Value of Atherosclerotic Plaque Characteristics and Pericoronary Adipose Tissue in Predicting Outcomes in Familial Hypercholesterolaemia: Should CCTA be Carried out in all Adult Patients With FH?

2021 ◽  
Vol 30 ◽  
pp. S95
Author(s):  
B. Jaltotage ◽  
J. Pang ◽  
A. Abraham ◽  
A. Krishnan ◽  
B. Chow ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Atherosclerotic Plaque ◽  
Familial Hypercholesterolaemia ◽  
Adult Patients

Abstract 5822: Atherosclerotic Plaque Inflammation Synchronize With Inflammatory Activity OF Visceral Fat

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Eung Ju Kim ◽  
Hong Seog Seo ◽  
Sungeun Kim ◽  
Jin Oh Na ◽  
Jae Hyoung Park ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Atherosclerotic Plaque ◽  
Visceral Adipose Tissue ◽  
Visceral Fat ◽  
Subcutaneous Fat ◽  
Fdg Uptake ◽  
Coronary Syndrome ◽  
Significant Difference ◽  
Plaque Inflammation ◽  
Visceral Adipose

Background: Visceral adipose tissue is thought to confer increased cardiovascular risk through leukocyte infiltration and increased adipose macrophage activity. Previous positron emission tomography (PET) studies using fluorodeoxyglucose (FDG) demonstrated that increased FDG uptake could reflect the severity of inflammation in atherosclerotic plaque. We hypothesized that active atherosclerotic change in the major arteries would accompany increased inflammation within visceral fat and it could be detected in humans using combined FDG PET/computed tomography (CT). Methods: We observed 44 consecutive subjects with cardiovascular disease. For all of them, an one-hour PET/CT (from brain to foot) was performed after injection of FDG (370–555 MBq). FDG uptake in the aorta or its major branches was evaluated visually and semiquantitatively. Maximal standard uptake values (SUV) of the highest regions of interest were calculated in the subcutaneous fat and visceral fat area, separately. Results: Significant FDG uptake in the arterial wall was noted in 21 patients (plaque positive; PP group), all of whom have experienced acute cardiovascular events (acute coronary syndrome or ischemic stroke) within a week. The other 23 patients (plaque negative; PN group) had chronic stable angina or asymptomatic carotid stenosis. Visceral fat SUV was significantly higher as compared to subcutaneous fat SUV (0.49± 0.15 vs. 0.15± 0.05, p< 0.001) in PP group, whereas there was no significant difference in PN group (0.18± 0.07 vs. 0.16± 0.03, p= 0.622). When we compared two groups, PP group showed higher visceral fat SUV than PN group (p< 0.001). In terms of subcutaneous fat SUV, the results were similar in two groups (p= 0.773). Conclusions: We demonstrated that atherosclerotic plaque inflammation was associated with increased inflammation within visceral fat. Our results need to be confirmed by comparison with histologic or other imaging findings. Further evaluation to determine whether metabolic activity of visceral adipose tissue is a marker or mediator of vascular inflammation is also needed.

scholarly journals Regional Adipose Tissue Associations With Calcified Atherosclerotic Plaque: African American-Diabetes Heart Study

Obesity ◽  
2010 ◽  
Vol 18 (10) ◽  
pp. 2004-2009 ◽  
Author(s):  
Jasmin Divers ◽  
Lynne E. Wagenknecht ◽  
Donald W. Bowden ◽  
J. Jeffrey Carr ◽  
R. Caresse Hightower ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
African American ◽  
Atherosclerotic Plaque ◽  
Heart Study ◽  
Diabetes Heart Study

PPARgamma: from adipose tissue to the atherosclerotic plaque

1998 ◽  
Vol 139 (4) ◽  
pp. 363-364 ◽  
Author(s):  
J. Lopez-Liuchi ◽  
C. Meier
Keyword(s):  
Adipose Tissue ◽  
Atherosclerotic Plaque

scholarly journals Bladder drug mirabegron exacerbates atherosclerosis through activation of brown fat-mediated lipolysis

2019 ◽  
Vol 116 (22) ◽  
pp. 10937-10942 ◽  
Author(s):  
Wenhai Sui ◽  
Hongshi Li ◽  
Yunlong Yang ◽  
Xu Jing ◽  
Fei Xue ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Atherosclerotic Plaque ◽  
Ldl Cholesterol ◽  
Uncoupling Protein ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Cerebrovascular Diseases ◽  
Plaque Development ◽  
Brown Adipose

Mirabegron (Myrbetriq) is a β3-adrenoreceptor agonist approved for treating overactive bladder syndrome in human patients. This drug can activate brown adipose tissue (BAT) in adult humans and rodents through the β3-adrenoreceptor-mediated sympathetic activation. However, the effect of the mirabegron, approved by the US Food and Drug Administration, on atherosclerosis-related cardiovascular disease is unknown. Here, we show that the clinical dose of mirabegron-induced BAT activation and browning of white adipose tissue (WAT) exacerbate atherosclerotic plaque development. In apolipoprotein E−/− (ApoE−/−) and low-density lipoprotein (LDL) receptor−/− (Ldlr−/−) mice, oral administration of clinically relevant doses of mirabegron markedly accelerates atherosclerotic plaque growth and instability by a mechanism of increasing plasma levels of both LDL-cholesterol and very LDL-cholesterol remnants. Stimulation of atherosclerotic plaque development by mirabegron is dependent on thermogenesis-triggered lipolysis. Genetic deletion of the critical thermogenesis-dependent protein, uncoupling protein 1, completely abrogates the mirabegron-induced atherosclerosis. Together, our findings suggest that mirabegron may trigger cardiovascular and cerebrovascular diseases in patients who suffer from atherosclerosis.

scholarly journals Estimation of the prevalence of cholesteryl ester storage disorder in a cohort of patients with clinical features of familial hypercholesterolaemia

2018 ◽  
Vol 56 (1) ◽  
pp. 112-117
Author(s):  
Pauline Ashfield-Watt ◽  
Kate Haralambos ◽  
Rhiannon Edwards ◽  
Delyth Townsend ◽  
Rob Gingell ◽  
...  
Keyword(s):  
Cholesteryl Ester ◽  
Allele Frequency ◽  
Storage Disease ◽  
Familial Hypercholesterolaemia ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Splice Junction ◽  
European Population ◽  
Adult Patients ◽  
Routine Testing

Background and aim Familial hypercholesterolaemia is caused by variants in the low-density lipoprotein cholesterol metabolic pathway involving LDLR, APOB and PCSK9 genes. A national genetic testing service in Wales, UK has observed that no familial hypercholesterolaemia variant is found in almost 80% patients with the familial hypercholesterolaemia phenotype. It has recently been suggested that some adult patients with a familial hypercholesterolaemia phenotype may have cholesteryl ester storage disease which can also present as a mixed hyperlipidaemia. The commonest genetic cause of cholesteryl ester storage disease is an exon 8 splice junction variant in the LIPA gene (rs116928232, c.894G>A; E8SJM) previously found to have an allele frequency of 0.0011 (1 in 450 individuals) in a large European population. This study investigated the prevalence of the E8SJM in patients with a familial hypercholesterolaemia phenotype in Wales, UK. Method A total of 1203 patients with a clinical suspicion of familial hypercholesterolaemia but no familial hypercholesterolaemia variant were invited to participate. Of these, 668 patients provided informed written consent. Stored DNA samples from 663 patients were genotyped for the E8SJM variant. Results Three heterozygotes were identified (allele frequency 0.0023). Whole gene sequencing of the LIPA gene was undertaken in these three individuals, but no other variants were found. Therefore, there were no cholesteryl ester storage disease patients (homozygote or compound heterozygote) identified in this cohort. Conclusion The allele frequency 0.0023 (1 in 221 individuals) for the E8SJM variant was more prevalent in this cohort than in a European population study; however, no cholesteryl ester storage disease homozygotes were identified. We found no evidence to support routine testing for cholesteryl ester storage disease in adult patients with a familial hypercholesterolaemia phenotype.

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