What is the R‑on‑T phenomenon on an electrocardiogram?

R-on-T Phenomenon on ECG

The R-on-T phenomenon occurs when a premature ventricular complex (PVC) falls on the T wave of the preceding beat, coinciding with the vulnerable period of ventricular repolarization when regional dispersion of refractoriness creates conditions for potential reentry and life-threatening arrhythmias. 1, 2

Electrocardiographic Definition

• The R-on-T phenomenon is the superimposition of an ectopic ventricular beat on the T wave of a preceding beat 3
• This timing is critical because the T wave represents transmural dispersion of repolarization, when some ventricular regions have recovered excitability while others remain refractory 2
• The vulnerable period corresponds to the T wave on the surface ECG, creating conditions where unidirectional block and reentry can be initiated 1

Mechanisms of Arrhythmia Initiation

Two distinct mechanisms exist for R-on-T arrhythmogenesis:

• "R-to-T" mechanism: A PVC arising focally from one region propagates into another region with delayed recovery, resulting in unidirectional conduction block and reentry initiation 1
• "R-from-T" mechanism: The PVC is causally generated from the repolarization gradient itself (the T wave), rather than being a separate event—the trigger arises directly from the underlying tissue instabilities that create the vulnerable substrate 1
• The R-on-T phenomenon may result from transmural propagation of phase 2 reentry or phase 2 early afterdepolarization, potentially initiating polymorphic ventricular tachycardia or fibrillation 2

Clinical Significance and Risk Assessment

The actual arrhythmic risk of R-on-T is substantially lower than historically believed:

• R-on-T VPCs are rare events, representing only 1.8% of total VPCs in acute myocardial infarction patients 4
• R-on-T is not a critical determinant of primary ventricular fibrillation in acute myocardial infarction and represents few of the initiating beats of paroxysmal ventricular tachycardia 3
• When the capacity for sustained repetitive beating has not been clinically evident, R-on-T is unlikely to result in ventricular tachyarrhythmias, even in coronary heart disease 3
• R-on-T VTs occur more frequently during thrombolysis than after (0.8 vs 0.05 VPCs/hour), and when they occur, they are significantly faster than non-R-on-T VTs (374 ± 56 ms vs 411 ± 69 ms) 4

High-Risk Clinical Contexts

R-on-T carries meaningful risk in specific settings:

• Acute myocardial infarction: The inability to always identify precursors of tachyarrhythmias strengthens the argument for prophylactic treatment 3
• Pacemaker malfunction: Asynchronous ventricular pacing or loss of sensing in synchronous pacemakers can cause R-on-T phenomenon leading to polymorphic ventricular tachycardia and cardiac arrest 5
• Brugada syndrome and early repolarization syndrome: These conditions involve prominent transmural voltage gradients during repolarization that increase vulnerability to R-on-T triggered arrhythmias 2

Common Pitfalls

• Do not assume all R-on-T events will trigger sustained arrhythmias—the vast majority do not result in dangerous rhythms 3, 4
• Recognize that R-on-T represents at worst only a small risk in terms of sudden death outside the acute myocardial infarction setting 3
• In pacemaker patients, verify proper sensing function to prevent iatrogenic R-on-T phenomenon from pacing stimuli 5
• Consider both trigger suppression and substrate modification when designing antiarrhythmic strategies, as R-from-T mechanisms require addressing underlying dynamic tissue instabilities simultaneously 1