Abstract
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.
Highlights
Viral myocarditis is myocardial inflammation due to a viral infection
It is thought to be a major cause of sudden cardiac death (SCD) in the pediatric and adolescent population (Steinberger et al, 1996)
One study found that infants who suffered from SCD had mild fever and insomnia several days prior to their deaths, suggesting infection as a major contributor in this group (Gaaloul et al, 2016)
Summary
It is thought to be a major cause of sudden cardiac death (SCD) in the pediatric and adolescent population (Steinberger et al, 1996). One study found that infants who suffered from SCD had mild fever and insomnia several days prior to their deaths, suggesting infection as a major contributor in this group (Gaaloul et al, 2016). At least 20 viruses have been implicated in myocarditis, but the commonest virus involved are Parvovirus B19 (PVB19), human herpes virus 6, adenovirus and coxsackievirus B3 (CVB3; Gaaloul et al, 2012). Not all viral infections are the same: cardiotropic viruses are known to infect >90% of the human population, yet only 1–5% of these will develop viral myocarditis as proven histologically (Andreoletti et al, 2009)
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