It was previously thought that hypertrophic cardiomyopathy is the leading cause of sudden cardiac death in athletes. This was also extrapolated to the general population. Thereby, exercise was restrained in patients with hypertrophic cardiomyopathy. However, recent studies have shown that hypertrophic cardiomyopathy is not the main cause of sudden cardiac death, and moderate exercise is not only safe but beneficial for patients with hypertrophic cardiomyopathy. With the accumulation of evidence, relevant guidelines recommend low-intensity exercise from the beginning, then gradually recommend moderate-high intensity exercise for patients with hypertrophic cardiomyopathy. This suggests that we should rediscover the value of exercise in patients with hypertrophic cardiomyopathy. It is now widely accepted that patients with hypertrophic cardiomyopathy can benefit from the positive effects of exercise through an individualized exercise prescription based on a comprehensive assessment. This review summarizes the evidence showing patients with hypertrophic cardiomyopathy can exercise safely, and the methods to formulate related exercise prescriptions.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10262002 | PMC |
http://dx.doi.org/10.3724/zdxbyxb-2022-0323 | DOI Listing |
JACC Cardiovasc Imaging
January 2025
National Amyloidosis Centre, University College London, Royal Free Campus, Rowland Hill Street, London, United Kingdom.
Cardiac amyloidosis represents a unique disease process characterized by amyloid fibril deposition within the myocardial extracellular space. Advances in multimodality cardiac imaging enable accurate diagnosis and facilitate prompt initiation of disease-modifying therapies. Furthermore, rapid advances in multimodality imaging have enriched understanding of the underlying pathogenesis, enhanced prognostication, and resulted in the development of imaging-based markers that reflect the amyloid burden, which is of increasing importance when assessing the response to treatment.
View Article and Find Full Text PDFJACC Heart Fail
January 2025
Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia, USA. Electronic address:
Mol Ther
January 2025
Department of Biology, Concordia University, 7141 Sherbrooke St. W H4B 1R6, Montreal, Canada; Department of Physics, Concordia University, 7141 Sherbrooke St. W H4B 1R6, Montreal, Canada. Electronic address:
CRISPR-Cas9 ribonucleoproteins (RNPs) have been heavily considered for gene therapy due to their high on-target efficiency, rapid activity and lack of insertional mutagenesis relative to other CRISPR-Cas9 delivery formats. Genetic diseases such as hypertrophic cardiomyopathy currently lack effective treatment strategies and are prime targets for CRISPR-Cas9 gene editing technology. However, current in-vivo delivery strategies for Cas9 pose risks of unwanted immunogenic responses.
View Article and Find Full Text PDFJ Electrocardiol
December 2024
Crown Princess Victoria Children's Hospital, Dept of Biomedical and Clinical Sciences, Dept of Pediatrics, Linköping University, Sweden; Pediatric Heart Centre, Skåne University Hospital and Dept of Clinical Sciences, Lund University, Sweden. Electronic address:
Background: Myocardial fibrosis, expressed as late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR), is an important risk factor for malignant cardiac events in hypertrophic cardiomyopathy (HCM). However, CMR is not easily available, expensive, also needing intravenous access and contrast.
Objective: To determine if derived vectorcardiographic spatial QRS-T angles, an aspect of advanced ECG (A-ECG), can indicate LGE to appropriately prioritize young HCM-patients for CMR.
Eur Heart J
January 2025
Hypertrophic Cardiomyopathy Center, Department of Cardiology, Sakakibara Heart Institute, 3-16-1 Asahi-cho, Fuchu, Tokyo 183-0003, Japan.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!