Epicardial adipose tissue (EAT) plays a role in cardiac physiology and may contribute to the development of coronary artery disease. Our objective was to determine whether there was a significant difference in gene expression in EAT compared to subcutaneous adipose tissue (SAT) and to identify potential relationships. MEDLINE and EMBASE were searched using the key terms "Epicardial Adipose Tissue" or "Epicardial Fat" in combination with "RNA", "mRNA", or "gene". The entry criteria were studies that presented primary data including expression levels of mRNA in human EAT compared with SAT and an expression of variance (SD). Genes identified by 2 or more studies were evaluated. Genes that showed significant change in expression between EAT and SAT were examined using the Gene Functional Classification analytical tool in Database for Annotation, Visualization and Integrated Discovery and cross-validated by ToppGene. Seventeen genes were identified from 25 studies. Meta-analysis showed that 10 genes (ADORA1, adiponectin, AGT, ADM, CATA, IL-1β, MCP-1, RBP-4, TNF-α, UCP-1) were significantly different in EAT. Gene Functional Classification analysis yielded 23 clusters with significant relationships. The top clusters were focused on responses to glucocorticoid stimulus, regulation of apoptosis, cellular ion homeostasis, and responses to hormone stimulus. Genetic analysis shows that EAT is discretely different from SAT. ADORA1, adiponectin, AGT, ADM, CATA, IL-1β, MCP-1, RBP-4, TNF-α, and UCP-1 may play significant roles in the unique physiology of EAT and/or its role in pathophysiology, through mechanisms as diverse as steroid hormone responses and regulation of apoptosis.

Gene expression and associations were examined in a model of heart failure with preserved ejection fraction (HFpEF), a condition with minimal effective treatment. Genes with at least two studies showing significant changes in Dahl rat with heart failure were examined by meta-analysis. Significantly increased in expression were iNOS, p47phox, ADM, ANP, OPN, ACE, MCP-1, GP91PHOX, ICAM-1, TGF-β1, CTGF, ET-1, p22phox, ETB, BNP, ETA, MMP13, Col1a1, MMP2, TIMP1, Col3a1, Il-1β, β-MHC, ECE1, MMP14, AGT, and MMP9. In contrast, GLUT4, VEGF, eNOS, HIF-1α, and PGC1-α were significantly decreased in expression. The top biological process clusters identified in Database for Annotation, Visualization and Integrated Discovery, ToppGene, and PANTHER were collagen metabolic process, cellular ion homeostasis, regulation of cell migration, and response to decreased oxygen levels. These data suggest refocusing understanding of the pathophysiology of HFpEF to pathways involved in collagen metabolism, cell migration likely for inflammatory cells, and responses to decreased oxygen levels. Abbreviations Inducible nitric oxide synthase (INOS), neutrophil cytosolic factor 1 (p47phox), adrenomedullin (ADM), atrial natriuretic peptide (ANP), osteopontin (OPN/SPP1), angiotensin converting enzyme (ACE), monocyte chemotactic protein 1 (MCP-1), cytochrome b-245 beta polypeptide (gp91phox), intercellular adhesion molecule 1 (ICAM-1), transforming growth factor beta 1 (TGF-β1), connective tissue growth factor (CTGF), endothelin-1 (ET-1), cytochrome B-245, alpha polypeptide (p22phox), endothelin receptor type B (ETB/EDNRB), brain natriuretic peptide (BNP), endothelin receptor type A (ETA/EDNRA), matrix metallopeptidase 13 (MMP13), type I collagen (Col1a1), matrix metallopeptidase 2 (MMP2), TIMP metallopeptidase inhibitor 1 (TIMP1), Type III collagen (Col3a1), interleukin 1 beta (IL-1β), beta myocin heavy chain (β-MHC), endothelin converting enzyme 1 (ECE1) matrix metallopeptidase 14 (MMP14), angiotensinogen (AGT), angiotensin II receptor Type 1 (AT1R), cytochrome C oxidase I (COX1), fms-like tyrosine kinase 1 (FLT1), TIMP metallopeptidase inhibitor 2 (TIMP2), phospholamban (PLN), vascular cell adhesion molecule 1 (VCAM1), extracellular matrix (ECM).

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Fabry disease (FD) is an X-linked lysosomal storage disorder caused by mutations in the galactosidase A (GLA) gene that result in deficient galactosidase A enzyme and subsequent accumulation of glycosphingolipids throughout the body. The result is a multi-system disorder characterized by cutaneous, corneal, cardiac, renal, and neurological manifestations. Increased left ventricular wall thickness represents the predominant cardiac manifestation of FD. As the disease progresses, patients may develop arrhythmias, advanced conduction abnormalities, and heart failure. Cardiac biomarkers, point-of-care dried blood spot testing, and advanced imaging modalities including echocardiography with strain imaging and magnetic resonance imaging (MRI) with T1 mapping now allow us to detect Fabry cardiomyopathy much more effectively than in the past. While enzyme replacement therapy (ERT) has been the mainstay of treatment, several promising therapies are now in development, making early diagnosis of FD even more crucial. Ongoing initiatives involving artificial intelligence (AI)-empowered interpretation of echocardiographic images, point-of-care dried blood spot testing in the echocardiography laboratory, and widespread dissemination of point-of-care ultrasound devices to community practices to promote screening may lead to more timely diagnosis of FD. Fabry disease should no longer be considered a rare, untreatable disease, but one that can be effectively identified and treated at an early stage before the development of irreversible end-organ damage.

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The objective was to improve the management of patients with hypertension (HTN) and coronary artery disease (CAD), utilizing a model which integrates 3 determinants of coronary blood flow (CBF)-CAD severity, diastolic blood pressure (DBP), and left ventricular (LV) mass. We validated non-parametric equations for CBF estimation in a consecutive patient sample (N = 81) with HTN and CAD. There was a highly significant correlation (r = .565; P < .01) between clinical DBP and estimated CBF. Greater LV mass and more severe CAD shifted the relationship towards less CBF at the same DBP. LV mass was more critical when DBP >70 mm Hg. Estimated changes in CBF at different DBP considering the severity of CAD and LV mass can be calculated. In summary, the severity of CAD from coronary CT or coronary angiography combined with LV mass from echocardiography permits clinicians to guide the extent of, or target for, DBP to avoid seriously compromising CBF. | INTRODUCTIONTarget diastolic blood pressure (DBP) for patients with hypertension (HTN) and coronary artery disease (CAD) has been the subject of some controversy because of the need to lower blood pressure (BP) to pre- The purpose of this study was to produce a better treatment strategy for patients with hypertension and CAD. Specifically, we sought to use the degree of coronary stenosis from either coronary angiography or coronary computed tomography angiography (CCTA) and to integrate it with LV mass in order to develop a patient-specific approach for blood pressure management in patients with hypertension and coronary artery disease. | METHODS | Patient populationThe study population consisted of patients who attended a cardiology clinic at a university hospital. A retrospective case review was con-

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