Role of Purkinje Fibers in Post-Infarction Ventricular Tachycardia

Bogun, Frank; Good, Eric; Reich, Stephen; Elmouchi, Darryl; Igic, Petar; Tschopp, David; Dey, Sujoya; Wimmer, Alan P.; Jongnarangsin, Krit; Oral, Hakan; Chugh, Aman; Pelosi, Frank; Morady, Fred

doi:10.1016/j.jacc.2006.07.062

Cited by 136 publications

(102 citation statements)

References 12 publications

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“…U pacjentów z VF i podstawową strukturalną chorobą serca, a także u osób z idiopatycznym VF można zidentyfikować PVC wywodzące się z różnych miejsc w układzie włókien Purkinjego lub z RVOT jako bodźce wyzwalające VF i potencjalne cele ablacji przezcewnikowej [467,[584][585][586][587][588]. U pacjentów z częstymi epizodami VF należy rozważyć ablację przezcewnikową PVC wyzwalających nawroty VF, ale zależy to od występowania takich pobudzeń podczas zabiegu, najczęściej po epizodzie VF lub burzy elektrycznej z licznymi epizodami VF.…”

Section: Idiopatyczne Migotanie Komórunclassified

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

Priori

Blomström‐Lundqvist²,

Mazzanti³

et al. 2015

Kardiol Pol

233

337

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Section: Idiopatyczne Migotanie Komórunclassified

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

Priori

Blomström‐Lundqvist²,

Mazzanti³

et al. 2015

Kardiol Pol

233

337

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“…Horowitz et al 9 and Arnar et al 10 showed that the subendocardial Purkinje network was the origin of ventricular arrhythmias occurring 24 h after myocardial infarction in dog models, and there is emerging evidence that Purkinje arborization is a dominant source of triggers for polymorphic VT or ven- tricular fibrillation in patients with various clinical conditions. [4][5][6][7][8][11][12][13][14][15][16][17] Ablation of these triggers eliminates further arrhythmias. The electrocardiographic and electrophysiological characteristics of incessant VT in the present patient were similar to those in previous reports [4][5][6][7][8][11][12][13][14][15][16][17] (ie, all premature ventricular beats originated from the distal Purkinje network and the sources were eliminated by focal energy delivery).…”

Section: Discussionmentioning

confidence: 99%

Successful Catheter Ablation for Incessant Ventricular Tachycardia in a Patient With Hypertrophic Cardiomyopathy

Okumura

Watanabe

Ohkubo

et al. 2007

Circ J

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onomorphic ventricular tachycardia (VT) in the presence of structural heart disease is largely attributable to anatomically bound macro-re-entry involving regions of myocardial scarring or the bundle branches. 1 In contrast; repetitive, idiopathic right and left ventricular (LV) outflow tract VTs are attributable to triggered activity or abnormal automaticity of the ventricular myocardium. 2,3 There is evidence that triggers originating from distal Purkinje arborization play an important role in the initiation of malignant arrhythmias such as polymorphic VT and ventricular fibrillation in a variety of clinical scenarios. [4][5][6][7][8] We report a patient with hypertrophic cardiomyopathy (HCM) in whom life-threatening repetitive monomorphic VTs developed. Radiofrequency (RF) ablation targeting the Purkinje-like potentials preceding the VT prevented recurrence. Case ReportA 35-year-old man with HCM presented with recurrent episodes of palpitation and chest discomfort. Electrocardiographic monitoring during palpitation showed an incessant nonsustained, wide QRS tachycardia with a QRS duration of 130 ms at 180-200 beats/min. On admission to hospital, 12-lead ECG showed incessant nonsustained VT with right bundle branch block (RBBB) morphology and a northwest axis deviation (Fig 1). Intravenous lidocaine and verapamil were effective in terminating the VT but ineffective in preventing recurrence. A 12-lead ECG obtained during sinus rhythm after intravenous administration of verapamil showed poor R wave progression in the precordial leads (Fig 2). The signal-averaged ECG was recorded during sinus rhythm after intravenous administration of 5 mg of verapamil. Oral administration of -blocker, class I antiarrhythmic drugs (pilsicainide and cibenzoline), and amiodarone was ineffective in preventing the VT. The late potential was positive (filtered QRS duration: 139 ms, root mean square voltage of the terminal 40 ms of the filtered QRS complex: 6.6 V; the duration of low-amplitude signals <40 V of the terminal filtered QRS complex: 56 ms). Transthoracic echocardiography showed nonobstructive HCM (LV ejection fraction: 88.8%, left atrial dimension: 36.9 mm, LV end-diastolic dimension: 31.8 mm, LV enddiastolic dimension: 13.4 mm, interventricular septum thickness: 19.4 mm, LV posterior wall thickness: 10.9 mm) and 2-dimensional echocardiography showed mid-septal hypertrophy. After written informed consent was given by the patient, coronary angiography, left ventriculography and electrophysiologic study were performed in the postabsorptive state after all antiarrhythmic drugs, except amiodarone, had been discontinued for at least 5 lives. Coronary angiography was normal and left ventriculography showed there was neither obstruction in the LV nor pressure gradients within the LV or between the LV and aorta. Three diagnostic catheters were inserted via the femoral veins and placed at the high right atrium, His bundle position and right ventricular apex. A decapolar catheter was inserted into the coronary sinus via the right int...

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“…Here, the earliest bipolar signal is recorded and, concomitantly, a fast negative intrinsicoid deflection is also recorded in the unipolar recording from [16,17] . A rare but interesting form of focal VT has been described in patients with postinfarction ischemic cardiomyopathy [18,19] . In this form, the arrhythmogenic focus originates from surviving Purkinje fibers at the border zone of myocardial necrosis.…”

Section: Methodsmentioning

confidence: 99%

Role of catheter ablation of ventricular tachycardia associated with structural heart disease

Ponti

2011

WJC

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In patients with structural heart disease, ventricular tachycardia (VT) worsens the clinical condition and may severely affect the short-and long-term prognosis. Several therapeutic options can be considered for the management of this arrhythmia. Among others, catheter ablation, a closed-chest therapy, can prevent arrhythmia recurrences by abolishing the arrhythmogenic substrate. Over the last two decades, different techniques have been developed for an effective approach to both tolerated and untolerated VTs. The clinical outcome of patients undergoing ablation has been evaluated in multiple studies. This editorial gives an overview of the role, methodology, clinical outcome and innovative approaches in catheter ablation of VT. De Ponti R. Role of catheter ablation of ventricular tachycardia associated with structural heart disease.

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Role of Purkinje Fibers in Post-Infarction Ventricular Tachycardia

Abstract: The Purkinje system may be part of the re-entry circuit in patients with post-infarction monomorphic VT, resulting in a type of VT with a relatively narrow QRS complex that mimics fascicular VT.

Cited by 136 publications

References 12 publications

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death

Successful Catheter Ablation for Incessant Ventricular Tachycardia in a Patient With Hypertrophic Cardiomyopathy

Role of catheter ablation of ventricular tachycardia associated with structural heart disease

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