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Focal Monomorphic Ventricular Tachycardia As The First Manifestation Of Amyloid Cardiomyopathy  [cached]
Srikanth Seethala,Sandeep Jain,N. Paul Ohori,Sara Monaco
Indian Pacing and Electrophysiology Journal , 2010,
Abstract: 52-year-old patient presented with palpitation and well tolerated monomorphic ventricular tachycardia. He had normal echocardiogram and coronary angiogram 3 months prior to presentation. Surface EKG revealed regular wide-complex tachycardia with right bundle branch block morphology and right inferior axis. In conjunction with recent negative cardiac evaluation, this suggested idiopathic focal ventricular tachycardia from anterolateral basal left ventricle. CARTO based activation mapping confirmed the presence of VT focus in that area. Radiofrequency ablation at the site of perfect pacemap resulted in a partial suppression of the focus. Echocardiogram was subsequently performed because of progressive dyspnea. It revealed asymmetrical thickening of posterolateral left ventricle, with delayed enhancement on contrast magnetic resonance imaging. Fine needle aspiration of abdominal fat stained with Congo red confirmed the diagnosis of systemic AL amyloidosis due to IgG λ-light chain deposition. Consequently, the patient underwent placement of implantable defibrillator and hematopoetic stem cell transplantation. He remains in excellent functional status 18 months after presentation.
Pattern of initiation of monomorphic ventricular tachycardia in recorded intracardiac electrograms  [cached]
Majid Haghjoo,Arash Arya,Mohammad Ali Sadr-Ameli
Indian Pacing and Electrophysiology Journal , 2005,
Abstract: Background: By analyzing stored intracardiac electrograms during spontaneous monomorphic ventricular tachycardia (VT), we examined the patterns of the VT initiation in a group of patients with implantable cardioverter defibrillators (ICDs). Methods: Stored electrograms (EGMs) were monomorphic VTs and at least 5 beats before the initiation and after the termination of VT were analyzed. Cycle length, sinus rate, and the prematurity index for each episode were noted. Results: We studied 182 episodes of VT among 50 patients with ICDs. VPC-induced (extrasystolic initiation) episode was the most frequent pattern (106; 58%) followed by 76 episodes (42%) in sudden-onset group. Among the VPC-induced group, VPCs in 85 episodes (80%) were different in morphology from subsequent VT. Sudden-onset episodes had longer cycle lengths (377±30ms) in comparison with the VPC-induced ones (349±29ms; P= 0.001). Sinus rate before VT was faster in the sudden-onset compared to that in VPC-induced one (599±227ms versus 664±213ms; P=0.005). Both of these episodes responded similarly to ICD tiered therapy. There was no statistically significant difference in coupling interval, prematurity index, underlying heart disease, ejection fraction, and antiarrhythmic drug usage between two groups (P=NS). Conclusions: Dissimilarities between VT initiation patterns could not be explained by differences in electrical (coupling interval, and prematurity index) or clinical (heart disease, ejection fraction, and antiarrhythmic drug) variables among the patients. There is no association between pattern of VT initiation and the success rate of electrical therapy.
Vasopressin improves outcome in out-of-hospital cardiopulmonary resuscitation of ventricular fibrillation and pulseless ventricular tachycardia: a observational cohort study
Stefek Grmec, Stefan Mally
Critical Care , 2005, DOI: 10.1186/cc3967
Abstract: The present study was conducted in a prehospital setting and included patients with ventricular fibrillation or pulseless ventricular tachycardia undergoing one of three treatments: group I patients received only adrenaline 1 mg every 3 minutes; group II patients received one intravenous dose of arginine vasopressine (40 IU) after three doses of 1 mg epinephrine; and patients in group III received vasopressin 40 IU as first-line therapy. The cause of cardiac arrest (myocardial infarction or other cause) was established for each patient in hospital.A total of 109 patients who suffered nontraumatic cardiac arrest were included in the study. The rates of restoration of spontaneous circulation and subsequent hospital admission were higher in vasopressin-treated groups (23/53 [45%] in group I, 19/31 [61%] in group II and 17/27 [63%] in group III). There were also higher 24-hour survival rates among vasopressin-treated patients (P < 0.05), and more vasopressin-treated patients were discharged from hospital (10/51 [20%] in group I, 8/31 [26%] in group II and 7/27 [26%] group III; P = 0.21). Especially in the subgroup of patients with myocardial infarction as the underlying cause of cardiac arrest, the hospital discharge rate was significantly higher in vasopressin-treated patients (P < 0.05). Among patients who were discharged from hospital, we found no significant differences in neurological status between groups.The greater 24-hour survival rate in vasopressin-treated patients suggests that consideration of combined vasopressin and adrenaline is warranted for the treatment of refractory ventricular fibrillation or pulseless ventricular tachycardia. This is especially the case for those patients with myocardial infarction, for whom vasopressin treatment is also associated with a higher hospital discharge rate.Survival after cardiopulmonary resuscitation (CPR) with adrenaline (epinephrine) therapy is disappointing [1,2]. The use of adrenaline is associated with increased m
Late Presentation of Recurrent Monomorphic Ventricular Tachycardia following Minimally Invasive Mitral Valve Repair due to Epicardial Injury  [PDF]
Harry L. South,Moses Osoro,Tjuan Overly
Case Reports in Cardiology , 2014, DOI: 10.1155/2014/976494
Abstract: We report a 73-year-old male with late onset monomorphic ventricular tachycardia following mitral valve repair (MVR). Typically, injury to epicardial arteries following mitral valve repair/replacement presents immediately as ventricular tachycardia/fibrillation, difficulty weaning from cardiopulmonary bypass, worsening ECG changes, increasing cardiac biomarkers, or new wall motion abnormalities. Our case illustrates a “late complication” of a distorted circumflex artery following mitral valve repair and the importance of early diagnostic angiography and percutaneous intervention. 1. Introduction In experienced centers mitral valve repair has low mortality rates and excellent outcomes. The Cleveland Clinic and Mayo Clinic report 30 day mortality rates of 0.3% and 0.9%, respectively [1, 2]. Injury to the circumflex artery during MVR is a recognized complication, albeit rare. The proximity of the circumflex artery to the anterolateral commissure of the mitral valve predisposes the artery to injury during mitral valve surgery [3, 4]. Acute occlusion of the circumflex artery may manifest immediately as ventricular arrhythmia, difficulty weaning from cardiopulmonary bypass, ST elevation myocardial infarction, or new wall motion abnormality [5]. We report a late onset sustained monomorphic ventricular tachycardia (SMVT) secondary to distortion of the circumflex artery following mitral valve repair. 2. Case Report A 73-year-old male with mitral regurgitation presented to his primary cardiologist with symptoms of increasing dyspnea on exertion. As part of the diagnostic workup, a transthoracic echocardiogram (TTE) was performed which revealed significant pulmonary hypertension (estimated pulmonary artery pressures of 50–55?mmHg), not previously seen on prior TTE. Moderate mitral valve insufficiency with prolapse of the posterior leaflet and normal right ventricular function was also present. Past medical history was significant for hyperlipidemia, chronic obstructive pulmonary disease, chronic kidney disease (stage 3), and benign prostatic hypertrophy. The decision was made by the primary cardiologist to refer the patient for mitral valve repair. In anticipation of the aforementioned procedure a left and right cardiac catheterization was performed which showed a left dominant system with nonobstructive coronary artery disease, normal left ventricular function, right ventricular pressures of 68/9?mmHg, pulmonary artery pressures of 63/30?mmHg, and a pulmonary capillary wedge pressure of 21?mmHg. The patient was then referred for cardiothoracic surgeon
Tuberculous myocarditis presenting as a refractory ventricular tachycardia of biventricular origin  [PDF]
MP Gautam,G Sogunuru,G Subramanyam,RC Viswanath
Journal of College of Medical Sciences-Nepal , 2011, DOI: 10.3126/jcmsn.v7i2.6686
Abstract: Ventricular tachycardia (VT) is one of the difficult clinical problems for the physician. Its evaluation and treatment are complicated because of its life-threatening nature and urgent need of rapid management. Any process that creates myocardial scar tissue could be the substrate for ventricular tachycardia. The coronary artery disease is the most common cause of myocardial scar. The dilated cardiomyopathies, hypertrophic cardiomyopathy, right ventricular dysplasia, Chagas disease, sarcoidosis, myocarditis including tubercular and other chronic granulomatous conditions and surgical incisions in the ventricle also can create myocardial scar and can lead to ventricular tachycardia. Occasionally, the arrhythmia may be well-tolerated, but in most of the situations it is associated with grave, life-threatening hemodynamic compromise. Regardless of the arrhythmia mechanism, the severity of clinical symptoms and hemodynamic compromise determines the urgency with which VT must be treated. Rarely, patients present with repetitive runs of nonsustained or sustained VT despite the medical treatment and poorly respond to the conventional treatment. Such refractory VT may cause a tachycardia-induced cardiomyopathy in long run. In such cases, long-term management also include looking beyond the VT and work up for the possible and treatable cause of VT. Here we are presenting a case report of a young patient with tubercular myocarditis who has presented to us with recurrent ventricular tachycardia of both right bundle and left bundle branch block morphology and LV dysfunction. A review of literature has been carried out on causes and management of refractory VT.
Monomorphic Outflow Tract Ventricular Tachycardia: Unique Presenting Manifestation of Gitelman's Syndrome
Subba Reddy Vanga,Chandra Annapureddy,Mazda Biria,Dhanunjaya Lakkireddy
Journal of Atrial Fibrillation , 2010, DOI: 10.4022/jafib.v1i10.560
Abstract: Outflow Tract Ventricular Tachycardia (OTVT) is typically seen in young to middle aged people with structurally normal hearts. These arrhythmias are triggered by emotional or stress factors and that responds to medications. Electrolyte abnormalities rarely cause ventricular arrhythmia. Gitelman's syndrome, a rare autosomal recessive renal disorder causes hypokalemia, metabolic alkalosis and hypomagnesaemia . This disorder is often benign with mild clinical symptoms and excellent long-term prognosis. We present a case of Gitelman's syndrome with symptomatic OTVT as initial manifestation.
Sustained Ventricular Tachycardia and Cardiogenic Shock due to Scorpion Envenomation  [PDF]
Carlos Henrique Miranda,Karina Tozatto Maio,Henrique Turin Moreira,Marcos Moraes,Viviane Imaculada do Carmo Custodio,Antonio Pazin-Filho,Palmira Cupo
Case Reports in Medicine , 2014, DOI: 10.1155/2014/251870
Abstract: We describe a case of severe scorpion envenomation in an adult patient, with the presence of very rapid sustained ventricular tachycardia followed by cardiogenic shock, which was reversed by scorpion antivenom administration. Scorpion venom causes cardiac changes that can lead to an environment favoring arrhythmogenesis. 1. Introduction Scorpion stings occur in many areas of the world, mainly in rural regions of countries with a hot climate [1]. A total of 51,457 scorpion stings were reported in Brazil during the year of 2010 [2]. Because of its frequency, the World Health Organization considers scorpion envenomation as the second most important type of poisoning caused by animals around the world [3]. The majority of these incidents are not serious, with local pain being the only clinical manifestation. However, severe complications such as acute pulmonary edema and cardiogenic shock can occur, mainly in children [1, 4]. We report here an unusual presentation of a case of severe scorpion envenoming complicated by acute pulmonary edema and cardiogenic shock in an adult patient, with the presence of very rapid sustained ventricular tachycardia during the early phase. 2. Case Presentation A 25-year-old woman with no previous disease was admitted to an emergency department after being stung in a toe by an unidentified animal when she was walking at night in a place infested with scorpions in an urban area near the local cemetery. A few minutes after the sting, she had important local pain and paresthesia of her entire left leg associated with several episodes of emesis, profuse sweating, mild respiratory distress, hypertension, and tachycardia. She first sought primary medical care, with clinical examination showing blood pressure of ?mm?Hg and a heart rate of 156?bpm. The electrocardiogram showed sustained ventricular tachycardia with very fast heart rate of approximately 300?bpm associated with a right bundle branch block pattern (Figure 1(a)). Amiodarone was initiated and the sinus rhythm was restored after some minutes, with the patient then being taken to our hospital. During this initial evaluation, no analgesics or antihypertensive agents were administered. Figure 1: Electrocardiogram of a 25-year-old woman showing an episode of sustained ventricular tachycardia (SVT) with very fast heart rate (approximately 300?bpm) after scorpion envenomation (a). Upon admission to the hospital, the electrocardiogram showed sinus tachycardia associated with QTc interval prolongation (550?ms) after SVT reversal (b). A chest radiograph shows pulmonary edema with a
Exercise Induced Non-Sustained Ventricular Tachycardia and Indication for Invasive Management
Shahriar Dadkhah, Samaneh Dowlatshahi, Korosh Sharain and Roza Sharain
Clinical Medicine Insights: Cardiology , 2012, DOI: 10.4137/CMC.S8504
Abstract: Diagnostic stress echo testing is commonly performed in patients with known or suspected cardiovascular disease. There has been considerable debate in management of exercise induced non-sustained ventricular tachycardia (NSVT). In this case report, we present our experience with a case of exercise induced NSVT, and subsequent angiographically significant left anterior descending (LAD) coronary artery lesion.
Resetting of Cardiac Ventricular Tachycardia Storm with Intravenous Potassium Chloride: A Case Report  [PDF]
Gal Sella, Sharon L. Kracoff
Case Reports in Clinical Medicine (CRCM) , 2018, DOI: 10.4236/crcm.2018.72013
Abstract: Ventricular Tachycardia Storm (VTS) with hemodynamic instability is a life-threatening arrhythmia more often presents in patients with structural heart disease. Lack of response to cardioversion and/or antiarrhythmic drugs will have fatal consequences. We report a case of a hemodynamically unstable patient with Ventricular Tachycardia Storm refractory to intravenous antiarrhythmic medications, which finally responded to a slow bolus of IV potassium chloride. This case emphasizes the importance of identifying an electrolyte imbalance as a possible cause of a Ventricular Tachycardia storm and its rapid correction as an addition to the usual pharmacological treatment.
The impact of syncope during clinical presentation of sustained ventricular tachycardia on total and cardiac mortality in patients with chronic Chagasic heart disease
Leite, Luiz Roberto;Fenelon, Guilherme;Paes, ?ngela Tavares;de Paola, Angelo Amato Vincenzo;
Arquivos Brasileiros de Cardiologia , 2001, DOI: 10.1590/S0066-782X2001001100005
Abstract: objective: to assess the impact of syncope during sustained ventricular tachycardia on total and cardiac mortality in patients with chronic chagasic heart disease. methods: we assessed 78 patients with sustained ventricular tachycardia and chronic chagas' heart disease. the mean age was 53±10 years, 45 were males, and the mean ejection fraction was 49.6±13%. the patients were divided into 2 groups according to the presence (gi=45) or absence (gii=33) of syncope during sustained ventricular tachycardia. results: after a mean follow-up of 49 months, total mortality was 35% (28 deaths), 22 deaths having a cardiac cause (78.6%). no difference was observed in total (33.3% x 39.4%) and cardiac (26.7% x 30.3%) mortality, or in nonfatal sustained ventricular tachycardia between gi and gii patients (57.6% x 54.4%, respectively). however, the presence of syncope during recurrences was significantly greater in those patients who had had the symptom from the beginning (65.4% x 18.1%, p<0.01). conclusion: syncope during the presentation of sustained ventricular tachycardia is not associated with an increase in total or cardiac mortality in patients with chronic chagas' heart disease. however, syncope during the recurrence ventricular tachycardia is greater in patients experiencing syncope in the first episode, of sustained ventricular tachycardia.
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