Repetitive Monomorphic Ventricular Tachycardia Research Articles

Verapamil-sensitive idiopathic left ventricular tachycardia and concomitant atrioventricular nodal reentrant tachycardia

We describe the case of a young patient with runs of repetitive monomorphic left ventricular tachycardia. He was diagnosed with verapamil-sensitive, idiopathic left ventricular tachycardia (ILVT) and underwent an electrophysiological study, in which dual atrioventricular (AV) nodal physiology was evident, with an AV nodal reentrant tachycardia (AVNRT) being easily and reproducibly induced. Both the AVNRT and the ILVT were successfully ablated using high-density electroanatomical mapping and an open-irrigation catheter. In conclusion, verapamil-sensitive ILVT might coexist with AVNRT. In case of invasive therapy, a thorough electrophysiological evaluation is mandatory to exclude or treat other co-existing reentrant supraventricular arrhythmias.

The clinical and electrophysiological characteristics of nonsustained repetitive monomorphic ventricular tachycardia from the left His-Purkinje system.

Repetitive monomorphic ventricular tachycardia (RMVT) arising from the left His-Purkinje system can occasionally be encountered during clinical practice. We describe eight cases as a unique entity in this study to characterize the clinical and electrophysiological features of the patients. Eight patients with frequent palpitation (five men with median age of 28 years) were included in the study from January 2003 to July 2018. Twelve-lead ECG (Electrocardiogram), Holter, and echocardiographic tests were performed after medical history interrogations and physical examinations. Antiarrhythmic drug therapy was essential to all patients, and catheter ablation was attempted if the patients could not tolerate or were not responsive to drug therapy. No patients had a history of syncope and a family history of sudden cardiac death. ECGrecording was characterized by frequent ventricular extrasystoles, ventricular couplets, and salvos of nonsustained VT competitive with sinus rhythm. The QRS morphology of ectopic beats was in the right bundle branch block pattern with severe left axis deviation. The width of the QRS complex from ECG was 135ms (120-140) during ventricular tachycardia. Verapamil had no effect on all VT individuals. Enlargement of the left ventricle was found in two patients. Four out of six cases were successful with catheter ablation treatment. RMVT arising from the left His-Purkinje system is a special arrhythmic and nonverapamil-sensitive entity. The electrophysiological mechanism of this treatment appears to be focal firing, which is amendable to catheter ablation in symptomatic and high-burden patients.

Tachycardia-induced cardiomyopathy due to repetitive monomorphic ventricular ectopy in association with isolated left ventricular non-compaction : online article - case report

Isolated left ventricular non-compaction is a rare genetic disorder manifesting mainly with heart failure, ventricular arrhythmias and systemic embolism. Isolated ventricular tachycardia originating from the right ventricular outflow tract is an arrhythmia that can be treated medically and/or by radiofrequency catheter ablation. Here, we report a case of an asymptomatic 16-year-old boy with a new diagnosis of dilated cardiomyopathy, left ventricular noncompaction and right ventricular outflow tract tachycardia. Electrophysiological studies and radiofrequency ablation of the right ventricular outflow tract tachycardia resulted in normalisation of left ventricular systolic function. This is the first case reporting left ventricular non-compaction in association with tachycardia-induced cardiomyopathy secondary to repetitive monomorphic right ventricular outflow tract tachycardia.

Long-Term Effect of Continuing Sports Activity in Competitive Athletes With Frequent Ventricular Premature Complexes and Apparently Normal Heart

The long-term outcome of athletes with frequent ventricular premature complexes (VPCs) and apparently normal heart has not been fully clarified. To evaluate the clinical and prognostic significance of VPCs and the influence of continuing sports activity during follow-up, we studied 120 healthy athletes (96 men; median age 16 years) in whom frequent VPCs (>100 VPCs/24 hours) were discovered by chance during preparticipation screening. All athletes were followed up for a median of 84 months. During follow-up, 96 underwent serial 24-hour Holter recording and 62 underwent serial echocardiography. The median number of VPCs/24 hours on basal Holter was 3,760. During follow-up, 81 athletes continued sports activity, whereas 39 did not. No athlete died or developed overt heart disease. The median number of VPCs/24 hours decreased in both athletes who continued sports activity and those who did not (from 3,805 to 1,124, p <0.0001 and from 5,787 to 1,298, p <0.0001, respectively). During follow-up, left ventricular ejection fraction slightly decreased to <55% in 9 of 62 athletes who, in respect to the remaining 53, had more VPCs/24 hours both in the basal state (12,000 vs 3,880) and during follow-up (10,702 vs 1,368), and a longer follow-up (95 vs 36 months). In conclusion, (1) frequent VPCs in athletes without heart disease have a long-term benign prognostic significance, (2) sporting activity does not modify this benign outcome, (3) during follow-up, the burden of VPCs decreases whether or not subjects continue sports activity, and (4) in 14.5% of athletes, ejection fraction slightly decreases over time.

Subcutaneous implantable defibrillator: State-of-the art 2013

The subcutaneous implantable cardioverter-defibrillator (S-ICD) has recently been approved for commercial use in Europe, New Zealand and the United States. It is comprised of a pulse generator, placed subcutaneously in a left lateral position, and a parasternal subcutaneous lead-electrode with two sensing electrodes separated by a shocking coil. Being an entirely subcutaneous system it avoids important periprocedural and long-term complications associated with transvenous implantable cardioverter-defibrillator (TV-ICD) systems as well as the need for fluoroscopy during implant surgery. Suitable candidates include pediatric patients with congenital heart disease that limits intracavitary lead placements, those with obstructed venous access, chronic indwelling catheters or high infection risk, as well as young patients with electrical heart disease (e.g., Brugada Syndrome, long QT syndrome, and hypertrophic cardiomyopathy). Nevertheless, given the absence of intracavitary leads, the S-ICD is unable to offer pacing (apart from short-term post-shock pacing). It is therefore not suitable in patients with an indication for antibradycardia pacing or cardiac resynchronization therapy, or with a history of repetitive monomorphic ventricular tachycardia that would benefit from antitachycardia pacing. Current data from initial clinical studies and post-commercialization "real-life" case series, including over 700 patients, have so far been promising and shown that the S-ICD successfully converts induced and spontaneous ventricular tachycardia/ventricular fibrillation episodes with associated complication and inappropriate shock rates similar to that of TV-ICDs. Furthermore, by using far-field electrograms better tachyarrhythmia discrimination when compared to TV-ICDs has been reported. Future results from ongoing clinical studies will determine the S-ICD system's long-term performance, and better define suitable patient profiles.

Catheter ablation of ventricular tachycardia originating from the diverticulum of the right ventricular outflow tract

Ventricular tachyarrhythmias from the right ventricular outflow tract (RVOT) are well recognized.1 In most cases, such arrhythmias are idiopathic because of the presence of a structurally normal heart. However, this ‘normal heart’ can sometimes be due to the early stage of heart disease or minor abnormalities that cannot be detected by routine examination. We report one case with ventricular tachycardia (VT) originating from the diverticulum of the RVOT. The electrocardiographic and electrophysiological characteristics, mapping and ablation strategies, and detailed images are described in this report. A 62-year-old man with a repetitive monomorphic VT with a typical RVOT origin morphology for 19 years was referred for catheter ablation. The echocardiogram did not suggest any evidence of structural heart disease and revealed a normal left ventricular ejection fraction. The oral administration of amiodarone was initially effective, but the patient was referred for an electrophysiological assessment and catheter ablation because of the side effects of amiodarone and reoccurrence of syncope. Ambulatory monitoring did not reveal any large burden of premature ventricular contractions. The 12-lead electrocardiogram (ECG) during the VT demonstrated a left bundle branch block (LBBB) and inferior axis morphology with a late QRS transition in the precordial lead, V4. The QRS complexes had a tall positive component without a notch in the inferior leads and a Qr pattern in lead I ( Figure 1A ). Figure 1 ( A ) Left panel: the 12-lead electrocardiogram of clinical ventricular tachycardia. Right panel: perfect pace mapping was obtained with an almost 11/12 match to clinical ventricular tachycardia morphology from the target site in the diverticulum. ( B ) The local fragmented, low-voltage electrograms at the earliest site which preceded the onset of QRS during ventricular tachycardia by 23 ms was recorded at the same site. ECG, electrocardiogram; VT, ventricular tachycardia. An electrophysiological study was performed under a fasting state …

Tachycardia-Induced Cardiomyopathy in Patients With Idiopathic Ventricular Arrhythmias: The Incidence, Clinical and Electrophysiologic Characteristics, and the Predictors

Idiopathic ventricular arrhythmias in the form of monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) can cause tachycardia-induced cardiomyopathy (TICMP). The aim of this study was to determine the incidence, clinical and electrophysiologic characteristics, and the predictors of TICMP in patients with idiopathic ventricular arrhythmias. Study population consisted of 249 consecutive patients (148 F/101 M, 45 ± 20 y/o) with frequent PVCs and/or VT. All patients underwent transthoracic echocardiography and 24-hour Holter monitoring. TICMP was defined as left ventricular ejection fraction (LVEF) of ≤50% in the absence of any detectable underlying heart disease and improvement of LVEF ≥15% following effective treatment of index ventricular arrhythmia. Seventeen (6.8%) patients had TICMP. Patients with TICMP compared to patients with preserved LVEF were more likely to be male (65% vs 39%, P = 0.043) and asymptomatic (29% vs 9%, P = 0.018), and were more likely to have higher PVC burden (29.4 ± 9.2 vs 8.1 ± 7.4, P < 0.001), persistence of PVCs throughout the day (65% vs 22%, P = 0.001), and repetitive monomorphic VT (24% vs 0.9%, P < 0.001). PVC burden of 16% by ROC curve analysis best separated the patients with TICMP compared to patients with preserved LVEF (sensitivity 100%, specificity 87%, area under curve 0.96). TICMP was relatively common (∼1 in every 15 patients) in our study population. The predictors of TICMP were male gender, absence of symptoms, PVC burden of ≥16%, persistence of PVCs throughout the day, and the presence of repetitive monomorphic VT.

Repetitive Monomorphic Ventricular Tachycardia as a Manifestation of Suboptimally Treated Thyrotoxicosis

Monomorphic ventricular tachycardia (VT) is a unique manifestation of hyperthyroidism. We present the case of a 41-year-old male with a history of hyperthyroidism presenting with palpitations secondary to non-sustained episodes of monomorphic VT. Cardiac arrhythmias due to thyrotoxicosis are perpetually supraventricular in origin. Monomorphic VT in the setting of thyrotoxicosis in the absence of structural heart disease is exceedingly rare. After starting propranolol and increasing the dose of methimazole, the patient had no further episodes of VT. It is important to recognize repetitive monomorphic VT as an understated but important manifestation of thyrotoxicosis. Propranolol is associated with an excellent response in these patients and anti-thyroid medications such as methimazole effectively reverse thyrotoxicity.

Magnesium Sensitive, Adenosine Resistant, Repetitive Monomorphic Ventricular Tachycardia

Repetitive monomorphic ventricular tachycardia (RMVT) is characterized by episodes of ventricular ectopy and nonsustained VT exacerbated by catecholamines. Because this arrhythmia is frequently adenosine sensitive, its mechanism is believed to be cyclic adenosine monophosphate-mediated triggered activity due to delayed afterdepolarizations. We present a case of RMVT associated with significant hypomagnesemia (serum level = 1.1 mg/dL), which did not respond to intravenous (IV) adenosine and terminated repeatedly after IV magnesium. Electrophysiologic study demonstrated an origin from the left sinus of Valsalva, which was successfully ablated. The combination of adenosine resistance and magnesium sensitivity may be consistent with an atypical RMVT mechanism related to inhibition of sodium-potassium adenosine triphosphatase (Na(+)-K(+) ATPase).

Termination of idiopathic sustained monomorphic ventricular tachycardia by intravenous adenosine in a pregnant woman

A 34-year-old pregnant woman presented to the emergency department with the complaints of palpitations at 32 weeks gestation. The diagnosis of right ventricular outflow tract ventricular tachycardia (VT) was made. Intravenous 5 mg of metoprolol and 25 mg of diltiazem did not terminate the VT. Ten milligrams of adenosine were administered. Within 10 s of adenosine administration, sustained VT converted to repetitive monomorphic VT and within 30 s to normal sinus rhythm. The mother and the foetus tolerated the medications well. Non-stress test for the assessment of the foetal well-being was normal.

Outcome of Radiofrequency Catheter Ablation as a non-pharmacological therapy for idiopathic Ventricular Tachycardia.

To determine the outcome of Radiofrequency Catheter Ablation (RFCA) as a non-pharmacological curative therapy for idiopathic Ventricular Tachycardia (VT) and to identify procedure-related complications. Descriptive study. The Armed Forces Institute of Cardiology and National Institute of Heart Diseases, Rawalpindi, from February 2001 to October 2008. Ninety eight consecutive patients with idiopathic VT, resistant to drug therapy, who underwent Electrophysiology Studies (EPS) radiofrequency catheter ablation were enrolled. Clinical and electrophysiological variables were recorded and a descriptive analysis was done. Out of the 98 patients, 79 were males (80.6%). The mean age was 33.29+11.93 years. Modes of presentation were sustained VT, Repetitive Monomorphic VT (RMVT), Non-sustained VT (NSVT) and Ventricular Premature Beats (VPBs). Right Ventricular Outflow Tract (RVOT) VT was found in 37 patients, 37 had Idiopathic Left Ventricular Tachycardia (ILVT), 20 had Left Ventricular Outflow Tract (LVOT) VT, and Inflow Right Ventricular Tachycardia (IRVT) was found in 7 patients. Other sites of origin of VT were infrequent. Eight patients had dual morphologies of VT. Atrioventricular Nodal Re-entry Tachycardia (AVNRT) was found in 8 patients. RFCA was successful in abolishing inducible VT in 88 patients. One patient developed complete AV block requiring a permanent pacemaker. Results of this study confirm a high degree of success and safety of radiofrequency catheter ablation as curative therapy for idiopathic ventricular tachycardia.

Mechanism of outflow tract tachycardia

m s l m c c t ntroduction ithin the last decade, considerable progress has been made ith respect to delineating the cellular and molecular mechnisms for a number of arrhythmogenic syndromes that sed to be classified under the generic category “idiopathic entricular tachycardia.” Mutations in ion channels as well s structural proteins that result in either hyperor hypounctioning of a given signal are thought to underlie the ong QT, Brugada, short QT, and catecholaminergic polyorphic ventricular tachycardia (VT) syndromes. Affected ndividuals are relatively young, have little or no evidence f structural heart disease, and usually present with polyorphic VT or ventricular fibrillation (VF). In some of hese syndromes, enhanced adrenergic stimulation is a reqisite trigger for initiation of the arrhythmia. Based on xtrapolation of experimental data, the predominant clinical echanism underlying these arrhythmias is thought to be onreentrant; however, phase 2 reentry possibly accounts or the arrhythmias associated with Brugada syndrome. The most common form of VT that occurs in the absence f structural heart disease originates from the ventricular utflow tract. Originally associated with a right ventricular utflow tract origin, it now is recognized that the arrhythmia lso can originate from the left ventricular outflow tract in early 20% of patients.1,2 Unlike ventricular arrhythmias ssociated with monogenic mutational syndromes, outflow ract tachycardia is a stable, organized arrhythmia that is ssociated with a uniform ECG morphology and most often anifests with a left bundle branch block, inferior-axis onfiguration. Although the arrhythmia initially was associted with exercise-induced sustained VT, it now is appreciated hat the clinical presentation of outflow tract arrhythmia can be rotean. For example, in addition to exercise-induced susained VT, the arrhythmia may occur at rest and present as onsustained VT (often as repetitive monomorphic VT) or

Catheter Ablation for Ventricular Tachycardia

Sustained ventricular tachycardia (VT) is an important cause of morbidity and sudden death in patients with heart disease.1 Implantable cardioverter-defibrillators (ICDs) terminate VT episodes, reducing the risk of sudden death. Recurrent VT develops in 40% to 60% of patients who receive an ICD after an episode of spontaneous sustained VT. A first episode of VT occurs in ≈20% of patients within 3 to 5 years after ICD implantation for primary prevention of sudden death in high-risk groups.2–4 ICD shocks reduce quality of life and are associated with an increased risk of death.2–4 Antiarrhythmic drug therapy with amiodarone or sotalol reduces VT episodes but with disappointing incidence of side effects and efficacy.2 Catheter ablation is useful for reducing VT episodes and can be life-saving when VT is incessant.1,5,6 Idiopathic VTs occur in patients without structural heart disease and rarely cause sudden death. Electrophysiological study with catheter ablation is often warranted to confirm the diagnosis, to provide further evidence for the absence of ventricular scar or other disease, and often to cure the arrhythmia. Ablation is also an option for symptomatic nonsustained VT and frequent ventricular ectopy in these patients.1 The appearance of the VT on ECG often suggests its likely cause and associated heart disease (Figure 1). Monomorphic VT has the same QRS complex from beat to beat, indicating repetitive ventricular activation from a structural substrate or focus that can be targeted for ablation. Most are due to reentry through regions of ventricular scar.7 Figure 1. ECG types of VT and most common causes are shown with characteristic ECG features of selected VTs. LBBB indicates left bundle-branch block; LVOT, LV outflow tract; RBBB, right bundle-branch block; L, left; and R, right. Polymorphic VTs have a changing ventricular activation sequence that can be due to …

Repetitive Monomorphic Ventricular Tachycardia Associated with Exercise

The case of a 45-year-old man suffering from a catecholamine-sensitive ventricular tachycardia originating from the right ventricular outflow tract is reported. The authors describe a novel noninvasive treatment strategy for the management of this patient.

373 Electrocardiographic characteristics of repetitive monomorphic right ventricular tachycardia originating near the HIS-bundle

373 Electrocardiographic characteristics of repetitive monomorphic right ventricular tachycardia originating near the HIS-bundle

Surgery

Surgery

373 Electrocardiographic characteristics of repetitive monomorphic right ventricular tachycardia originating near the HIS-bundle

373 Electrocardiographic characteristics of repetitive monomorphic right ventricular tachycardia originating near the HIS-bundle

Safety and efficacy of catheter ablation of repetitive monomorphic ventricular tachycardia arising from the sinus of Valsalva guided by intracardiac echocardiography

Safety and efficacy of catheter ablation of repetitive monomorphic ventricular tachycardia arising from the sinus of Valsalva guided by intracardiac echocardiography

Peripartum Cardiomyopathy Presenting with Repetitive Monomorphic Ventricular Tachycardia

A 30-year-old asymptomatic pregnant woman at 38 weeks' gestation was noticed to have repetitive monomorphic ventricular tachycardia. A dilated left ventricle with moderately reduced systolic function was found on echocardiographic examination. To the best of our knowledge, a case of peripartum cardiomyopathy presenting with repetitive monomorphic ventricular tachycardia has not been previously reported.

Diagnosis and treatment of idiopathic ventricular tachycardia.

Idiopathic ventricular tachycardia in patients with an anatomically normal heart is a distinct entity whose management and prognosis differs from ventricular tachycardia associated with structural heart disease. The tachycardia's QRS morphology on surface electrocardiogram (ECG) predicts the site of origin and is commonly classified as right ventricular tachycardia or left ventricular tachycardia. The tachycardia is further characterized by clinical features such as repetitive monomorphic ventricular tachycardia (VT), paroxysmal sustained VT, or catecholamine dependent VT. The responsiveness of VT to adenosine or verapamil is useful in differentiating the mechanism, which may be reentry or triggered activity. Patients generally tolerate the tachycardia but may present with dizziness, syncope, or palpitations. Sudden cardiac death is rare in this patient population. Patient work-up should include 12-lead ECG, signal-averaged ECG, ambulatory ECG recording, stress testing, and tests to rule out structural heart disease such as echocardiography, cardiac angiography, endomyocardial biopsy, or magnetic resonance imaging. Treatment options include pharmacotherapy or catheter ablation. Although the prognosis of these patients remains excellent, they should continue to have periodic cardiac follow-up to rule out latent progressive heart disease such as arrhythmogenic right ventricular dysplasia or cardiomyopathy or other forms of cardiomyopathies.