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New options for young people with dyslipidemia: The future is bright!
Atherosclerosis
December 2024
Jesselson Integrated Heart Center, The Eisenberg R&D Authority, Shaare Zedek Medical Center and Faculty of Medicine, Hebrew University of Jerusalem, Israel.
In p53-deficient cancers, targeting cholesterol metabolism has emerged as a promising therapeutic approach, given that p53 loss dysregulates sterol regulatory element-binding protein 2 (SREBP-2) pathways, thereby enhancing cholesterol biosynthesis. While cholesterol synthesis inhibitors such as statins have shown initial success, their efficacy is often compromised by the development of acquired resistance. Consequently, new strategies are being explored to disrupt cholesterol homeostasis more comprehensively by inhibiting its synthesis and intracellular transport.
View Article and Find Full Text PDFAmerican society for preventive cardiology 2024 cardiovascular disease prevention: Highlights and key sessions.
Am J Prev Cardiol
March 2025
Division of Cardiology, Wake Forest University, Winston-Salem, NC, USA.
Groundbreaking strategies for preventive cardiology were showcased at the 2024 American Society for Preventive Cardiology (ASPC) Congress on Cardiovascular Disease (CVD) Prevention held in Salt Lake City, Utah, from August 2nd to 4th, 2024. The event featured 69 moderators and 13 scientific sessions comprised of 98 topics, 36 satellite events, 133 poster presentations, and 27 lifestyle classes. The conference highlighted innovative strategies focused on integrating cardiovascular, kidney, and metabolic health, presenting a cohesive approach for managing complex, interrelated conditions.
View Article and Find Full Text PDFFamilial hypercholesterolemia - Targeted whole gene sequencing as a diagnostic approach.
Atheroscler Plus
March 2025
Department of Laboratory Medicine, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Background And Aims: Familial hypercholesterolemia (FH) and other disorders with similar features are common genetic disorders that remain underdiagnosed and undertreated, due in part to the cost of screening. The aim of this study was to design and implement a whole gene targeted NGS panel for the molecular diagnosis of FH and statin intolerance with an emphasis on high quality variant calling, including copy number analysis.
Methods: A whole gene panel for hybridisation-based short read NGS was designed for the dominant FH-genes low density lipoprotein receptor (), apolipoprotein B (APOB), proproteinconvertas subtilisin/kexin type 9 (PCSK9), apolipoprotein E (APOE) and the recessive FH-genes low density lipoprotein receptor adaptor protein 1 (), ATP binding cassette subfamily member 5/8 (ABCG5/8) and lipase A, lysosomal acid type (), as well as solute carrier organic anion transporter family member 1B1 (), not an FH gene but linked to statin intolerance.
The impact of new-onset atrial fibrillation in the setting of acute coronary syndrome.
J Cardiol
January 2025
Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China; Kent and Medway Medical School, Canterbury, Kent, UK; School of Nursing and Health Studies, Hong Kong Metropolitan University, Hong Kong, China.
Approximately 10 % of patients who have suffered from myocardial infarction develop new-onset atrial fibrillation (AF). Coronary artery disease implicating atrial branches has been associated with AF. The following variables have been associated with new-onset AF in the setting of acute coronary syndrome: older age, history of hypertension, history of angina, history of stroke, chronic renal failure, body mass index, no statin use, worse nutritional status, worse Killip class, admission heart rate ≥ 85 bpm, complete atrioventricular block, Glasgow prognostic score, Syntax score, CHEST score > 3, PRECISE-DAPT score ≥ 25, left ventricular ejection fraction ≤40 %, increased left atrial diameter, E/E' ratio > 12, epicardial fat tissue thickness, and thrombolysis in myocardial infarction flow < 3.
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