Can EAT be an INOCA goalkeeper

Figures

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  Figure 1. The clinical diagnostic assessment of INOCA. (Created with BioRender.com).

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  Figure 2. The mechanism of INOCA. INOCA is represented by CMD. It can be caused by oxidative stress, adipokines produced by EAT, changes in circulating factor concentrations in plasma, and changes in ESL. CMD is determined by a combination of factors including endothelial dysfunction, vascular smooth muscle cell hyperreactivity, vascular remodeling, vascular fibrosis, and changes in macrophage function (see text for details). A possible adjustment procedure is proposed for this. CMD: coronary microvascular dysfunction.*Green represents several conditions that produce CMD under abnormal EAT; brown represents pathways that promote inflammation; yellow represents pathways that inhibit inflammation. (Created with BioRender.com).

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  Figure 3. Several possible relationships between inflammatory EAT and the pathogenesis of INOCA. Inflammation causes EAT to secrete cytokines and adipokines, altering the function of the vascular endothelium and the phenotype of macrophages. In turn, it affects the function of vascular smooth muscle, the remodeling of microvascular density, deposition of subcutaneous plaque lipids, and the mesenchymal fibrosis. These may affect perfusion of myocardial blood flow, leading to the development of INOCA. (Created with BioRender.com).

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  Figure 4. The methods used to measure the quantity and quality of EAT. Quantification of EAT has seen improvements over the years attributed to the advancements in non-invasive imaging techniques: CT, as well as CMR, PET. Evaluation indicators as thickness, volume, and density. EAT under chronic inflammation shifts from brown fat to white fat. The quality of the EAT was changed, such as inflammatory status, the type of adipokines, and microRNA. The cytokines and adipokines within the EAT can be measured by quantitative RT-PCR and ELISA. Cytokines correlate with the presence of CAD, severity, and coronary artery calcification, but not with circulating cytokines in plasma. EAT inflammation was independent of several clinical variables (obesity, diabetes, or chronic therapy with statins or ACE inhibitors). (Created with BioRender.com).