The classical 'r-on-T' phenomenon

摘要

? 2015 Cardiological Society of India. ? 2015 Cardiological Society of India. 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. 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.