Programmed ventricular stimulation in arrhyhtmogenic myocarditis: Foraging into the unknown!

Owing to myriad clinical manifestations including ventricular arrhythmias, risk of sudden cardiac death (SCD), and innovation in various imaging techniques and role of immunomodulators have resulted in a newfound interest in the management of inflammatory cardiomyopathies. Specific protocol based imaging techniques, electroanatomical mapping guided biopsy has translated in the enhanced diagnosis of myocardial inflammation and diagnosis of the scar. With respect to myocarditis, the emphasis in the treatment lies in the determination of whether acute inflammation exists or not as the management can be vastly different with some specific indications for immunosuppressive and antiarrhythmic medications. Cardiac magnetic resonance imaging with scar‐quantification and metabolic imaging (T2‐mapping) has emerged as the primary tool for the noninvasive assessment of myocarditis. It is well‐established that late gadolinium‐enhancement is associated with increased all‐cause mortality and SCD in patients with nonischemic cardiomyopathy independent of the left ventricular ejection fraction. In this issue of the Journal of Cardiovascular Electrophysiology, Peretto et al report the findings of their elegantly conducted study on the utility of programmed ventricular stimulation (PVS) in patients with active vs prior arrhythmic myocarditis. The authors’ endeavor to elucidate the nuances of this less‐understood topic in electrophysiology is commendable. This prospective study, with a coherent design and arduous follow‐up, concluded that invasive PVS is safe and significantly associated with follow‐up malignant ventricular arrhythmia (MVA) episodes. This association was more accurate in patients with prior myocarditis as opposed to those with active myocarditis. To determine whether myocarditis is active or not, the authors propose the use of endomyocardial biopsy (EMB) as a risk‐ stratification tool. Given that the current guidelines do not confer a role for PVS in myocarditis, the present study is a useful adjunct to the existing literature. Peretto et al devised a practical way of dividing their study sample into active and nonactive myocarditis. This stratification assumes importance given the pathophysiology of VA in myocarditis. Myocardial scar which can be seen in “cold myocarditis” serves as a substrate for reentrant monomorphic ventricular tachycardia (VT) and the zones of slow conduction in the cardiomyopathic ventricle help sustaining reentrant circuits. Conversely, active inflammation seen in “hot myocarditis” can lead to arrhythmias due to multiple mechanisms such as abnormal automaticity, triggered activity, and reentry, thus casting a wide net of arrhythmogenic complications, including polymorphic VT and ventricular fibrillation (VF). The investigators then went on to perform electrophysiologic studies (EPS) with PVS on all of these patients, after the cardiovascular magnetic resonance (CMR) but before the results of EMB were available. The lack of T2‐mapping techniques with CMR and the timing of EPS before biopsy results essentially meant that the physicians could only suspect the presence of active inflammation based on the clinical presentation and laboratory data. While this could be seen as a limitation of the study, as the authors point out, this aided in minimizing the selection bias that would have occurred otherwise.