The "R-on-T" phenomenon: an update and critical review. | Semantic Scholar (2024)

Exercise-induced ventricular tachycardia is a rare complication of treadmill stress test and occurs in patients with heart disease, is frequently preceded by "exertional hypotension," and is not related to the R on T phenomenon.

The mechanism of arrhythmias following acute infarction, whether enhanced auto-maticity or re-entry or both, appears to vary depending on the time after coronary occlusion, and it is probable that minute differences in the way the premature beat is conducted may decide whether or not re- entry succeeds.

The time from "warning arrhythmias" to the development of ventricular fibrillation in many patients was short, thus limiting the administration of antiarrhythmic agents, and an increase in heart rate appeared to be a predisposing factor in the initiation of vents.

Patients with congestive cardiomyopathy or congestive heart failure and nonsustained paroxysmal ventricular tachycardia are at a high risk for sudden death and are ideal candidates for prophylactic interventions.

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The observation that 41% of primary ventricular fibrillation was initiated by a late-coupled ventricular premature beat suggests that ventricular vulnerability during acute myocardial infarction may extend throughout most of the cardiac cycle and is not necessarily confined to the QT interval.

Results favor re-entry as the mechanism of tachycardia in group A patients and abnormal automaticity seems more likely in group B, while in one patient with chronic recurrent VT the arrhythmia could be terminated by a single atrial premature beat.

It is suggested that the coupling interval of a ventricular ectopic is a poor predictor of ventricular tachycardia in the early phases of acute myocardial infarction.

VF is more likely to be induced by early VPBs in the presence of clinical and electrocardiographic evidence of myocardial infarction, long ventricular cycle lengths, Q-T prolongation, and increase in the T wave amplitude, associated with increased inhom*ogeneity of excitability in ventricular myocardium.

An inverse relation was found between the prematurity of the tachycardia-initiating prematureBeat and the interval between the premature beat and the first beat of tachycardsia, a finding suggestive of a re-entry mechanism.

It is concluded that not all ventricular arrhythmia are potentially lethal and while atropine, pacing, and lidocaine successfully suppress most benign arrhythmias, they appear considerably less effective in suppressing those faster arrh rhythmias that frequently lead to the precipitation of VF.

Warning arrhythmias are not considered good criteria for institution of antiarrhythmic therapy in order to prevent primary ventricular fibrillation (PVF), and in patients with sinus rhythm there may be an association between heart rate and onset of PVF.

The available evidence favors the conclusion that, after a single premature systole, the phenomenon is caused by re-entry of circulating wave fronts which involve smaller and smaller blocks of myocardium, each of which develops an independent excitation.

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