Charles Antzelevitch – författare

This addition to the Clinical Approaches to Tachyarrhythmias (CATA) Series, written by the investigators who discovered and probed the Brugada Syndrome, discusses the history, etiology, pathology and clinical manifestations of sudden death. From diagnosis, prognosis, to therapeutic approaches using the latest in cathater ablation techniques, electrophysiological surgery, and genetic appraisal, the work is a testimony to the author''s investigation. Using clinical cases in Thailand and Laos, they further unravel the syndrome''s molecular mechanisms, studying related syndromes, such as the long-QT syndrome, infant death, and arryhthmogenic right ventricular cardiomyopathy.

By being informed of the electrophysiological abnormalities that contribute to familial and genetic diseases, physicians, cardiologists and all those who care for patients with cardiac arrhythmias will be better able to identify and treat patients in whom the Brugada Syndrome may strike next.

Electrical Disease of the Heart, 2nd Edition, volume 2, covers the diagnostic and treatment options available in the management of electrical diseases and with its companion volume provides the latest developments in the field of experimental and clinical cardiac electrophysiology, genetics, pharmacology and interventional therapies of various clinical arrhythmogenic entities. This book is highly relevant to a broad audience, ranging from medical and graduate students, to clinicians and scientists.

An understanding of basic science is crucial for physicians who treat heart rhythm disorders. This issue summarizes the basic science of arrhythmias, including both acquired and inherited heart rhythm disorders. The basic mechanisms of arrhythmia are reviewed as are the mechanisms of atrial fibrillation. The issue is an excellent refresher for practicing cardiac electrophysiologists as well as a helpful resource for residents and fellows.

"Electrical Diseases of the Heart: Genetics, Mechanisms, Treatment, Prevention" provides a unique contemporary and succinct distillation of the current status of recently delineated electrical diseases of the heart, emphasizing their common and diverse clinical features. The latest developments in the field of experimental and clinical cardiac electrophysiology, genetics, pharmacology and interventional therapies of various clinical arrhythmogenic entities are featured and discussed in terms of recent advances in basic and clinical science. The book is divided into 7 major parts. Each part consists of chapters (total of 64) dealing with related topics. Each chapter is outlined with objectives, key points, current perspectives, and recommendations for future investigations and includes established and evidence-based knowledge, the authors'' personal opinions, areas of controversy, and future trends.

J wave syndromes are one of the hottest topics in cardiology today. Cardiac arrhythmias associated with Brugada syndrome (BrS) or an early repolarization (ER) pattern in the inferior or infero-lateral ECG leads are thought to be mechanistically linked to accentuation of transient outward current (Ito)-mediated J waves. Although BrS and ER syndrome (ERS) differ with respect to magnitude and lead location of abnormal J waves, they are thought to represent a continuous spectrum of phenotypic expression termed J wave syndromes. ERS is divided into three subtypes with the most severe, Type 3, displaying an ER pattern globally in the inferior, lateral and right precordial leads. BrS has been linked to mutations in 19 different genes, whereas ERS has been associated with mutations in 7 different genes.

There is a great deal of confusion as to how to properly diagnose and treat the J wave syndromes as well as confusion about the underlying mechanisms. The demonstration of successful epicardial ablation of BrS has provided new therapeutic options for the management of this syndrome for which treatment alternatives are currently very limited, particularly in the case of electrical storms caused by otherwise uncontrollable recurrent VT/VF. An early repolarization pattern is observed in 2-5% of the US population. While it is clear that the vast majority of individuals exhibiting an ER pattern are not at risk for sudden cardiac death, the challenge moving forward is to identify those individuals who truly are at risk and to design safe and effective treatments.

J wave syndromes are one of the hottest topics in cardiology today. Cardiac arrhythmias associated with Brugada syndrome (BrS) or an early repolarization (ER) pattern in the inferior or infero-lateral ECG leads are thought to be mechanistically linked to accentuation of transient outward current (Ito)-mediated J waves. Although BrS and ER syndrome (ERS) differ with respect to magnitude and lead location of abnormal J waves, they are thought to represent a continuous spectrum of phenotypic expression termed J wave syndromes. ERS is divided into three subtypes with the most severe, Type 3, displaying an ER pattern globally in the inferior, lateral and right precordial leads. BrS has been linked to mutations in 19 different genes, whereas ERS has been associated with mutations in 7 different genes.

There is a great deal of confusion as to how to properly diagnose and treat the J wave syndromes as well as confusion about the underlying mechanisms. The demonstration of successful epicardial ablation of BrS has provided new therapeutic options for the management of this syndrome for which treatment alternatives are currently very limited, particularly in the case of electrical storms caused by otherwise uncontrollable recurrent VT/VF. An early repolarization pattern is observed in 2-5% of the US population. While it is clear that the vast majority of individuals exhibiting an ER pattern are not at risk for sudden cardiac death, the challenge moving forward is to identify those individuals who truly are at risk and to design safe and effective treatments.