Mechanisms Underlying Antiarrhythmic Properties of Cardioprotective Agents Impacting Inflammation and Oxidative Stress.

Katarina Andelova,Miroslav Barancik,Barbara Szeiffova Bacova,Narcis Tribulova,Peter Hlivak,Matus Sykora

doi:10.3390/ijms23031416

Katarina Andelova, Miroslav Barancik + Show 4 more

Open Access

https://doi.org/10.3390/ijms23031416

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Abstract

The prevention of cardiac life-threatening ventricular fibrillation and stroke-provoking atrial fibrillation remains a serious global clinical issue, with ongoing need for novel approaches. Numerous experimental and clinical studies suggest that oxidative stress and inflammation are deleterious to cardiovascular health, and can increase heart susceptibility to arrhythmias. It is quite interesting, however, that various cardio-protective compounds with antiarrhythmic properties are potent anti-oxidative and anti-inflammatory agents. These most likely target the pro-arrhythmia primary mechanisms. This review and literature-based analysis presents a realistic view of antiarrhythmic efficacy and the molecular mechanisms of current pharmaceuticals in clinical use. These include the sodium-glucose cotransporter-2 inhibitors used in diabetes treatment, statins in dyslipidemia and naturally protective omega-3 fatty acids. This approach supports the hypothesis that prevention or attenuation of oxidative and inflammatory stress can abolish pro-arrhythmic factors and the development of an arrhythmia substrate. This could prove a powerful tool of reducing cardiac arrhythmia burden.

Highlights

Cardiac arrhythmias remain a serious global clinical issue
The following chapters present updated findings on the antiarrhythmic properties and the established and putative underlying mechanisms of: (1) the sodium-glucose transport protein 2 inhibitor (SGLT2i) novel drug for diabetes treatment; (2) the statins, and especially atorvastatin, which are the most widespread long-standing treatment for dyslipidemia and (3) natural cardio-protective omega-3 FA used in numerous clinical trials
Rosuvastatin reduced autonomic nerve-sprouting combined with decreased mRNA and tyrosine hydroxylase protein expression levels in atrial tissues following acute myocardial infarction [180]. These findings provide understanding of the mechanism statins use to decrease the risk of atrial fibrillation (AF) occurrence after heart attack

Summary

Introduction

Cardiac arrhythmias remain a serious global clinical issue. The current treatment of stroke-provoking atrial fibrillation (AF) and life-threatening ventricular fibrillation (VF) employs invasive approaches with implanted cardioversion devices and catheter ablation of pro-arrhythmic triggers [1,2,3,4,5,6,7,8]. While many of the cardio-protective compounds which exhibit antiarrhythmic properties are potent anti-oxidative and anti-inflammatory agents [13,20,21,22,23] These most likely target the primary mechanisms of pro-arrhythmia. The clinical benefits of inflammation-and redox-related therapies [10,32,33] can be achieved by personalized medicine, and this will provide innovative approaches for precision medicine This focused review-article highlights the growing mechanistic link between inflammation and oxidative stress and arrhythmogenesis, and outlines the established and putative mechanisms which underlie the antiarrhythmic properties of selected compounds acknowledged to influence inflammation and oxidative stress. It is emphasized that a healthy lifestyle which avoids cardiovascular risk factors, with their attendant inflammation and oxidative stress, is highly effective in preventing the occurrence of both atrial and ventricular arrhythmias

Inflammation and Redox Disorders Linked with Cardiac Arrhythmia Burden

Antiarrhythmic Efficacy of SGLT2 Inhibitors

Antiarrhythmic Efficacy of Statins

Antiarrhythmic Efficacy of Omega-3 Fatty Acids

Findings

Conclusions