Evidence Of Ventricular Tachycardia Research Articles

CE-454610-3 VT STORM DUE TO HYPERTROPHIC CARDIOMYOPATHY TREATED WITH ALCOHOL SEPTAL ABLATION

Radiofrequency (RF) ablation is a guideline-recommended therapy for ventricular tachycardia (VT). However, certain locations can be inaccessible through endocardial or epicardial approach. There are several documented unconventional techniques in these cases where VT is either treatment-refractory to RF ablation, or ablation is unlikely to be successful due to deep intramural substrate. N/A N/A A 66-year-old gentleman with a history of coronary artery disease (CAD) presents with four days of palpitations and lightheadedness to the emergency department. An ECG was performed which showed monomorphic VT from a basal septal focus. He was hemodynamically stable and thus started on a lidocaine drip and intermittent metoprolol IV pushes with conversion to sinus rhythm. Given the history of CAD, primary differential concerns were ischemia-mediated or scar-mediated VT. Thus, the patient underwent a coronary angiogram which revealed stable non-obstructive CAD. The patient then underwent a cardiac MRI which revealed severe asymmetric left ventricular hypertrophy measuring up to 18 mm in the mid-basal interventricular septum with mid-myocardial late gadolinium enhancement in the same area. This was most consistent with hypertrophic cardiomyopathy (HCM) as the etiology for the patient’s VT. As the patient continued to have significant ventricular ectopy and recurrent bouts of sustained VT on medical management, options for VT ablation were discussed. Overall, given the deep intramural location of the suspected VT substrate, endocardial and epicardial approaches were thought to have a low probability of success. Transarterial coronary ethanol ablation (TCEA) of the septum was thought to have the highest likelihood of success at controlling the patient’s VT in the setting of HCM. The patient underwent successful TTE guided TCEA of the first septal branch. Left ventricular outflow tract (LVOT) gradient improved from 45 to 17 mmHg. The patient was observed for 24 hours without evidence of VT. An ICD was subsequently implanted for secondary prevention. The patient was discharged in stable condition on an oral beta blocker without any additional anti-arrhythmic medications. In patients with VT due to HCM where there is a deep intramural substrate not amenable to traditional RF catheter ablation, TCEA is a reasonable approach. We describe a case of successful TCEA in both decreasing a patient’s LVOT gradient as well as cessation of the patient’s treatment refractory VT.

Frequent ventricular extrasystoles after heart transplantation: a late presentation of amiodarone-induced thyrotoxicosis: a case report.

BackgroundThere is a lack of information about a mixed type of amiodarone-induced thyrotoxicosis (AIT) after heart transplantation (HTx) with no amiodarone treatment in almost 1 year. Frequent ventricular extrasystoles (VES) associated with a mixed type of AIT can often be treated using thiamazole and prednisolone, without the need for specific antiarrhythmic treatment.Case summaryWe present a clinical case of a 65-year-old heart transplanted male patient with frequent VES associated with mixed type of AIT. Recipient had managed with amiodarone prior to HTx but there were no indications for it after the surgery. One year after antiarrhythmic treatment was discontinued, monomorphic VES (total amount: 27 472/day) were diagnosed. In addition, our investigation revealed that thyrotoxicosis developed. Prednisolone and thiamazole were added to the treatment with positive outcomes. The antithyroid treatment had been discontinued after 9 months and results of the 24-h Holter electrocardiogram monitoring showed only two VES/24 h.DiscussionThe case highlights the association of amiodarone, thyroid disorders, and VES. In mixed type AIT or if diagnosis is uncertain, it is reasonable to use mixed therapy. Next is to decide whether you need special treatment for VES. There was no evidence of ventricular tachycardia. Thyroid function tests remained normal off antithyroid medications and the total amount of VES significantly decreased. There were no indications for any antiarrhythmic treatment or ablation.

Ventricular tachycardia: a hospital perspective.

To describe the etiology and outcome in patients with ventricular tachycardia in our patient population. A descriptive study. The study was conducted at the Aga Khan University Hospital from November 2002 to October 2003. We enrolled 58 patients who presented to the emergency room with clinical and electrocardiographic evidence of ventricular tachycardia (VT) and/or who developed it during the inpatient stay at the Aga Khan University Hospital. Medical records were retrieved through the computerized data retrieval system. Patients above 18 years of age were included. Those with a pacemaker or who developed VT during electrophysiological testing were excluded. A pre-designed proforma was filled for all patients who fulfilled the inclusion criteria. All patients were worked up for etiological causes of ventricular tachycardia. Outcomes in the form of death or discharge were recorded. There were 58 patients who suffered ventricular tachycardias during the study period. These included 70.7 %( 42) males and 29.3 %( 16) females. Mean age of the patients was 57.06+/-11.84 years. Emergency room admissions accounted for 55.2% and ventricular tachycardia was seen in 44.8% during the inpatient stay. Unresponsiveness was the presenting symptom in 25.9%, chest pain in 24.1%, palpitations in 13.8% and ghabrahat in 12.1% patients. Myocardial ischemia was seen in 43.5% of the patients while 23.2% had cardiomyopathy, followed by 33.3% miscellaneous. Out of the patients who had myocardial ischemia (43.5%), 76.6% had non-ST elevation myocardial infarction, 20 % patients had ST elevation myocardial infarction and 3.3% had unstable angina. Hemodynamic instability was noted in 50%, who subsequently required defibrillation. The mortality among these patients with VT was 13.7%. Myocardial ischemia was most commonly seen in patients with ventricular tachycardia in our group of patients. Ventricular tachycardia is associated with a significant mortality of 13.7%.

Orthostatic blood pressure test for risk stratification in patients with hypertrophic cardiomyopathy.

BackgroundHypertrophic cardiomyopathy (HCM) is the most common cause of sudden cardiac death (SCD) in young adults, mainly ascribed to ventricular tachycardia (VT). Assuming that VT is the major cause of (pre-) syncope in HCM patients, its occurrence is essential for SCD risk stratification and primarily preventive ICD-implantation. However, evidence of VT during syncope is often missing. As the differentiation of potential lethal causes for syncope such as VT from more harmless reasons is crucial, HCM patients were screened for orthostatic dysregulation by using a simple orthostatic blood pressure test.MethodsOver 15 months (IQR [9;20]) 100 HCM patients (55.8±16.2 yrs, 61% male) were evaluated for (pre-)syncope and VT (24h-ECGs, device-memories) within the last five years. Eighty patients underwent an orthostatic blood pressure test. Logistic regression models were used for statistical analysis.ResultsIn older patients (>40 yrs) a positive orthostatic test result increased the chance of (pre-) syncope by a factor of 63 (95%-CI [8.8; 447.9], p<0.001; 93% sensitivity, 95%-CI [76; 99]; 74% specificity, 95%-CI [58; 86]). No correlation with VT was shown. A prolonged QTc interval also increased the chance of (pre-) syncope by a factor of 6.6 (95%-CI [2.0; 21.7]; p=0.002).ConclusionsThe orthostatic blood pressure test is highly valuable for evaluation of syncope and presyncope especially in older HCM patients, suggesting that orthostatic syncope might be more relevant than previously assumed. Considering the high complication rates due to ICD therapies, this test may provide useful information for the evaluation of syncope in individual risk stratification and may help to prevent unnecessary device implantations, especially in older HCM patients.

Successful surgical treatment for recurrent cardiac fibroma 21 years after resection.

Cardiac fibromas are rare benign tumors usually seen in the pediatric population. Generally, long-term survival after surgical resection is favorable, and recurrence of fibroma has been hardly reported. Herein, we report a case of a 34-year-old woman who presented with ventricular tachycardia 21 years after resection of a cardiac fibroma and was found to have a recurrent giant cardiac fibroma. We performed a complete resection of the recurrent fibroma. At the 2-year follow-up, she remains asymptomatic with no evidence of ventricular tachycardia or recurrence of fibroma.

A case of idiopathic ventricular tachycardia in a 14-year-old obese patient due to golden berry fruit extract pills for weight loss

Several studies have determined an association between obesity and increased risk of cardiac arrhythmia. Currently, due to the increased frequency of obesity, food-, plant-, and drug-based therapies for weight loss have gained great attention. A 14-year-old female patient presented with complaints of palpitation of one-hour onset. Blood pressure was 110/70 mmHg and peripheral pulses were present. She had been using golden berry extract pill three times a day for 10 days. The electrocardiogram showed nonsustained monomorphic ventricular tachycardia (VT). Echocardiographic examination and cardiac magnetic resonance imaging (MRI) were normal. She returned to sinus rhythm following amiodarone infusion. She refused the electrophysiologic study, which plays a vital role in the diagnosis and establishment of the appropriate therapy. Although there was no decrease in body mass index (BMI) of the patient during the two-year follow-up, she had no complaint or evidence of VT on intermittent rhythm Holter studies. This case suggests the primary role of golden berry extract use in the development of VT, rather than obesity.

Surgical Treatment of Giant Intramural Left Ventricular Fibroma in an Adult Patient with Refractory Ventricular Tachycardia

Cardiac fibromas are rare benign tumors predominantly diagnosed in children and teenagers. We report a 57-year-old male patient with class II dyspnea and angina. During electrocardiographic assessment, recurrent ventricular tachycardia was present and magnetic resonance imaging revealed a giant (12.5 × 5 × 4 cm) intramural left ventricular tumor compatible with cardiac fibroma. After surgical biopsy and histological confirmation, open-heart surgical resection was successfully performed. After nine months of follow up, the patient remains asymptomatic without evidence of ventricular tachycardia.

Sudden Death in an Emery–Dreifuss Muscular Dystrophy Patient with an Implantable Defibrillator

We report the first case of witnessed sudden death of an Emery-Dreifuss muscular dystrophy (EDMD) patient with a properly functioning implantable cardioverter-defibrillator (ICD). This 38-yr-old woman with normal left ventricular function had a history of recurrent syncope and nonsustained ventricular tachycardia, for which a single-chamber ventricular ICD was implanted. She later collapsed suddenly and unexpectedly while at home, with witnesses present, and was found cyanotic with pulseless electrical activity by the emergency squad. This event took place in the setting of previously documented hypercapnic ventilatory insufficiency, for which she had refused the use of respiratory muscle aids to normalize alveolar ventilation. Subsequent interrogation of the ICD demonstrated normal function, with no evidence of ventricular tachycardia or ventricular fibrillation. In the hospital, her myocardial function was found to be normal by echocardiography. Further workup revealed that the patient had severe anoxic encephalopathy. She was eventually made "do not resuscitate," and she died on the sixth day of hospitalization. An autopsy was performed, and no obvious cause for the sudden death could be established. Review of the clinical presentation, with all the data available, suggests acute respiratory failure as the likely primary cause of this patient's sudden death, which then secondarily led to the observed pulseless electrical activity of the heart. The use of respiratory muscle aids--in particular, noninvasive mechanical ventilation to prevent chronic hypercapnia and cor pulmonale--is crucial for EDMD patients with symptomatic ventilatory insufficiency, for whom sudden deaths may not necessarily be of primarily cardiac origin.

Heterogeneous sympathetic innervation in German shepherd dogs with inherited ventricular arrhythmia and sudden cardiac death.

Recently, a colony of German shepherd dogs with inherited spontaneous cardiac arrhythmias and associated sudden death has been developed and characterized. Due to the median age of onset of the arrhythmia (4.5 months), the tendency for the arrhythmia to occur during REM sleep or after exercise, and the absence of structural heart disease, we hypothesized a developmental abnormality of the sympathetic innervation to the heart. We studied 11 dogs from this colony, ranging in age from 6 months to 6 years, and four 7-month-old German shepherd dogs unrelated to the colony as controls. We imaged the distribution of functional myocardial sympathetic innervation and perfusion with [123I]metaiodobenzylguanidine (MIBG) and 201Tl, respectively. Sympathetic nerve distribution was evaluated morphologically by immunocytochemical localization of tyrosine hydroxylase. All of the hearts showed evidence of a regional decrease in MIBG uptake, ranging from 5.3% to 53.4% of the myocardium, whereas control dogs showed homogeneous MIBG uptake. Immunocytochemical studies on sections from regions with decreased MIBG uptake showed a striking paucity of nerves compared with regions with normal MIBG uptake, confirming denervation. When the dogs were grouped into those with (n=6) and without (n=5) evidence of ventricular tachycardia on ambulatory ECG, the group with ventricular tachycardia showed 35+/-16.5% denervation, whereas the group without ventricular tachycardia showed 12+/-5.6% denervation (P<.02). Abnormal heterogeneous sympathetic innervation exists in these dogs with inherited ventricular arrhythmia and sudden cardiac death. Mechanisms relating the presence and extent of regional denervation to the incidence of ventricular arrhythmia remain to be defined.

Long-term clinical outcome of right bundle branch radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia.

The study assessed the long-term outcome of patients undergoing radiofrequency ablation of the right bundle for bundle branch reentrant ventricular tachycardia. Bundle branch reentrant tachycardia was diagnosed in 16 patients (ejection fraction 31% +/- 15%) who underwent electrophysiology study in our laboratory. All patients had His-Purkinje system conduction delay with mean HV interval of 68 +/- 8 ms. After ablation, right bundle branch block developed in 15 patients. One patient developed complete heart block, which was anticipated. One patient died of heart failure 9 months after ablation. Two patients were successfully bridged to heart transplantation 0.5 and 13 months, respectively, after ablation. Two patients received implantable defibrillators for other ventricular tachycardias. One patient had syncope 11 months after ablation, but there was no evidence of ventricular tachycardia or heart block in repeat electrophysiology study. This patient died suddenly 29 months after ablation. The remaining nine patients were alive and well for a mean follow-up of 19 +/- 10 months. Radiofrequency ablation of the right bundle branch is an effective therapy for treatment of bundle branch reentrant ventricular tachycardia. Survival is excellent provided that other types of ventricular tachycardia, when present, are treated as well. This technique may be helpful in management of patients who have unacceptable frequent shocks from their implanted defibrillators and may be helpful in avoiding implantation of such a device completely in others. In some patients with terminal heart failure and incessant ventricular tachycardia, this procedure can function as a bridge to cardiac transplantation.

Verapamil for the suppression of idiopathic ventricular tachycardia of left bundle branch block-like morphology

This study examines the efficacy of verapamil for the suppression of idiopathic ventricular tachycardia (VT) of left bundle branch block LBBB-like morphology. Forty-two patients (mean age 36.2 ± 12.1 years; 20 men and 22 women) with VT and without any underlying cardiac abnormality on clinical examination and noninvasive investigation were studied. The inducibility of clinical VT was examined by treadmill exercise testing and programmed ventricular stimulation (PVS). In 29 patients VT was inducible by exercise testing, in 24 by PVS, and in 23 there was evidence of VT on Holter monitoring. After baseline testing, patients were treated with verapamil 120 mg thrice daily for at least 5 half-lives for the drug to load before evaluation. With Holter monitoring, 74% of patients with evidence of VT at baseline testing demonstrated a change of status from nonsustained VT to no VT or from sustained VT to nonsustained VT. Four patients had nonsustained VT during verapamil treatment but no VT at baseline. There was a significant reduction in the number of ventricular ectopic beats over 24 hours (baseline: 15541 ± 17599 vs verapamil treatment: 8892 ± 15582, p < 0.01). Exercise-induced VT was suppressed in 56% of patients with VT during baseline testing, but no effect of verapamil on the tachycardia was observed in 26%. The remaining patients demonstrated a partial response to verapamil; the rate of VT was unchanged, although the duration of the runs was reduced. Sustained monomorphic VT was inducible in only 5 patients, of whom 4 were rendered noninducible; 1 patient remained inducible. However, of the 13 patients with nonsustained VT inducible at baseline, 4 became sustained, of which 2 were hemodynamically unstable. There was no obvious difference in the age or sex distribution of the patients, axis of VT, presence of abnormal cardiac histology, or late potentials among patients responding to verapamil during Holter monitoring or exercise testing. VT of an inferior axis was more likely to respond to verapamil, whereas VT of a superior axis did not respond to verapamil during Holter monitoring. We conclude that idiopathic VT of LBBB-like morphology can be suppressed in approximately two thirds of the patients by verapamil. In patients with a partial response, the rate of VT is unaffected. Some patients exhibit exacerbation of the arrhythmia and verapamil should be avoided in these cases.

A new intraoperative approach for endocardial mapping of ventricular tachycardia

Results of operation for control of ventricular tachycardia have improved since endocardial mapping techniques have been developed that allow a directed approach to the problem. In some patients, a limitation of established techniques has been difficulty in initiating the arrhythmia after a ventriculotomy has been made to allow introduction of endocardial recording electrodes. This paper describes a transatrial approach for endocardial mapping with a balloon array of 112 electrodes, which has been used intraoperatively in 15 patients. Surgical success in this group has been compared to that obtained in a similar group of patients in whom standard techniques of intraoperative mapping were used. With our new balloon technique we have been able to easily induce and map multiple episodes of ventricular tachycardia in all cases. On the basis of detailed endocardial maps, the locations of earliest activation and possible reentry loops have been identified and ablated with either endocardial excision or application of the cryoprobe. When indicated, concomitant procedures including aneurysm resection (9/15) and bypass grafting (14/15) have been performed. Hospital mortality in this group was 20%. None of the deaths have been related to recurrent ventricular tachycardia or complications of the mapping technique. Postoperative electrophysiologic studies performed at 2 weeks have been normal in 11 of 12 or 92% of patients. To date (mean follow-up 12 +/- 6 months) there has been no clinical recurrence or evidence of ventricular tachycardia by Holter monitoring in these patients. We conclude that the transatrial balloon approach to endocardial mapping facilitates intraoperative induction of ventricular tachycardia, allows complete mapping during multiple runs of the arrhythmia without prolonging cardiopulmonary bypass time, and improves results of operation using standard ablation techniques.

Prognostic implications of complex ventricular ectopy in patients with and without structural heart disease. A study based on programmed electrical stimulation

Fifty-six patients with complex ventricular premature beats (Lown grade IVa, IVb), but no evidence of ventricular tachycardia on 48 hours of continuous monitoring were evaluated by programmed electrical stimulation. Thirty patients had coronary atherosclerotic heart disease, 3 had valvular heart disease, 2 had cardiomyopathy and 21 had no structural heart disease. Programmed stimulation identified two groups of subjects: Group I comprised 11 patients in whom ventricular tachycardia was induced and Group II comprised 45 patients (which included 21 patients without heart disease) in whom no ventricular tachycardia was induced. The incidence of left ventricular dysfunction (ejection fraction <40%) was significantly higher in Group I as compared to Group II ( P < 0.001). There was, however, no difference between the grade of ventricular ectopy, HV interval or the incidence of bundle branch block between the 2 groups. Patients with inducible ventricular tachycardia (Group I) were put on laboratory directed anti-arrhythmic drug therapy. Patients without inducible tachycardia (Group II) were not given anti-arrhythmic therapy. The patients were followed up for 34 ± 10 months. The incidence of sudden death (36.3% vs 6.6%, P < 0.001) was significantly higher in Group I as compared to Group II. No patients without structural heart disease died during the follow-up. Programmed electrical stimulation fails to induce ventricular tachycardia in patients with complex ventricular ectopy but no structural heart disease. It is, however, possible to define a high risk subset in patients with structural heart disease and complex ectopy. The high risk patients with inducible ventricular tachycardia do not seem to benefit by anti-arrhythmic drugs, which may independently increase the risk of sudden death in treated patients. Patients in whom ventricular tachycardia is not inducible have better left ventricular function, a good long-term prognosis and do not require anti-arrhythmic agents.

Coronary artery surgery for recurrent ventricular arrhythmias in patients with variant angina

Two patients with Prinzmetal's variant angina had recurrent episodes of resting chest pain, ST segment elevation, QRS widening, ventricular tachycardia, and ventricular fibrillation. These episodes were unresponsive to medical therapy including lidocaine, procaine amide, and quinidine sulfate. Coronary arteriography revealed severe obstructive coronary artery disease, involving more than one coronary artery, in both patients. Aorticocoronary saphenous vein grafts were utilized to bypass significant disease in each patient. In one patient blood flow through the grafts was measured at 90 and 65 ml per minute, respectively, at operation and patent grafts were demonstrated six months postoperatively. Neither patient has had recurrence of chest pain or evidence of ventricular tachycardia at one year or 2 1 2 years postoperatively. Postoperative resting and maximal exercise ECG's are normal. Coronary artery surgery may be an effective method of therapy for ischemic ventricular tachycardia when medical therapy fails.

A-V dissociation revisited

We have touched upon the semantic impasse that plagues discussions of A-V dissociation and given our reasons for preferring to avoid the terms interference, complete and incomplete A-V dissociation, and nonparoxysmal A-V nodal tachycardia. We have stressed Pick's admirable dictum that A-V dissociation is never a primary disturbance, described the various ways in which the term is used, and defended as virtually inescapable the use of A-V dissociation in a quasi-specific way for a group of cognate arrhythmias that would otherwise be nameless. We have described and illustrated many of the mechanisms that lead to dissociation with special attention to related phenomena and variants including: isorhythmic dissociation, fusion beats, the “zone” of potential dissociation, dissociated nodal pacemakers, paired capture beats, altered contours of capture beats and the many variants resulting from block-dissociation, including the effects of concealed and supernormal conduction. We have placed emphasis on the bedside diagnosis of A-V dissociation and have stressed 2 important pitfalls, namely, the folly of diagnosing complete A-V block in the presence of A-V dissociation with accelerated idionodal or idioventricular rhythms; and the doubtful value of signs of dissociation as evidence of ventricular tachycardia. Finally, we have briefly alluded to certain modes of therapy applicable to various patterns of A-V dissociation.