The classical “R-on-T” phenomenon (2024)

Abstract

The polymorphic ventricular tachycardia (PVT) is uncommon arrhythmia with multiple causes and has been classified according to whether they are associated with long QT interval or normal QT. Whereas “Torsade de pointes (TdP)” is an uncommon and distinctive form of PVT occurring in a setting of prolonged QT interval, which may be congenital or acquired (congenital or acquired), “PVT with normal QT” is associated with myocardial ischemia, electrolyte abnormalities (hypokalemia), mutations of the cardiac sodium channel (Brugada syndrome), and the ryanodine receptor (catecholaminergic PVT). This distinction is crucial because of the differing etiologies and management of these arrhythmias. Moreover, the PVT in the setting of acute MI generally occurs during the hyperacute phase, is related to ischemia (“ischemic PVT”) and is not associated with QT prolongation. It is triggered by ventricular extrasystoles with very short coupling interval (the “R-on-T” phenomenon) and is not pause-dependent. However, recently there has been described a new PVT during the “healing phase” of MI in patients with no evidence of ongoing ischemia and following excessive QT prolongation, the electrophysiologic abnormality being a “pause-dependent infarct-related TdP” due to a LQTS in healing MI patients. Therefore, “ischemic PVT” differs from “infarct-related TdP” in terms of pathophysiology and ECG manifestations.

Keywords: R-on-T phenomenon, Polymorphic ventricular tachycardia, Torsade de pointes

The “R-on-T phenomenon” was first described by Smirk in 1949 as “R waves interrupting T waves”.1,2 In 1966, Francois Dessertenne described a specific electrocardiographic form of polymorphic ventricular tachycardia (PVT) characterized by changing amplitude of the complexes with a characteristic twist around the isoelectric baseline with prolonged QT interval, which he termed “torsades de pointes” (TdP).3 In its most typical form, sudden slowing of heart rate (i.e., pauses) invariably precede each burst of TdP, and the recurrent arrhythmia is referred to as “pause-dependent TdP”.4 Indeed, the PVT is uncommon arrhythmia with multiple causes, and has been classified according to whether they are associated with long QT interval or normal QT.5,6 Contemporary classifications of the long QT syndrome (LQTS) refer to the congenital LQTS as “adrenergic dependent” and to the acquired LQTS as “pause dependent”.4 Whereas “TdP” is a form of PVT occurring in a setting of prolonged QT interval, which may be congenital or acquired, “PVT with normal QT” is associated with myocardial ischemia, electrolyte abnormalities (hypokalemia), mutations of the cardiac sodium channel (Brugada syndrome), and the ryanodine receptor (catecholaminergic PVT).6 This distinction is crucial because of the differing etiologies and management of these arrhythmias. A 59-year-old male patient presented to the emergency department approximately 1h after experiencing a severe crushing retrosternal chest pain with radiation to his left arm. No metabolic abnormalities such as hyponatremia, hypocalcemia, hypomagnesemia, or hypermagnesemia were noted. The most striking feature of the patient's ECG was its newly detected PVT, which was consistent with, but not diagnostic of, TdP initiated by “R-on-T” phenomenon (Fig.1, arrows). ECG taken immediately after successful electrical defibrillation revealed ST elevation in V1–3 suggesting hyperacute anterior myocardial infarction (MI) (Fig.2). Emergency coronary angiography showed a total occlusion of the middle part of the left anterior descending artery, which was successfully revascularized with a bare metal stent.

PVT in the setting of acute MI generally occurs during the hyperacute phase, is related to ischemia, and is not associated with QT prolongation.7 They are triggered by ventricular extrasystoles with very short coupling interval (the “R-on-T” phenomenon) and is not pause-dependent.8 Therefore, “ischemic PVT” differs from “infarct-related TdP” in terms of pathophysiology and ECG manifestations.8 Although some investigators have used the term “TdP” to describe PVT during MI,9,10 the available illustrations suggest that the majority of the patients had “ischemic PVT” with short QT interval. Recently, Halkin etal described a new PVT during the “healing phase” of MI in patients with no evidence of ongoing ischemia and following excessive QT prolongation, therefore, named it as “pause-dependent/infarct related TdP” due to a LQTS in healing MI patients. Although our patient had PVT that fulfilled the morphologic criterion for TdP, it was associated with normal QTc (393ms), thereby precluding the diagnosis of TdP, and we preferred to use the term “ischemic PVT” instead ofTdP.

Conflicts of interest

The authors have none to declare.

References