Myocardial fat is often seen at cardiac computed tomography (CT) and magnetic resonance (MR) imaging of healthy adults and patients with myocardial diseases. Physiologic myocardial fat develops with aging and is commonly seen at CT in the anterolateral right ventricular (RV) free wall and RV outflow tract with normal or thickened RV myocardium and a normal-sized RV in elderly patients. Pathologic conditions with myocardial fat include healed myocardial infarction (MI); arrhythmogenic RV cardiomyopathy or dysplasia (ARVC); and others, such as cardiac lipoma, lipomatous hypertrophy of the interatrial septum, tuberous sclerosis complex, dilated cardiomyopathy, and cardiomyopathy with muscular dystrophy. In patients with healed MI, CT and MR imaging show fat in left ventricular myocardium that is of normal thickness or thin and follows the distribution of the coronary artery; CT often depicts fat in mostly subendocardial regions. In patients with ARVC, characteristic CT and MR imaging findings include a thin RV outflow tract and free wall caused by subepicardial fatty infiltration; fat in the RV moderator band, trabeculae, and ventricular septum; and RV enlargement and wall motion abnormality. Recognition of patient age, characteristic locations of myocardial fat, myocardial thickness, and ventricular size helps in differentiating physiologic and pathologic myocardial fat at cardiac imaging; findings of wall motion abnormality and late gadolinium enhancement at MR imaging help narrow the diagnosis.
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http://dx.doi.org/10.1148/rg.306105519 | DOI Listing |
Nutrients
December 2024
Department of Nutrition, Georgia State University, 140 Decatur St SE, Atlanta, GA 30303, USA.
Dietary sulfur amino acid restriction (SAAR) elicits various health benefits, some mediated by fibroblast growth factor 21 (FGF21). However, research on SAAR's effects on the heart is limited and presents mixed findings. This study aimed to evaluate SAAR-induced molecular alterations associated with cardiac remodeling and their dependence on FGF21.
View Article and Find Full Text PDFNutrients
December 2024
Department of Food and Nutrition, Obesity/Diabetes Research Center, Hoseo University, 20 Hoseoro97bungil, BaeBang-Yup, Asan 31499, Republic of Korea.
Background: Myocardial infarction (MI) can range from mild to severe cardiovascular events and typically develops through complex interactions between genetic and lifestyle factors.
Objectives: We aimed to understand the genetic predisposition associated with MI through genetic correlation, colocalization analysis, and cells' gene expression values to develop more effective prevention and treatment strategies to reduce its burden.
Methods: A polygenic risk score (PRS) was employed to estimate the genetic risk for MI and to analyze the dietary interactions with PRS that affect MI risk in adults over 45 years ( = 58,701).
Int J Mol Sci
December 2024
Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA.
Hutchinson-Gilford progeria syndrome (HGPS) is a pediatric condition characterized by clinical features that resemble accelerated aging. The abnormal accumulation of a toxic form of the lamin A protein known as progerin disrupts cellular functions, leading to various complications, including growth retardation, loss of subcutaneous fat, abnormal skin, alopecia, osteoporosis, and progressive joint contractures. Death primarily occurs as the result of complications from progressive atherosclerosis, especially from cardiac disease, such as myocardial infarction or heart failure, or cerebrovascular disease like stroke.
View Article and Find Full Text PDFClin Transl Med
January 2025
Key Laboratory For Organ Failure Research, Ministry of Education of the People's Republic of China, Guangzhou, China.
Introduction: Heart failure with preserved ejection fraction (HFpEF) is a complex condition characterized by metabolic dysfunction and myocardial lipotoxicity. The roles of PTEN-induced kinase 1 (PINK1) and peroxiredoxin-2 (Prdx2) in HFpEF pathogenesis remain unclear.
Objective: This study aimed to investigate the interaction between PINK1 and Prdx2 to mitigate cardiac diastolic dysfunction in HFpEF.
Cardiovasc Diabetol
January 2025
Department of Clinical Pharmacy, School of Preclinical Medicine and Clinical Pharmacy, China Pharmaceutical University, 24 Tong jia Lane, Nanjing, 210009, People's Republic of China.
Background: Inflammatory diseases impair the reparative properties of endothelial progenitor cells (EPC); however, the involvement of diabetes in EPC dysfunction associated with myocardial infarction (MI) remains unknown.
Methods: A model was established combining high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic mice with myocardial infarction. The therapeutic effects of transplanted wild-type EPC, Nlrp3 knockout EPC, and Nlrp3 overexpression EPC were evaluated.
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