title: Significance of R-on-T phenomenon in early ventricular tachyarrhythmia susceptibility after acute myocardial infarction in the thrombolytic era.
abstract: We investigated the clinical significance and mechanism of the R-on-T phenomenon in the current thrombolytic era as potential precipitant of R-on-T-induced early ventricular tachyarrhythmias in patients with a thrombolysed acute myocardial infarction. We also examined the role of QT dispersion on ventricular vulnerability and its association with R-on-T-initiated ventricular tachyarrhythmias. A total of 93 patients underwent 24-hour Holter monitoring starting at hospital admission before thrombolysis. Patients were classified into 2 groups: those with (n = 76) and those without (n = 17) reperfusion according to electrocardiographic criteria. All R-on-T ventricular premature complexes (VPCs) and R-on-T-initiated arrhythmic events (ventricular tachycardia [VT], ventricular fibrillation) were counted to estimate arrhythmia density and severity in 2 time periods during and after completion of thrombolysis. Measurements of QT and QTc intervals and dispersion parameters were obtained on the 12-lead electrocardiogram before thrombolysis and at 24 hours in patients with and without R-on-T VTs. Overall, R-on-T VPCs were rarely observed (1.8% of total VPCs over 24 hours), occurring more frequently during than after thrombolysis (at a rate of 8 vs 0.6 VPCs/hour, p = NS) and at a higher rate during thrombolysis in nonreperfused than in perfused patients (15 vs 8/hour, p = NS). Three VF episodes were observed in 1 reperfused patient, and all were R-on-T initiated. Episodes of nonsustained R-on-T VTs (3.3% of total VTs over 24 hours) appeared more frequent during than after thrombolysis (at a rate of 0.8 vs 0.05 VPCs/ hour, p = NS), and compared with non-R-on-T VTs they were significantly faster (374 +/- 56 ms vs 411 +/- 69 ms; p < 0.05), with a trend toward longer duration. Our findings indicate that R-on-T VPCs and R-on-T VTs are early rare features in acute myocardial infarction, and do not serve as triggers of severe ventricular tachyarrhythmia. The study of ventricular repolarization did not elicit an identifiable risk factor of R-on-T VT susceptibility.
authors.affiliation: Cardiology Division, Patras University Medical School, Rio, Greece.
authors.forename: J A
authors.initials: JA
authors.lastname: Chiladakis
authors.forename: G
authors.initials: G
authors.lastname: Karapanos
authors.forename: P
authors.initials: P
authors.lastname: Davlouros
authors.forename: G
authors.initials: G
authors.lastname: Aggelopoulos
authors.forename: D
authors.initials: D
authors.lastname: Alexopoulos
authors.forename: A S
authors.initials: AS
authors.lastname: Manolis
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D004562:Electrocardiography; D015716:Electrocardiography, Ambulatory; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology*; D015425:Myocardial Reperfusion; D010960:Plasminogen Activators / Q000627:therapeutic use*; D017180:Tachycardia, Ventricular / Q000503:physiopathology*; D015912:Thrombolytic Therapy; D018879:Ventricular Premature Complexes / Q000503:physiopathology*
chemical_list: D010960:Plasminogen Activators