than by systemic effects. In conclusion, abdominal visceral fat and epicardial fat may thus contribute to coronary atherosclerosis by distinct mechanisms in nonobese individuals.

scholarly journals The Associations of Epicardial Adipose Tissue With Coronary Artery Disease and Coronary Atherosclerosis

2014 ◽  
Vol 55 (3) ◽  
pp. 197-203 ◽  
Author(s):  
Se-Hong Kim ◽  
Ju-Hye Chung ◽  
Beom-June Kwon ◽  
Sang-Wook Song ◽  
Whan-Seok Choi
Keyword(s):  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Coronary Atherosclerosis ◽  
Epicardial Adipose Tissue ◽  
Artery Disease
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