Novel mechanism of postinfarction ventricular tachycardia originating in surviving left posterior Purkinje fibers.
BACKGROUND
Other than bundle branch reentry and interfascicular reentry, monomorphic postmyocardial infarction (post-MI) reentrant ventricular tachycardia (VT) including the His-Purkinje system has not been reported. Verapamil-sensitive idiopathic left VT includes the left posterior Purkinje fibers but develops in patients without structural heart disease.


OBJECTIVE
The purpose of this study was to describe a novel mechanism of reentrant VT arising from the left posterior Purkinje fibers in patients with a prior MI.


METHODS
The study consisted of four patients with a prior MI and symptomatic heart failure who underwent electrophysiologic study and catheter ablation for VT showing right bundle branch block (n = 3) or atypical left bundle branch block (n = 1) morphology with superior axis. In two patients, the VT frequently emerged during the acute phase of MI and required emergency catheter ablation.


RESULTS
Clinical VT was reproducibly induced by programmed stimulation. In three patients, both diastolic and presystolic Purkinje potentials were sequentially recorded along the left ventricular posterior septum during the VT, whereas in the fourth patient, only presystolic Purkinje potentials were observed. During entrainment pacing from the right atrium, diastolic Purkinje potentials were captured orthodromically and demonstrated decremental conduction properties, whereas presystolic Purkinje potentials were captured antidromically and appeared between the His and QRS complex. Radiofrequency energy delivered at the site exhibiting a Purkinje-QRS interval of 58 +/- 26 ms successfully eliminated the VTs without provoking any conduction disturbances.


CONCLUSIONS
Reentrant monomorphic VT originating from the left posterior Purkinje fibers, which is analogous to idiopathic left VT, can develop in the acute or chronic phase of MI. Catheter ablation is highly effective in eliminating this VT without affecting left ventricular conduction.
Hayashi
Meiso
M
First Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
Kobayashi
Yoshinori
Y
Iwasaki
Yu-ki
YK
Morita
Norishige
N
Miyauchi
Yasushi
Y
Kato
Takao
T
Takano
Teruo
T
D000368:Aged; D018780:Body Surface Potential Mapping; D002037:Bundle-Branch Block / Q000209:etiology / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D017115:Catheter Ablation; D015986:Confounding Factors, Epidemiologic; D003937:Diagnosis, Differential; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology / Q000601:surgery; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000453:epidemiology / Q000503:physiopathology* / Q000601:surgery; D011690:Purkinje Fibers / Q000503:physiopathology* / Q000601:surgery; D017180:Tachycardia, Ventricular / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery