Contents


Preface

Knowledge of cardiac arrhythmias has significantly improved in the last several decades. Although most cases are benign and easy to evaluate and treat, arrhythmias are sometimes challenging to differentiate, requiring quick recognition and response. The worst-case scenario is a hemodynamically unstable arrhythmia that may lead to heart failure or cardiac arrest that necessitates cardiopulmonary

A translational approach means implementing laboratory science into real-life clinical practice. Improvements in the science of arrhythmias have led to a decrease in morbidity and even mortality. Efforts to understand arrhythmic mechanisms have led to experimental modelling of arrhythmogenesis. These models are based on hypoxic-ischemic reperfusion myocardial insult, arrhythmogenic stimulating factors induced by electrolyte imbalance or administration of certain drugs. Over the last fifteen years, new methods of genetic testing have been developed that reveal new hereditary factors behind arrhythmias (e.g., cardiomyopathies), though

The key to the effective and appropriate treatment of clinical arrhythmias is the identification of etiology. The classical diagnosis is based on a thorough analysis of the patient's ECG. Causative therapy is driven by further clinical examination, laboratory testing of blood samples, imaging studies (e.g., echocardiography, CT and MRI scans), and invasive cardiac procedures. Patients suffering from arrhythmic cardiac arrest require immediate diagnostics and therapeutics regardless of setting

This book contains eight chapters in which the contributing authors highlight special aspects of the current scientific knowledge on cardiac arrhythmias.

The molecular background of catecholaminergic and calcium-dependent ventricular tachycardias is a point of interest since the latter may lead to sudden cardiac death. Genetic mutations in components of the calcium signaling pathway may induce dysregulation of calcium leading to overload, and this may be the pathway to target for therapy. Ryanodine receptors could be useful interventional gates to prevent

The COVID-19 pandemic has devastated daily medical and social life. Affecting mainly the respiratory tract and causing acute respiratory distress syndrome (ARDS), COVID infection has direct and indirect effects on the heart itself via secondary thrombogenicity, ischemia, myocarditis, and electrical inhomogeneity. The newly developed antiviral agents have potential proarrhythmic effects with or without the ischemic insult of the myocardial tissue. This proarrhythmic burden spurred scientists to begin using an endo-, mid myo-, and epicardial myocyte anisotropic preparation model for testing the safety of the first-used "anti-COVID" agent hydroxychloroquine. The latter acts electrophysiologically differently on myocardial cells in hypokalemic, COVID-associated ischemic, or overdosed

resuscitation and complex intensive care.

genetics-driven therapy is still lacking.

in order to increase their chances of survival.

catecholaminergic ventricular arrhythmias.

circumstances.
