The authors made a retrospective analysis of case histories of 201 patients who had died of fatal cardiac arrhythmias. The predictors of their death were ventricular fibrillation in 133 (66.2%) patients, asystole in 68 (32.8%), electromechanical dissociation in 2 (1%). Terminal sinus tachycardia, atrial fibrillation and flutter, the second-third degree atrioventricular block, the third-fifth grade ventricular extrasystole were the most common clinical and electrocardiographic prodromes of ventricular fibrillation. In the development of the latter, various mixed disturbances of cardiac rhythm and conduction in combination with prolonged Q-T interval were of more unfavorable value. Asystole was more frequently preceded by the second-third degree atrioventricular block, complete bundle branch block, third-fifth grade ventricular extrasystole, atrial fibrillation and flutter, and various mixed disturbances of cardiac rhythm and conduction. Cardiac arrhythmias and conduction disturbance with prolonged Q-T interval were found to be precursors of asystole in 84.8%.
Download full-text PDF |
Source |
---|
Arrhythm Electrophysiol Rev
December 2024
Department of Medicine, Division of Cardiovascular Medicine, Vanderbilt University Medical Center Nashville, TN, US.
Idiopathic arrhythmias originating from the mitral and tricuspid annuli are commonly encountered in clinical practice. This review focuses on distinguishing features of ventricular arrhythmias arising from these structures and the importance of distinguishing idiopathic arrhythmias from those associated with structural heart disease. Each region along the mitral and tricuspid annuli (including the cardiac crux and para-Hisian region) is then discussed separately, with a particular emphasis on the ablation strategies and pitfalls for each.
View Article and Find Full Text PDFBackground: Patients with arrhythmogenic cardiomyopathy (ACM) due to pathogenic variants in , the gene for the desmosomal protein plakophilin-2, are being enrolled in gene therapy trials designed to replace the defective allele via adeno-associated viral (AAV) transduction of cardiac myocytes. Evidence from experimental systems and patients indicates that ventricular myocytes in ACM have greatly reduced electrical coupling at gap junctions and reduced Na current density. In previous AAV gene therapy trials, <50% of ventricular myocytes have generally been transduced.
View Article and Find Full Text PDFBackground: Long QT Syndrome Type-2 (LQT2) is due to loss-of-function variants. encodes K 11.1 that forms a delayed-rectifier potassium channel in the brain and heart.
View Article and Find Full Text PDFArrhythmogenic cardiomyopathy (ACM) is a genetic form of heart failure that affects 1 in 5000 people globally and is caused by mutations in cardiac desmosomal proteins including , and Individuals with ACM suffer from ventricular arrhythmias, sudden cardiac death, and heart failure. There are few effective treatments and heart transplantation remains the best option for many affected individuals. Here we performed single nucleus RNA sequencing (snRNAseq) and spatial transcriptomics on myocardial samples from patients with ACM and control donors.
View Article and Find Full Text PDFJ Korean Med Sci
January 2025
Division of Cardiology, Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Background: The ionic mechanism underlying Brugada syndrome (BrS) arises from an imbalance in transient outward current flow between the epicardium and endocardium. Previous studies report that artemisinin, originally derived from a Chinese herb for antimalarial use, inhibits the Ito current in canines. In a prior study, we showed the antiarrhythmic effects of artemisinin in BrS wedge preparation models.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!