Myocarditis and cardiac channelopathies: A deadly association?

Salerno, F.; Girerd, Nicolas; Chalabreysse, Lara; Billaud, Geneviève; Lina, Bruno; Chevalier, Philippe

doi:10.1016/j.ijcard.2011.01.019

Cited by 20 publications

(14 citation statements)

References 9 publications

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“…Interestingly, not only were ventricular arrhythmias observed during the acute phase of the myocarditis but persistent ECG changes were observed after the inflammation has subsided, suggesting underlying abnormalities in ion channel function, predisposing to arrhythmogenesis during myocarditis. Indeed, as pointed out by these authors (Salerno et al, 2011 ), this could be due to temperature-dependent alterations in ion channel function (Pasquié, 2005 ). This notion is consistent with previous observations that infants suffering from SCD had mild fever before their deaths (Gaaloul et al, 2016 ), which would suggest fever as a trigger of the arrhythmia (Pasquié, 2005 ).…”

Section: Host-mediated and Viral-induced Inflammation And Can Promotementioning

confidence: 90%

Section: Host-mediated and Viral-induced Inflammation And Can Promotementioning

confidence: 99%

“…Finally, there may be interaction between genetic predisposition of ion channel dysfunction and viral myocarditis (Salerno et al, 2011 ; Juhasz et al, 2014 ). In a case series, patients who suffered from viral myocarditis complicated by ventricular fibrillation showed electrocardiographic features of Brugada, early repolarization and short QT syndromes (Salerno et al, 2011 ). Interestingly, not only were ventricular arrhythmias observed during the acute phase of the myocarditis but persistent ECG changes were observed after the inflammation has subsided, suggesting underlying abnormalities in ion channel function, predisposing to arrhythmogenesis during myocarditis.…”

Section: Host-mediated and Viral-induced Inflammation And Can Promotementioning

confidence: 99%

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

et al. 2016

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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.

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Section: Host-mediated and Viral-induced Inflammation And Can Promotementioning

confidence: 90%

Section: Host-mediated and Viral-induced Inflammation And Can Promotementioning

confidence: 99%

Section: Host-mediated and Viral-induced Inflammation And Can Promotementioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2016

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“…Mutations in these ion channels are associated with cardiac arrhythmias, comprising the long QT syndrome, Brugada syndrome, cardiac conduction defect, familial atrial fibrillation, and the short QT syndrome (summarized at http://www.fsm.it/cardmoc). Recently, Salerno et al (20) suggested a link of ventricular arrhythmias in myocarditis with cardiac channelopathies. So far, it is unknown whether arrhythmias caused by enteroviral infections originate from impaired function of cardiac ion channels.…”

mentioning

confidence: 99%

Coxsackievirus B3 modulates cardiac ion channels

et al. 2013

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Infections with coxsackieviruses of type B (CVBs), which are known to induce severe forms of acute and chronic myocarditis, are often accompanied by ventricular arrhythmias and sudden cardiac death. The mechanisms underlying the development of virus-induced, life-threatening arrhythmias, which are phenotypically similar to those observed in patients having functionally impaired cardiac ion channels, remain, however, enigmatic. In the present study, we show, for the first time, modulating time-dependent effects of CVB3 on the cardiac ion channels KCNQ1, hERG1, and Cav1.2 in heterologous expression. Channel protein abundance in cellular plasma membrane and patterns of their subcellular distribution were altered in infected murine hearts. The antiviral compound AG7088 did not prevent these effects on channels. In silico analyses of infected human myocytes suggest pronounced alterations of electrical and calcium signaling and increased risk of arrhythmogenesis. These modifications are attenuated by the common Asian polymorphism KCNQ1 P448R, a genetic determinant preventing coxsackievirus-induced effects in vitro. This study provides a previously unknown explanation for the development of arrhythmias in enteroviral myocarditis, which will help to develop therapeutic strategies for arrhythmia treatment.

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“…Several rhythm disturbances have been observed in myocarditis, including sinus tachycardia, atrial, and, sometimes fatal, ventricular arrhythmias. 11 , 12 Electrically sensitive foci in inflamed or scared areas because of myocarditis can give rise to PVCs. When a PVC occurs in a vulnerable period of a preceding T-wave, it can trigger ventricular arrhythmias, which is the likely mechanism responsible for VT in our patient.…”

Section: Discussionmentioning

confidence: 99%

A Case of Myocarditis and Near-Lethal Arrhythmia Associated With Interleukin-2 Therapy

Sarcon

et al. 2018

Journal of Investigative Medicine High Impact Case Reports

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We present a case of a 48-year-old female who developed myocarditis and near fatal arrhythmias during high dose Il-2 therapy for metastatic renal cancer. On day 5 of therapy, the patient developed sudden onset chest pain, elevated cardiac enzymes and ST segment changes on EKG. Coronary angiogram was normal, however echocardiogram showed reduced ejection fraction and hemodynamic measurements showed elevated bilateral elevated filling pressures. The patient then developed episodes of recurrent ventricular arrhythmia, precipitated by bradycardia and PVC, requiring defibrillation and temporary pacemaker placement. Endomycardial biopsy was nonspecific showing fibrosis with subsequent cardiac MRI showed evidence of myocardial edema, consistent with Il-2 induced myocarditis in the setting of no prior cardiac history. After the discontinuation of Il-2 therapy, the patient displayed clinical improvement as well as improved ejection fraction. This case brings attention to the cardiac toxicities associated with high dose Il-2 therapy including potentially lethal arrhythmias and highlights the importance of careful cardiac screening prior to initiation of treatment.

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Myocarditis and cardiac channelopathies: A deadly association?

Cited by 20 publications

References 9 publications

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

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

Coxsackievirus B3 modulates cardiac ion channels

A Case of Myocarditis and Near-Lethal Arrhythmia Associated With Interleukin-2 Therapy

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