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Hunting for Prospective Molecular Approaches to Prevent Cardiac Arrhythmias
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Hunting for Prospective Molecular Approaches to Prevent Cardiac Arrhythmias

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 April 2025 | Viewed by 13741

Special Issue Editor

Dr. Narcis Tribulova

E-Mail Website
Guest Editor
Centre of Experimental Medicine, Institute for Heart Research, Slovak Academy of Sciences, 84104 Bratislava, Slovakia
Interests: inflammation; redox disorder; heart diseases; arrhythmia substrate; cardiac connexin-43; Cx-hemichannels; antiarrhythmic mechanisms of tested agents; omega-3 fatty acids; melatonin
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The prevention and management of cardiac rhythm disorders, including atrial and ventricular fibrillation, is still a hot topic in clinical medicine. The heart is an electromechanical pump, and its function involves complex and coordinated activity. Asynchrony in these events promotes the development of life-threatening cardiac arrhythmias. Thus, therapies for prevention and treatment require a fundamental understanding and the ability to visualize, perturb and control cardiac electrical activity. Accordingly, continuous efforts are being made to reveal pro-arrhythmia triggers and to determine pro-arrhythmia markers in specific cardiac conditions. In turn, research is being conducted to explore new approaches for rhythm control and the prevention/attenuation of dysrhythmias in jeopardized heart. The outcomes of this research may include novel insights into current cardio-protective agents or natural compounds exhibiting antiarrhythmic potential, as well as epigenetic approaches.

Dr. Narcis Tribulova
Guest Editor

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Keywords

  • inflamed and stressed heart
  • pro-arrhythmic autonomic misbalance
  • pro-arrhythmic hormone misbalance
  • cardiac channelopathies
  • connexins and hemichannels
  • conduction disturbances
  • novel anti-arrhythmic targets
  • multitargeted strategies
  • non-invasive antiarrhythmic approaches
  • antiarrhythmic potential of cardioprotective drugs

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Published Papers (6 papers)

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Research

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16 pages, 3007 KiB  
Article
Blockade of Melatonin Receptors Abolishes Its Antiarrhythmic Effect and Slows Ventricular Conduction in Rat Hearts
by Aleksandra V. Durkina, Barbara Szeiffova Bacova, Olesya G. Bernikova, Mikhail A. Gonotkov, Ksenia A. Sedova, Julie Cuprova, Marina A. Vaykshnorayte, Emiliano R. Diez, Natalia J. Prado and Jan E. Azarov
Int. J. Mol. Sci. 2023, 24(15), 11931; https://doi.org/10.3390/ijms241511931 - 25 Jul 2023
Cited by 2 | Viewed by 1926
Abstract
Melatonin has been reported to cause myocardial electrophysiological changes and prevent ventricular tachycardia or fibrillation (VT/VF) in ischemia and reperfusion. We sought to identify electrophysiological targets responsible for the melatonin antiarrhythmic action and to explore whether melatonin receptor-dependent pathways or its antioxidative properties [...] Read more.
Melatonin has been reported to cause myocardial electrophysiological changes and prevent ventricular tachycardia or fibrillation (VT/VF) in ischemia and reperfusion. We sought to identify electrophysiological targets responsible for the melatonin antiarrhythmic action and to explore whether melatonin receptor-dependent pathways or its antioxidative properties are essential for these effects. Ischemia was induced in anesthetized rats given a placebo, melatonin, and/or luzindole (MT1/MT2 melatonin receptor blocker), and epicardial mapping with reperfusion VT/VFs assessment was performed. The oxidative stress assessment and Western blotting analysis were performed in the explanted hearts. Transmembrane potentials and ionic currents were recorded in cardiomyocytes with melatonin and/or luzindole application. Melatonin reduced reperfusion VT/VF incidence associated with local activation time in logistic regression analysis. Melatonin prevented ischemia-related conduction slowing and did not change the total connexin43 (Cx43) level or oxidative stress markers, but it increased the content of a phosphorylated Cx43 variant (P-Cx43368). Luzindole abolished the melatonin antiarrhythmic effect, slowed conduction, decreased total Cx43, protein kinase Cε and P-Cx43368 levels, and the IK1 current, and caused resting membrane potential (RMP) depolarization. Neither melatonin nor luzindole modified INa current. Thus, the antiarrhythmic effect of melatonin was mediated by the receptor-dependent enhancement of impulse conduction, which was associated with Cx43 phosphorylation and maintaining the RMP level. Full article
(This article belongs to the Special Issue Hunting for Prospective Molecular Approaches to Prevent Cardiac Arrhythmias)
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11 pages, 1502 KiB  
Article
Pro-Arrhythmic Potential of Accumulated Uremic Toxins Is Mediated via Vulnerability of Action Potential Repolarization
by Willem B. van Ham, Carlijn M. Cornelissen, Elizaveta Polyakova, Stephanie M. van der Voorn, Merel L. Ligtermoet, Jantine Monshouwer-Kloots, Marc A. Vos, Alexandre Bossu, Eva van Rooij, Marcel A. G. van der Heyden and Toon A. B. van Veen
Int. J. Mol. Sci. 2023, 24(6), 5373; https://doi.org/10.3390/ijms24065373 - 11 Mar 2023
Cited by 2 | Viewed by 1657
Abstract
Chronic kidney disease (CKD) is represented by a diminished filtration capacity of the kidneys. End-stage renal disease patients need dialysis treatment to remove waste and toxins from the circulation. However, endogenously produced uremic toxins (UTs) cannot always be filtered during dialysis. UTs are [...] Read more.
Chronic kidney disease (CKD) is represented by a diminished filtration capacity of the kidneys. End-stage renal disease patients need dialysis treatment to remove waste and toxins from the circulation. However, endogenously produced uremic toxins (UTs) cannot always be filtered during dialysis. UTs are among the CKD-related factors that have been linked to maladaptive and pathophysiological remodeling of the heart. Importantly, 50% of the deaths in dialysis patients are cardiovascular related, with sudden cardiac death predominating. However, the mechanisms responsible remain poorly understood. The current study aimed to assess the vulnerability of action potential repolarization caused by exposure to pre-identified UTs at clinically relevant concentrations. We exposed human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and HEK293 chronically (48 h) to the UTs indoxyl sulfate, kynurenine, or kynurenic acid. We used optical and manual electrophysiological techniques to assess action potential duration (APD) in the hiPSC-CMs and recorded IKr currents in stably transfected HEK293 cells (HEK-hERG). Molecular analysis of KV11.1, the ion channel responsible for IKr, was performed to further understand the potential mechanism underlying the effects of the UTs. Chronic exposure to the UTs resulted in significant APD prolongation. Subsequent assessment of the repolarization current IKr, often most sensitive and responsible for APD alterations, showed decreased current densities after chronic exposure to the UTs. This outcome was supported by lowered protein levels of KV11.1. Finally, treatment with an activator of the IKr current, LUF7244, could reverse the APD prolongation, indicating the potential modulation of electrophysiological effects caused by these UTs. This study highlights the pro-arrhythmogenic potential of UTs and reveals a mode of action by which they affect cardiac repolarization. Full article
(This article belongs to the Special Issue Hunting for Prospective Molecular Approaches to Prevent Cardiac Arrhythmias)
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9 pages, 2931 KiB  
Communication
SCN5A Variants as Genetic Arrhythmias Triggers for Familial Bileaflet Mitral Valve Prolapse
by Hager Jaouadi, Alexis Théron, Jérôme Hourdain, Hélène Martel, Karine Nguyen, Raja Habachi, Jean-Claude Deharo, Frédéric Collart, Jean-François Avierinos and Stéphane Zaffran
Int. J. Mol. Sci. 2022, 23(22), 14447; https://doi.org/10.3390/ijms232214447 - 21 Nov 2022
Cited by 2 | Viewed by 1480
Abstract
Mitral valve prolapse (MVP) is a common valvular heart defect with variable outcomes. Several studies reported MVP as an underestimated cause of life-threatening arrhythmias and sudden cardiac death (SCD), mostly in young adult women. Herein, we report a clinical and genetic investigation of [...] Read more.
Mitral valve prolapse (MVP) is a common valvular heart defect with variable outcomes. Several studies reported MVP as an underestimated cause of life-threatening arrhythmias and sudden cardiac death (SCD), mostly in young adult women. Herein, we report a clinical and genetic investigation of a family with bileaflet MVP and a history of syncopes and resuscitated sudden cardiac death. Using family based whole exome sequencing, we identified two missense variants in the SCN5A gene. A rare variant SCN5A:p.Ala572Asp and the well-known functional SCN5A:p.His558Arg polymorphism. Both variants are shared between the mother and her daughter with a history of resuscitated SCD and syncopes, respectively. The second daughter with prodromal MVP as well as her healthy father and sister carried only the SCN5A:p.His558Arg polymorphism. Our study is highly suggestive of the contribution of SCN5A mutations as the potential genetic cause of the electric instability leading to ventricular arrhythmias in familial MVP cases with syncope and/or SCD history. Full article
(This article belongs to the Special Issue Hunting for Prospective Molecular Approaches to Prevent Cardiac Arrhythmias)
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9 pages, 787 KiB  
Article
ECG Markers of Acute Melatonin Treatment in a Porcine Model of Acute Myocardial Ischemia
by Olesya G. Bernikova, Alena S. Tsvetkova, Alexey O. Ovechkin, Marina M. Demidova, Jan E. Azarov and Pyotr G. Platonov
Int. J. Mol. Sci. 2022, 23(19), 11800; https://doi.org/10.3390/ijms231911800 - 5 Oct 2022
Cited by 3 | Viewed by 1772
Abstract
In myocardial ischemia, melatonin confers antiarrhythmic action, but its electrocardiographic expression is unclear. We aimed to evaluate the effects of melatonin treatment on electrocardiogram (ECG) parameters reflecting major arrhythmogenic factors and to test the association of these parameters with ventricular fibrillation (VF) incidence. [...] Read more.
In myocardial ischemia, melatonin confers antiarrhythmic action, but its electrocardiographic expression is unclear. We aimed to evaluate the effects of melatonin treatment on electrocardiogram (ECG) parameters reflecting major arrhythmogenic factors and to test the association of these parameters with ventricular fibrillation (VF) incidence. Myocardial ischemia was induced by 40 min coronary artery occlusion in 25 anesthetized pigs. After induction of ischemia, 12 and 13 animals were given melatonin or placebo, respectively. Twelve-lead ECGs were recorded and durations of QRS, QT, Tpeak-Tend intervals and extrasystolic burden were measured at baseline and during occlusion. During ischemia, VF episodes clustered into early and delayed phases (<10 and >20 min, respectively), and QRS duration was associated with VF incidence. QT interval and extrasystolic burden did not differ between the groups. The Tpeak-Tend interval was progressively prolonged, and the prolongation was less pronounced in the treated animals. QRS duration increased, demonstrating two maxima (5–10 and 25 min, respectively). In the melatonin group, the earlier maximum was blunted, and VF development in this period was prevented. Thus, acute melatonin treatment prevented excessive prolongation of the QRS and Tpeak-Tend intervals in the porcine myocardial infarction model, and QRS duration can be used for the assessment of antiarrhythmic action of melatonin. Full article
(This article belongs to the Special Issue Hunting for Prospective Molecular Approaches to Prevent Cardiac Arrhythmias)
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Review

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21 pages, 10338 KiB  
Review
Connexin43, A Promising Target to Reduce Cardiac Arrhythmia Burden in Pulmonary Arterial Hypertension
by Matus Sykora, Barbara Szeiffova Bacova, Katarina Andelova, Tamara Egan Benova, Adriana Martiskova, Lin-Hai Kurahara, Katsuya Hirano and Narcis Tribulova
Int. J. Mol. Sci. 2024, 25(6), 3275; https://doi.org/10.3390/ijms25063275 - 14 Mar 2024
Viewed by 2025
Abstract
While essential hypertension (HTN) is very prevalent, pulmonary arterial hypertension (PAH) is very rare in the general population. However, due to progressive heart failure, prognoses and survival rates are much worse in PAH. Patients with PAH are at a higher risk of developing [...] Read more.
While essential hypertension (HTN) is very prevalent, pulmonary arterial hypertension (PAH) is very rare in the general population. However, due to progressive heart failure, prognoses and survival rates are much worse in PAH. Patients with PAH are at a higher risk of developing supraventricular arrhythmias and malignant ventricular arrhythmias. The latter underlie sudden cardiac death regardless of the mechanical cardiac dysfunction. Systemic chronic inflammation and oxidative stress are causal factors that increase the risk of the occurrence of cardiac arrhythmias in hypertension. These stressful factors contribute to endothelial dysfunction and arterial pressure overload, resulting in the development of cardiac pro-arrhythmic conditions, including myocardial structural, ion channel and connexin43 (Cx43) channel remodeling and their dysfunction. Myocardial fibrosis appears to be a crucial proarrhythmic substrate linked with myocardial electrical instability due to the downregulation and abnormal topology of electrical coupling protein Cx43. Furthermore, these conditions promote ventricular mechanical dysfunction and heart failure. The treatment algorithm in HTN is superior to PAH, likely due to the paucity of comprehensive pathomechanisms and causal factors for a multitargeted approach in PAH. The intention of this review is to provide information regarding the role of Cx43 in the development of cardiac arrhythmias in hypertensive heart disease. Furthermore, information on the progress of therapy in terms of its cardioprotective and potentially antiarrhythmic effects is included. Specifically, the benefits of sodium glucose co-transporter inhibitors (SGLT2i), as well as sotatercept, pirfenidone, ranolazine, nintedanib, mirabegron and melatonin are discussed. Discovering novel therapeutic and antiarrhythmic strategies may be challenging for further research. Undoubtedly, such research should include protection of the heart from inflammation and oxidative stress, as these are primary pro-arrhythmic factors that jeopardize cardiac Cx43 homeostasis, the integrity of intercalated disk and extracellular matrix, and, thereby, heart function. Full article
(This article belongs to the Special Issue Hunting for Prospective Molecular Approaches to Prevent Cardiac Arrhythmias)
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15 pages, 560 KiB  
Review
Left Ventricular Hypertrophy and Ventricular Tachyarrhythmia: The Role of Biomarkers
by Ljuba Bacharova, Marta Kollarova, Branislav Bezak and Allan Bohm
Int. J. Mol. Sci. 2023, 24(4), 3881; https://doi.org/10.3390/ijms24043881 - 15 Feb 2023
Cited by 5 | Viewed by 4084
Abstract
Left ventricular hypertrophy (LVH) refers to a complex rebuilding of the left ventricle that can gradually lead to serious complications—heart failure and life-threatening ventricular arrhythmias. LVH is defined as an increase in the size of the left ventricle (i.e., anatomically), therefore the basic [...] Read more.
Left ventricular hypertrophy (LVH) refers to a complex rebuilding of the left ventricle that can gradually lead to serious complications—heart failure and life-threatening ventricular arrhythmias. LVH is defined as an increase in the size of the left ventricle (i.e., anatomically), therefore the basic diagnosis detecting the increase in the LV size is the domain of imaging methods such as echocardiography and cardiac magnetic resonance. However, to evaluate the functional status indicating the gradual deterioration of the left ventricular myocardium, additional methods are available approaching the complex process of hypertrophic remodeling. The novel molecular and genetic biomarkers provide insights on the underlying processes, representing a potential basis for targeted therapy. This review summarizes the spectrum of the main biomarkers employed in the LVH valuation. Full article
(This article belongs to the Special Issue Hunting for Prospective Molecular Approaches to Prevent Cardiac Arrhythmias)
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