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 resuscitation and complex intensive care.

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 genetics-driven therapy is still lacking.

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 in order to increase their chances of survival.

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 catecholaminergic ventricular arrhythmias.

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 circumstances.

Bradycardia and heart failure together may be treated by cardiac implantable electronic devices (CIEDs). The pacing provides a better hemodynamic response, which is the aim of treating heart failure when the near-physiologic pacing sites are selected. To date, the first choice of device therapy for heart failure and the wide QRS complex is cardiac resynchronization therapy. "New-old" pacing methods are also tested to achieve better cardiac performance. The concept of pacing the bundle of His or left bundle branch has had a renaissance in the last five years. Despite the obvious benefits of pacing through the natural pacing conduction system of the heart, there are controversies on the skill-based and technical possibilities of it, limiting the widespread usage of the method.

Many supraventricular tachycardic arrhythmias have anatomical foci or accessory pathways in the background proven by electrophysiological diagnostic procedures. Most of these e.g. atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, atrial flutter, and atrial fibrillation can be treated by radiofrequency ablation. Few types of ventricular arrhythmias are also candidates for radiofrequency ablation, but most of them are treated with an implantable cardioverter-defibrillator (ICD) in addition to antiarrhythmic drug treatment. ICD was developed for primary and secondary prevention of ventricular arrhythmias and sudden cardiac death (SCD).

Sudden cardiac arrest is a major cause of mortality in developed countries. The incidence of out-of-hospital cardiac arrest is between 60 and 170 per 100,000 persons worldwide. Since the medical team is not present at the time of circulatory collapse in most cases, survival depends on the awareness and training of the people around the patient when the arrest occurs. Therefore, it is important to emphasize the relevance of the knowledge of the non-medical public recognizing cardiac arrest and providing basic life support until the emergency medical team arrives. The program of public access to automated defibrillators has also improved SCD mortality. In the era of widespread media coverage, more focus has been placed on SCD among athletes. Extreme sports activity, increased adrenaline release, lactic acidosis, and volume-electrolyte shifts may trigger SCD, which may be the first sign of undiagnosed heart disease in apparently healthy athletes. New guidelines in sports medicine suggest thorough examination and screening for underlying asymptomatic cardiac disorders.

Arrhythmias may cause a peri-arrest state or cardiac arrest in the hospital, intensive care unit, or even during anesthesia. Most of these cases occur because of stress due to surgery or hemostasis, volume, and electrolyte disorders, which are to be treated or corrected during the treatment of malignant arrhythmias.

After successful resuscitation, when the patient has returned the spontaneous circulation (ROSC), a special global systemic-ischemic reperfusion syndrome-induced multiple organ dysfunction may develop, which is defined as post-cardiac arrest syndrome. All the causative reversible factors should be promptly recognized and corrected to avoid the relapse of circulatory arrest. To prevent ischemic-reperfusion brain injury, a neuroprotective target temperature management (formerly mild therapeutic hypothermia) is part of the intensive care of patients suffering from a long-standing no-flow or low-flow perfusion before ROSC. These patients need special post-resuscitation intensive care, sedation, mechanical ventilation, and temperature management. As such, prognosis is difficult to estimate during the first 72–120 hours. Special protocols for prognostication cover the clinical neurological judgment, EEG, imaging modalities, and special neuron-specific biomarkers.

**V**

In conclusion, the translational approach to cardiac arrhythmias highlights interesting aspects of arrhythmia mechanisms as well as diagnostic and therapeutic methods. This book emphasizes a quick, critical, and thorough response to arrhythmias to prevent further deterioration of the patient. Knowledge of the basic molecular, cellular, and clinical background of arrhythmias is the foundation of clinical

**Endre Zima MD, Ph.D., Dr. med. habil.**

Intensive Care Specialist and Cardiologist, Head of Cardiac Intensive Care Unit,

Consultant Anesthesiologist,

Heart and Vascular Center, Semmelweis University, Budapest, Hungary

Professor,

appraisal and treatment.

In conclusion, the translational approach to cardiac arrhythmias highlights interesting aspects of arrhythmia mechanisms as well as diagnostic and therapeutic methods. This book emphasizes a quick, critical, and thorough response to arrhythmias to prevent further deterioration of the patient. Knowledge of the basic molecular, cellular, and clinical background of arrhythmias is the foundation of clinical appraisal and treatment.
