What Is the Arrhythmic Substrate in Viral Myocarditis? Insights from Clinical and Animal Studies

Sudden cardiac death (SCD) remains an unsolved problem in the twenty-first century. It is often due to rapid onset, ventricular arrhythmias caused by a number of different clinical conditions. A proportion of SCD patients have identifiable diseases such as cardiomyopathies, but for others, the causes are unknown. Viral myocarditis is becoming increasingly recognized as a contributor to unexplained mortality, and is thought to be a major cause of SCD in the first two decades of life. Myocardial inflammation, ion channel dysfunction, electrophysiological, and structural remodeling may play important roles in generating life-threatening arrhythmias. The aim of this review article is to examine the electrophysiology of action potential conduction and repolarization and the mechanisms by which their derangements lead to triggered and reentrant arrhythmogenesis. By synthesizing experimental evidence from pre-clinical and clinical studies, a framework of how host (inflammation), and viral (altered cellular signaling) factors can induce ion electrophysiological and structural remodeling is illustrated. Current pharmacological options are mainly supportive, which may be accompanied by mechanical circulatory support. Heart transplantation is the only curative option in the worst case scenario. Future strategies for the management of viral myocarditis are discussed.GT was awarded a BBSRC Doctoral Training Award and thanks for the Croucher Foundation for its generous support

What Is the Arrhythmic Substrate in Viral Myocarditis? Insights from Clinical and Animal Studies

Sudden cardiac death (SCD) remains an unsolved problem in the twenty-first century. It is often due to rapid onset, ventricular arrhythmias caused by a number of different clinical conditions. A proportion of SCD patients have identifiable diseases such as cardiomyopathies, but for others, the causes are unknown. Viral myocarditis is becoming increasingly recognized as a contributor to unexplained mortality, and is thought to be a major cause of SCD in the first two decades of life. Myocardial inflammation, ion channel dysfunction, electrophysiological, and structural remodeling may play important roles in generating life-threatening arrhythmias. The aim of this review article is to examine the electrophysiology of action potential conduction and repolarization and the mechanisms by which their derangements lead to triggered and reentrant arrhythmogenesis. By synthesizing experimental evidence from pre-clinical and clinical studies, a framework of how host (inflammation), and viral (altered cellular signaling) factors can induce ion electrophysiological and structural remodeling is illustrated. Current pharmacological options are mainly supportive, which may be accompanied by mechanical circulatory support. Heart transplantation is the only curative option in the worst case scenario. Future strategies for the management of viral myocarditis are discussed.GT was awarded a BBSRC Doctoral Training Award and thanks for the Croucher Foundation for its generous support

ACKNOWLEDGEMENT i

First of all, we are grateful to the organizers of INTERACT 2005, who have granted us the valuable opportunity to hold our Workshop “International COST294 Workshop on User Interface Quality Models (UIQM) ” in conjunction with the conference, and also provided the timely support for printing this Workshop’s Proceedings. Thanks must also go to the authors of the Workshop papers, whose contributions serve as rich sources of stimulation and inspiration to explore the issues of interest from multiple perspectives. The quality of the contributions could further be ensured and improved with the generous help of a group of reviewers, who are leading researchers and experts in the field of usability evaluation. Their prompt responses to our calls for peer review, and their effective as well as efficient review works are highly appreciated