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http://dx.doi.org/10.1161/CIRCULATIONAHA.124.066991 | DOI Listing |
Physiol Rep
January 2025
Department of Medicine, John A. Burns School of Medicine, University of Hawaii Mānoa, Honolulu, Hawaii, USA.
Inflammation and a metabolic shift from oxidative metabolism to glycolysis are common in the ischemic heart, the latter partly controlled by pyruvate kinase (muscle, PKM). We previously identified alternative splicing promoting the PKM2 isoform after myocardial infarction (MI). We examined the role of PKM2 physiological upregulation after MI, modeled by ligation of the left anterior descending coronary artery, using global PKM2 knockout (PKM2) mice.
View Article and Find Full Text PDFCureus
November 2024
Cardiology, Mount Sinai West Hospital, New York, USA.
The mechanism and severity of mitral valve (MV) regurgitation (MR) play a critical role in guiding treatment decisions. Transthoracic echocardiography (TTE) is the primary diagnostic modality for evaluating MV disease. Discordant findings on TTE can be further quantified through transesophageal echocardiography (TEE).
View Article and Find Full Text PDFFront Cardiovasc Med
December 2024
Chair of Preventive Pediatrics, Technical University of Munich, Munich, Germany.
[This corrects the article DOI: 10.3389/fcvm.2024.
View Article and Find Full Text PDFFront Cardiovasc Med
November 2024
Chair of Preventive Pediatrics, Technical University of Munich, Munich, Germany.
Cardio Vascular risk prevention in Germany has a gap between the ages of 20 and 30 years. We established a program for risk group identification in students and analyzed the screenings according to the ACCF/AHA Stages and NYHA functional classification. In a cross-sectional design, 596 participants completed a sports medical and motor performance check-up.
View Article and Find Full Text PDFEgypt Heart J
December 2024
Baqai Medical University, 51, Deh Tor, Gadap Road, Near Toll Plaza, SuperHighway,, P.O. Box 2407, Karachi, 75340, Sindh, Pakistan.
Background: A cardiac condition marked by excessive growth of heart muscle cells, hypertrophic cardiomyopathy (HCM) is a complex genetic disorder characterized by left ventricular hypertrophy, microvascular ischemia, myocardial fibrosis, and diastolic dysfunction. Obstructive hypertrophic cardiomyopathy (oHCM), a subset of HCM, involves significant obstruction in the left ventricular outflow tract (LVOT), leading to symptoms like dyspnea, fatigue, and potentially life-threatening cardiac events. With advancements in genetic understanding and the introduction of novel pharmacologic agents, including cardiac myosin inhibitors like mavacamten and aficamten, there is a paradigm shift in the therapeutic approach to oHCM.
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