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Aim: To study the associations between risk factors, clinical characteristics, severity of brachiocephalic artery (BCA) atherosclerosis and severity of coronary artery (CA) disease in patients with acute coronary syndrome (ACS).

Material And Methods: The study included patients with any type of ACS and obstructive coronary artery disease confirmed by coronary angiography. A quantitative analysis of coronary angiography data was performed with an assessment of the number of CAs with significant stenosis and calculation of the SYNTAX score.

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Our study aims to assess the robustness of myocardial radiomic texture features (RTF) to segmentation variability and variations across scanners with different field strengths, addressing concerns about reliability in clinical practices. We conducted a retrospective analysis on 45 pairs of CMR T1 maps from 15 healthy volunteers using 1.5 T and 3 T Siemens scanners.

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Hypervitaminosis D leads to toxic effects, including hypercalcemia, which can cause severe damage to various organs. Fetuin-A, a glycoprotein with anti-inflammatory properties, may protect tissues from such damage. This study explores the role of Fetuin-A in mitigating hypervitaminosis D-induced damage in renal, hepatic, and cardiac tissues.

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Background Ischemic late gadolinium enhancement (LGE) assessed with cardiac MRI is a well-established prognosticator in ischemic cardiomyopathy. However, the prognostic value of additional LGE parameters, such as extent, transmurality, location, and associated midwall LGE, remains unclear. Purpose To assess the prognostic value of ischemic LGE features to predict all-cause mortality in ischemic cardiomyopathy.

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Background: Myocardial fibrosis is a key healing response after myocardial infarction driven by activated fibroblasts. Gallium-68-labeled fibroblast activation protein inhibitor ([Ga]-FAPI) is a novel positron-emitting radiotracer that binds activated fibroblasts.

Objectives: The aim of this study was to investigate the intensity, distribution, and time-course of fibroblast activation after acute myocardial infarction.

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