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Heart Rhythm Dec 2023
Topics: Humans; Arrhythmias, Cardiac; Arrhythmogenic Right Ventricular Dysplasia
PubMed: 37709107
DOI: 10.1016/j.hrthm.2023.09.006 -
Circulation. Arrhythmia and... Feb 2024
Topics: Humans; Ventricular Fibrillation; Artificial Intelligence; Heart Arrest; Arrhythmias, Cardiac; Death, Sudden, Cardiac
PubMed: 38318697
DOI: 10.1161/CIRCEP.124.012760 -
Biomedicine & Pharmacotherapy =... Dec 2023Arrhythmia is one of the most common cardiovascular diseases. The search for new drugs to suppress various types of cardiac arrhythmias has always been the focus of... (Review)
Review
Arrhythmia is one of the most common cardiovascular diseases. The search for new drugs to suppress various types of cardiac arrhythmias has always been the focus of attention. In the past decade, the screening of antiarrhythmic active substances from plants has received extensive attention. These natural compounds have obvious antiarrhythmic effects, and chemical modifications based on natural compounds have greatly increased their pharmacological properties. The chemical modification of botanical antiarrhythmic drugs is closely related to the development of new and promising drugs. Therefore, the structural characteristics and action targets of natural compounds with antiarrhythmic effects are reviewed in this paper, so that pharmacologists can select antiarrhythmic lead compounds from natural compounds based on the disease target - chemical structural characteristics.
Topics: Humans; Anti-Arrhythmia Agents; Biological Products; Arrhythmias, Cardiac
PubMed: 37897974
DOI: 10.1016/j.biopha.2023.115762 -
Current Problems in Cardiology Sep 2023Arrhythmogenic cardiomyopathy (ACM) is a disease characterized by a progressive replacement of myocardium by fibro-adipose material, predisposing to ventricular... (Review)
Review
Arrhythmogenic cardiomyopathy (ACM) is a disease characterized by a progressive replacement of myocardium by fibro-adipose material, predisposing to ventricular arrhythmias (VA) and sudden cardiac death (SCD). Its prevalence is estimated at 1:2000 to 1:5000, with a higher incidence in males, and clinical onset is usually between the 2nd and 4th decade of life. The prevalence of ACM in SCD victims is relatively high, making it one of the most common etiologies in young patients with SCD, especially if they are athletes. Cardiac events occur more frequently in individuals with ACM who participate in competitive sports and/or high-intensity training. In effect, exercise activity can worsen RV function in cases of hereditary ACM. Estimating the incidence of SCD caused by ACM in athletes remains challenging, being reported frequency ranging from 3% to 20%. Here, we review the potential implications of exercising on the clinical course of the classical genetic form of ACM, as well as the diagnostic tools, risk stratification, and the different therapeutic tools available for managing ACM.
Topics: Male; Humans; Arrhythmias, Cardiac; Death, Sudden, Cardiac; Myocardium; Cardiomyopathies; Athletes; Arrhythmogenic Right Ventricular Dysplasia
PubMed: 37172878
DOI: 10.1016/j.cpcardiol.2023.101799 -
Journal of the American College of... Jul 2023Implantable cardioverter-defibrillators (ICDs) represent transformational technology, arguably the most significant advance in cardiovascular medicine in 50 years. The... (Review)
Review
Implantable cardioverter-defibrillators (ICDs) represent transformational technology, arguably the most significant advance in cardiovascular medicine in 50 years. The vision and determination of pioneers Mirowski and Mower was fundamental to this monumental achievement, working with limited resources and confronted by skepticism/criticism from medical establishment. The inventors were followed >35 years in which a multitude of innovative clinical scientists and engineers introduced technological advances leading to the sophisticated devices in practice today. A pivotal patient experiment with automated termination of ventricular fibrillation (1980) led to U.S. Food and Drug Administration approval. Transvenous lead systems converted ICDs from thoracotomy-based secondary prevention to primary prevention of sudden death devices in countless patients worldwide. ICD acceptance was solidified by prospective randomized controlled trials showing reduced mortality superior to antiarrhythmic drugs. ICDs eventually expanded from coronary disease to inherited arrhythmia conditions (eg, hypertrophic cardiomyopathy). The ICD breakthrough story demonstrates how significant progress is possible in medicine against all odds, given fearless imagination to pursue novel ideas that conflict with accepted wisdom.
Topics: Humans; Defibrillators, Implantable; Prospective Studies; Death, Sudden, Cardiac; Ventricular Fibrillation; Arrhythmias, Cardiac
PubMed: 37468191
DOI: 10.1016/j.jacc.2023.04.056 -
Journal of the American College of... Sep 2023Patients with congenital heart disease associated with a higher risk for ventricular arrhythmias (VA) and sudden cardiac death (SCD) can be divided conceptually into... (Review)
Review
Patients with congenital heart disease associated with a higher risk for ventricular arrhythmias (VA) and sudden cardiac death (SCD) can be divided conceptually into those with discrete mechanisms for reentrant monomorphic ventricular tachycardia (VT) (Group A) and those with more diffuse substrates (Group B). Part I of this review addresses Group A lesions, which predominantly consist of tetralogy of Fallot and related variants. Well-defined anatomic isthmuses for reentrant monomorphic VT are interposed between surgical scars and the pulmonary or tricuspid annulus. The most commonly implicated critical isthmus for VT is the conal septum that divides subpulmonary from subaortic outlets. Programmed ventricular stimulation can be helpful in risk stratification. Although catheter ablation is not generally considered an alternative to the implantable cardioverter-defibrillator (ICD) for prevention of SCD, emerging data suggest that there is a subset of carefully selected patients who may not require ICDs after successful monomorphic VT ablation.
Topics: Humans; Adult; Arrhythmias, Cardiac; Death, Sudden, Cardiac; Heart Defects, Congenital; Catheter Ablation; Defibrillators, Implantable
PubMed: 37673512
DOI: 10.1016/j.jacc.2023.06.034 -
Biomedicine & Pharmacotherapy =... Sep 2023Cardiac ventricular arrhythmia triggered by acute myocardial infarction (AMI) is a major cause of sudden cardiac death. We have reported previously that an increased...
Cardiac ventricular arrhythmia triggered by acute myocardial infarction (AMI) is a major cause of sudden cardiac death. We have reported previously that an increased serum level of circular RNA CDR1as is a potential biomarker of AMI. However, the possible role of CDR1as in post-infarct arrhythmia remains unclear. This study in MI mice investigated the effects and underlying mechanism of CDR1as in ventricular arrhythmias associated with MI. We showed that knockdown of CDR1as abbreviated the duration of the abnormally prolonged QRS complex and QTc intervals and decreased susceptibility to ventricular arrhythmias. Optical mapping demonstrated knockdown of CDR1as also reduced post-infarct arrhythmia by increasing the conduction velocity and decreasing dispersion of repolarization. Mechanistically, CDR1as led to the depletion of NAD and caused mitochondrial dysfunction by directly targeting the NAMPT protein and repressing its expression. Moreover, CDR1as aggravated dysregulation of the Na1.5 and Kir6.2 channels in cardiomyocytes, a change which was alleviated by the replenishment of NAD. These findings suggest that anti-CDR1as is a potential therapeutic approach for ischemic arrhythmias.
Topics: Mice; Animals; NAD; Nicotinamide Phosphoribosyltransferase; Arrhythmias, Cardiac; Myocardial Infarction; Death, Sudden, Cardiac
PubMed: 37542851
DOI: 10.1016/j.biopha.2023.115267 -
Heart (British Cardiac Society) Jun 2024
Review
Topics: Humans; Pregnancy; Female; Pregnancy Complications, Cardiovascular; Arrhythmias, Cardiac; Anti-Arrhythmia Agents; Electrocardiography
PubMed: 37993263
DOI: 10.1136/heartjnl-2023-322746 -
Pharmacology & Therapeutics Apr 2024Inherited cardiac arrhythmias are a group of genetic diseases predisposing to sudden cardiac arrest, mainly resulting from variants in genes encoding cardiac ion... (Review)
Review
Inherited cardiac arrhythmias are a group of genetic diseases predisposing to sudden cardiac arrest, mainly resulting from variants in genes encoding cardiac ion channels or proteins involved in their regulation. Currently available therapeutic options (pharmacotherapy, ablative therapy and device-based therapy) can not preclude the occurrence of arrhythmia events and/or provide complete protection. With growing understanding of the genetic background and molecular mechanisms of inherited cardiac arrhythmias, advancing insight of stem cell technology, and development of vectors and delivery strategies, gene therapy and stem cell therapy may be promising approaches for treatment of inherited cardiac arrhythmias. Recent years have witnessed impressive progress in the basic science aspects and there is a clear and urgent need to be translated into the clinical management of arrhythmic events. In this review, we present a succinct overview of gene and cell therapy strategies, and summarize the current status of gene and cell therapy. Finally, we discuss future directions for implementation of gene and cell therapy in the therapy of inherited cardiac arrhythmias.
Topics: Humans; Arrhythmias, Cardiac; Death, Sudden, Cardiac; Ion Channels; Cell- and Tissue-Based Therapy
PubMed: 38301770
DOI: 10.1016/j.pharmthera.2024.108596 -
Life Sciences Dec 2023Maladaptive ventricular remodeling is a major cause of ventricular arrhythmias following myocardial infarction (MI) and adversely impacts the quality of life of affected...
AIMS
Maladaptive ventricular remodeling is a major cause of ventricular arrhythmias following myocardial infarction (MI) and adversely impacts the quality of life of affected patients. Vericiguat is a new soluble guanylate cyclase (sGC) activator with cardioprotective properties. However, its effects on MI-induced ventricular remodeling and arrhythmias are not fully comprehended; hence, our research evaluated the effect of vericiguat on mice post-MI.
MATERIALS AND METHODS
Mice were divided into four treatment groups: Sham, Sham+Veri, MI, and MI + Veri. For the MI groups and MI + Veri groups, the left anterior descending (LAD) coronary artery was occluded to induce MI. Conversely, the Sham group underwent mock surgery. Vericiguat was administered orally daily for 28 days to the Sham+Veri and MI + Veri groups. Additionally, H9c2 cells were cultured for further mechanistic studies. Assessment methods included echocardiography, pathological analysis, electrophysiological analysis, and Western blotting.
KEY FINDINGS
Vericiguat reduced cardiac dysfunction and infarct size after MI. It also mitigated MI-induced left ventricular fibrosis and cardiomyocyte apoptosis. Vericiguat normalized the expression of ion channel proteins (Kv4.3, Kv4.2, Kv2.1, Kv1.5, Kv7.1, KCNH2, Cav1.2) and the gap junction protein connexin 43, reducing the susceptibility to ventricular arrhythmia. Vericiguat significantly inhibited MI-induced calcium/calmodulin-dependent protein kinase II (CaMKII) pathway activation in mice.
SIGNIFICANCE
Vericiguat alleviated MI-induced left ventricular adverse remodeling and arrhythmias through modulation of the CamkII signaling pathway.
Topics: Humans; Mice; Animals; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Ventricular Remodeling; Quality of Life; Myocardial Infarction; Arrhythmias, Cardiac; Signal Transduction
PubMed: 37866806
DOI: 10.1016/j.lfs.2023.122184