Ultrastructure of atrial cardiomyocytes in adrenalin myocardiodystrophy was studied in white rat experiments. Morphometrically, there was a reduced number of mitochondria and secretory granules in the atrial muscular cells, space characteristics of cardiomyocytes and their nuclei increased. The above rearrangement of the atrial cardiomyocytes indicates that adrenalin myocardiodystrophy is associated with a decline in synthetic and secretory function of the test cardiac muscular cells.
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NPJ Cardiovasc Health
December 2024
Department of Cardiology, Boston Children's Hospital, Boston, MA 02115, USA.
Atrial fibrillation (AF), the most common sustained arrhythmia, increases stroke and heart failure risks. Here we review genes linked to AF and mechanisms by which they alter AF risk. We highlight gene expression differences between atrial and ventricular cardiomyocytes, regulatory mechanisms responsible for these differences, and their potential contribution to AF.
View Article and Find Full Text PDFHeart Rhythm
January 2025
Department of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China; Xinjiang Key Laboratory of Cardiac Electrophysiology and Cardiac Remodeling, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China. Electronic address:
Pulsed-field ablation (PFA) offers notable advantages in atrial fibrillation (AF) ablation by selectively targeting cardiomyocytes via an irreversible electroporation mechanism, thereby minimizing damage to surrounding tissues. Although clinical studies demonstrate that PFA is both safe and effective, PFA-mediated hemolysis and potential acute kidney injury (AKI) development have been recently reported. This study comprehensively reviews the literature on PFA-associated hemolysis, analyzing the underlying mechanisms, risk factors, and preventive management strategies.
View Article and Find Full Text PDFCirc Genom Precis Med
January 2025
Centre for Heart Lung Innovation, University of British Columbia, Vancouver. (K.H., M.A., L.R., Y.L., A.S., H.H., L.R.B., Z.W.L.).
Background: Protein-truncating mutations in the titin gene are associated with increased risk of atrial fibrillation. However, little is known about the underlying pathophysiology.
Methods: We identified a heterozygous titin truncating variant (TTNtv) in a patient with unexplained early onset atrial fibrillation and normal ventricular function.
Int J Cardiol Heart Vasc
February 2025
Dept. of Cardiology, Erasmus University Medical Center, Rotterdam, the Netherlands.
Background: Areas of conduction disorders play an important role in both initiation and perpetuation of AF and can be recognized by specific changes in unipolar potential morphology. For example, EGM fractionation may be caused by asynchronous activation of adjacent cardiomyocytes because of structural barriers such as fibrotic strands. However, it is unknown whether there are sex differences in unipolar potential morphology.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Xinjiang Key Laboratory of Cardiac Electrophysiology and Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, China; Department of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830011, China. Electronic address:
Background: The antiarrhythmic effect of melatonin(MLT) has been demonstrated in several studies; however, this hypothesis has recently been contested. Our research seeks to determine if exogenous MLT supplementation can reduce atrial fibrillation (AF) susceptibility due to sleep deprivation (SD) by addressing Ca mishandling and atrial mitochondrial oxidative stress.
Methods: Adult rats received daily MLT or vehicle injections and were exposed to a modified water tank.
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