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Monomorphic Ventricular Tachycardia (monomorphic + ventricular_tachycardia)

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Medical Sciences100%

Selected Abstracts

Monomorphic Ventricular Tachycardia Induced by Cardiac Resynchronization Therapy in Patient with Severe Nonischemic Dilated Cardiomyopathy

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2006
AGUSTÍN BORTONE
We report the case of a patient with severe nonischemic dilated cardiomyopathy in whom cardiac resynchronization therapy (CRT) was the source of incessant, drug-resistant, monomorphic ventricular tachycardia (VT). VT recurrences were only resolutive with inactivation of CRT and reactivation of CRT reproduced VT occurrence. The possible pathophysiology of the VT and the potential ventricular proarrhythmic risk related to CRT are discussed. This report points out clearly that CRT can induce ventricular arrhythmias and suggests the need for CRT systematically associated with a defibrillation system. [source]

Characterization of the Electroanatomic Substrate for Monomorphic Ventricular Tachycardia in Patients with Nonischemic Cardiomyopathy

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2002
HENRY H. HSIA
HSIA, H.H., et al.: Characterization of the Electroanatomic Substrate for Monomorphic Ventricular Tachycardia in Patients with Nonischemic Cardiomyopathy. Ventricular arrhythmias are common in the setting of nonischemic cardiomyopathy. The etiology for the cardiomyopathy is frequently not identified and the label of "idiopathic" is applied. Interstitial fibrosis with conduction system involvement and associated left bundle branch block characterizes the disease process in some patients and the mechanism for monomorphic ventricular tachycardia is commonly bundle branch reentry. However, most patients with nonischemic cardiomyopathy have VT due to myocardial reentry and demonstrate marked myocardial fibrosis and electrogram abnormalities. Although patient specific, the overall distribution of electroanatomic abnormalities appears to be equal on the endocardium and epicardium. The extent of electrogram abnormalities appears to parallel arrhythmia presentation and/or inducibility. Patients with sustained uniform morphology VT have the most extensive endocardial and epicardial electrogram abnormalities. Magnetic electroanatomic voltage mapping provides a powerful tool to characterize the location and extent of the arrhythmia substrate. Basal left ventricular myocardial involvement, as indexed by the location of contiguous electrogram abnormalities, is common in patients with sustained VT and left ventricular cardiomyopathy. The relatively equal distribution of electrogram abnormalities on the endocardium and epicardium, and the results of mapping and ablation attempts, suggest that critical parts of the reentrant circuit may be epicardial. Unique features of the electroanatomic substrate associated with cardiomyopathy due to Chagas' disease, sarcoidosis, and arrhythmogenic right ventricular dysplasia are also discussed. [source]

Adenosine Induced Monomorphic Ventricular Tachycardia

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2000
DEEPIKA MISRA
Polymorphic ventricular tachycardia has been reported following the administration of adenosine for the treatment of SVT. We present a case of monomorphic ventricular tachycardia in a 75-year-old man following the intravenous administration of adenosine for stress testing. [source]

Increase in Ventricular Tachycardia Frequency After Biventricular Implantable Cardioverter Defibrillator Upgrade

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2003
JOSE M. GUERRA M.D.
We report the case of a patient in whom transvenous left ventricular pacing lead placement at the time of a biventricular upgrade led to an exacerbation of clinical monomorphic ventricular tachycardia (MVT). At implant, slow left ventricular pacing repeatedly induced sustained MVT. However, testing of the biventricular pacing showed no MVT inducibility, and the system was implanted. The patient was readmitted due to multiple episodes of the MVT observed at implant. The MVT was controlled with pharmacotherapy, allowing the patient to continue with biventricular pacing. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1245-1247, November 2003) [source]

Ventricular Flutter Induced During Electrophysiologic Studies in Patients with Old Myocardial Infarction:

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2003
Clinical, Electrophysiologic Predictors, Prognostic Significance
Introduction: Induction of ventricular flutter during electrophysiologic (EP) studies (similar to that of ventricular fibrillation [VF]) often is viewed as a nonspecific response with limited prognostic significance. However, data supporting this dogma originate from patients without previously documented ventricular tachyarrhythmias. We examined the significance of ventricular flutter in patients with and without spontaneous ventricular arrhythmias. Methods and Results: We conducted a cohort study of all patients with myocardial infarction (MI) undergoing EP studies at our institution. Of 344 consecutive patients, 181 had previously documented spontaneous sustained ventricular arrhythmias, 61 had suspected ventricular arrhythmias, and 102 had neither. Ventricular flutter was induced in 65 (19%) of the patients. Left ventricular ejection fraction was highest among patients with inducible VF (35 ± 13), lowest for patients with inducible sustained monomorphic ventricular tachycardia (SMVT; 27 ± 9), and intermediate for patients with inducible ventricular flutter (30 ± 10). Similarly, the coupling intervals needed to induce the arrhythmia were shortest for VF (200 ± 28 msec), intermediate for ventricular flutter (209 ± 27 msec), and longest for SMVT (230 ± 35 msec). During 5 ± 8 years of follow-up, the risk for ventricular tachycardia/VF was high for patients with SMVT and ventricular flutter and low for patients with inducible VF and noninducible patients (46%, 34%, 17%, and 14%, P < 0.005). Conclusion: Patients with inducible ventricular flutter appear to be "intermediate" between patients with inducible VF and patients with SMVT in terms of clinical and electrophysiologic correlates. However, the prognostic value of inducible ventricular flutter is comparable to that of SMVT. (J Cardiovasc Electrophysiol, Vol. 14, pp. 913-919, September 2003) [source]

Ineffectiveness of Precordial Thump for Cardioversion of Malignant Ventricular Tachyarrhythmias

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2007
OFFER AMIR M.D.
Background:The Precordial Thump (PT) is commonly used for cardiopulmonary resuscitations both in and out of hospitals. However, the support for its efficiency relies mainly on sporadic cases. In this current prospective large study, we tested the effectiveness and safety of PT in a wide range of malignant ventricular tachyarrhythmias. Methods: The study included 80 patients who underwent electrophysiological study and/or implantation of a cardiodefibrillator device. During these procedures, once a malignant ventricular tachyarrhythmia was induced, PT was used as the first treatment option. If the PT failed, other means were used to discontinue the arrhythmia. Results: Polymorphic ventricular tachycardia occurred in 32 (40%) patients, ventricular fibrillation in 28 (35%) patients, and 20 (25%) patients had sustained monomorphic ventricular tachycardia. Except in one patient with monomorphic ventricular tachycardia, the PT was unsuccessful in terminating any of the other malignant tachyarrhythmias, and internal or external defibrillation was eventually required in all other 79 (99%) patients. The PT was not associated with any damage either to the sternal bone, ribs, or to the cardiodefibrillator device. Conclusions: PT is not effective in terminating malignant ventricular tachyarrhythmia and should be reserved to a situation in which a defibrillator is not available. [source]

Monomorphic Ventricular Tachycardia Induced by Cardiac Resynchronization Therapy in Patient with Severe Nonischemic Dilated Cardiomyopathy

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2006
AGUSTÍN BORTONE
We report the case of a patient with severe nonischemic dilated cardiomyopathy in whom cardiac resynchronization therapy (CRT) was the source of incessant, drug-resistant, monomorphic ventricular tachycardia (VT). VT recurrences were only resolutive with inactivation of CRT and reactivation of CRT reproduced VT occurrence. The possible pathophysiology of the VT and the potential ventricular proarrhythmic risk related to CRT are discussed. This report points out clearly that CRT can induce ventricular arrhythmias and suggests the need for CRT systematically associated with a defibrillation system. [source]

Characterization of the Electroanatomic Substrate for Monomorphic Ventricular Tachycardia in Patients with Nonischemic Cardiomyopathy

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2002
HENRY H. HSIA
HSIA, H.H., et al.: Characterization of the Electroanatomic Substrate for Monomorphic Ventricular Tachycardia in Patients with Nonischemic Cardiomyopathy. Ventricular arrhythmias are common in the setting of nonischemic cardiomyopathy. The etiology for the cardiomyopathy is frequently not identified and the label of "idiopathic" is applied. Interstitial fibrosis with conduction system involvement and associated left bundle branch block characterizes the disease process in some patients and the mechanism for monomorphic ventricular tachycardia is commonly bundle branch reentry. However, most patients with nonischemic cardiomyopathy have VT due to myocardial reentry and demonstrate marked myocardial fibrosis and electrogram abnormalities. Although patient specific, the overall distribution of electroanatomic abnormalities appears to be equal on the endocardium and epicardium. The extent of electrogram abnormalities appears to parallel arrhythmia presentation and/or inducibility. Patients with sustained uniform morphology VT have the most extensive endocardial and epicardial electrogram abnormalities. Magnetic electroanatomic voltage mapping provides a powerful tool to characterize the location and extent of the arrhythmia substrate. Basal left ventricular myocardial involvement, as indexed by the location of contiguous electrogram abnormalities, is common in patients with sustained VT and left ventricular cardiomyopathy. The relatively equal distribution of electrogram abnormalities on the endocardium and epicardium, and the results of mapping and ablation attempts, suggest that critical parts of the reentrant circuit may be epicardial. Unique features of the electroanatomic substrate associated with cardiomyopathy due to Chagas' disease, sarcoidosis, and arrhythmogenic right ventricular dysplasia are also discussed. [source]

Radiofrequency Catheter Ablation of an Incessant Ventricular Tachycardia Following Valve Surgery

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2002
THORSTEN LEWALTER
LEWALTER, T., et al.: Radiofrequency Catheter Ablation of an Incessant Ventricular Tachycardia Following Valve Surgery. Sustained monomorphic ventricular tachycardia (VT) after valve surgery represents a clinical entity with different tachycardia mechanisms. This case report describes an incessant VT after tricuspid and aortic valve replacement that did not respond to antiarrhythmic drug treatment. The tachycardia exhibited VA block and a right bundle branch block pattern with left-axis deviation, suggesting ventricular excitation via the left posterior fascicle. The electrophysiological study was limited by the prosthetic tricuspid and aortic valve replacement, therefore a transseptal approach was necessary to obtain access to the ventricular myocardium. Radiofrequency catheter ablation was performed in the proximal left bundle or distal His region with termination of the incessant VT followed by complete AV block. After pacemaker implantation using a transvenous right atrial and an epicardial ventricular lead, no VT reoccurrence could be documented. [source]

Adenosine Induced Monomorphic Ventricular Tachycardia

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2000
DEEPIKA MISRA
Polymorphic ventricular tachycardia has been reported following the administration of adenosine for the treatment of SVT. We present a case of monomorphic ventricular tachycardia in a 75-year-old man following the intravenous administration of adenosine for stress testing. [source]

Idiopathic Left Ventricular Tachycardia Originating from the Mitral Annulus

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2005
KOJI KUMAGAI M.D.
Background: Radiofrequency catheter ablation (RFCA) can eliminate most idiopathic repetitive monomorphic ventricular tachycardias (RMVTs) originating from the right and left ventricular outflow tracts (RVOT, LVOT). Here, we describe the electrophysiological (EP) findings of a new variant of RMVT originating from the mitral annulus (MAVT). Methods and Results: MAVT was identified in 35 patients out of 72 consecutive left ventricular RMVTs from May 2000 to June 2004. All patients underwent an EP study and RFCA. The sites of origin of the MAVT were grouped into four groups according to the successful ablation sites around the mitral annulus. Group I included the anterior sites (n = 11), group II the anterolateral sites (n = 9), group III the lateral sites (n = 6), and group IV the posterior sites (n = 9). The MAVTs were a wide QRS tachycardia with a delta wave-like beginning of the QRS complex. The transitional zone of the R wave occurred between V1-V2 in all cases. The 12-lead electrocardiogram (ECG) pattern might reflect the site of the origin of MAVTs around the mitral annulus. We proposed an algorithm for predicting the site of the focus and the tactics needed for successful RFCA of the MAVT. Conclusions: We described the EP findings of the new variant of RMVT, MAVT. Most MAVTs could be eliminated by RF applications to the endocardial mitral annulus using our proposed tactics. [source]