Ventricular Tachycardia in Coronary Artery Disease

Ventricular arrhythmias are important contributors to morbidity and mortality in patients with coronary artery disease. Ventricular fibrillation accounts for the majority of deaths occurring in the acute phase of ischemia, whereas sustained, monomorphic ventricular tachycardia due to reentry generated in the scar tissue develops most often in the setting of healed myocardial infarction, especially in patients with lower left ventricular ejection fraction. Despite determinant advances in population education and myocardial infarction management, the ventricular tachycardia risk in the overall population with coronary artery disease continues to be a major problem in clinical practice. The initial evaluation of a patient presenting with ventricular tachycardia requires a 12-lead electrocardiogram, which can be helpful to confirm the diagnosis, suggest the presence of potential underlying heart disease, and identify the location of the ventricular tachycardia circuit. An invasive electrophysiologic study is usually crucial to determine the mechanism of the arrhythmia once induced and to provide guidance for ablation. The approach for ventricular tachycardia ablation depends on several factors, including inducibility, sustainability, and clinical tolerance of ventricular tachycardia. The paper also reviews other therapeutic options for patients with ventricular tachycardia associated with coronary artery disease, including antiarrhythmic drug therapy, surgical ablation, and current implantable cardioverter-defibrillator indications.     

Ventricular arrhythmias in ischemic heart disease

Ventricular arrhythmias remain the leading cause of death from coronary artery disease. This review summarizes current thinking in several areas relating to the pathophysiology, prognosis, and therapy of ventricular arrhythmias associated with acute and chronic coronary artery disease syndromes. The experimental basis of arrhythmias in the setting of acute myocardial ischemia and chronic myocardial infarction is described, stressing the important pathophysiologic differences between these two conditions. The effects of the autonomic nervous system as a key modulator of ischemic arrhythmogenesis are discussed. Insights, derived from endocardial mapping studies, into the nature of ventricular tachycardia in humans with chronic myocardial infarction are described, including implications for risk stratification and therapy to prevent arrhythmia recurrence. Current therapeutic principles are discussed in the management of ventricular arrhythmias associated with coronary artery disease, including pharmacologic approaches, surgical and catheter ablation, and automatic implantable cardioverting and defibrillating devices.     

经皮穿刺心外膜电-解剖标测及射频消融心肌梗死后室性心动过速的实验研究

目的探讨经心外膜途径在电-解剖标测系统指导下行射频消融治疗心肌梗死后室性心动过速的可行性和安全性。方法成年中华小型猪共7只,采用经皮穿刺的方法将球囊置于左前降支中下部,封堵150 min建立心肌梗死模型。3～5周后将心肌梗死模型猪,行电生理检查诱发室性心动过速。经胸穿刺进入心包腔,采用电-解剖标测系统在窦性心律下进行心外膜电压标测和线性消融。射频消融后再次行电生理检查,不能再诱发室性心动过速为消融成功。结果存活的心肌梗死模型的猪7只,3～5周后行电生理检查,共诱发出单形性室性心动过速共8种,7种表现为右束支阻滞图形,1种表现为左束支阻滞图形,室性心动过速(VT)周长平均在(338±66)ms。1只猪同时诱发心室颤动,电除颤转复窦性心律。7只猪心包穿刺均成功,完成心外膜电压标测,沿瘢痕区到二尖瓣环或正常心肌区逐点进行线性消融。射频消融后再次行电生理检查,6只猪不能再诱发室性心动过速。结论经胸穿刺进入心包腔行心外膜标测和消融治疗心肌梗死后室速的方法是安全可行的,心外膜标测消融心肌梗死后室速的方法可以作为心内膜消融的一种有效补充方法。     

Left ventricular aneurysm without coronary artery disease, incidence and clinical features: clinical analysis of 11 cases

OBJECTIVE: To examine the incidence, underlying disease and clinical features of left ventricular aneurysm (LVA) not related to coronary artery occlusion. METHODS: Retrospective review of consecutive patients who underwent both left ventriculography and coronary angiography. PATIENTS: LVA was confirmed in 11 of 2,348 consecutive patients (0.47%). RESULTS: The location of LVA was mainly in the apical region (81.8%). In five of the 11 patients (45.5%), the underlying heart disease was hypertrophic cardiomyopathy (HCM), including 4 patients of dilated phase and one patient of midventricular type. The serial ECG changes from left ventricular hypertrophy to abnormal Q wave and endomyocardial biopsy were useful for the differential diagnosis of these cases against myocardial infarction. The underlying disease of the remaining patients was: myocarditis (2 patients), arrhythmogenic right ventricular dysplasia (1 patient), Chagas' disease (1 patient), glycogen storage disease (1 patient), and sarcoidosis (1 patient). Ventricular tachycardia appeared in 9 of 11 cases (81.8%) including 2 patients with sustained ventricular tachycardia. CONCLUSION: LVA formation without coronary artery disease was a rare phenomenon. The underlying disease was varied but the incidence of hypertrophic cardiomyopathy in the dilated phase was comparatively high. Ventricular tachycardia was a significant complication in these patients.     

A Comparative Study of Intracoronary Iced Saline Versus Intracoronary Antiarrhythmic Drugs to Identify the Ventricular Tachycardia-Related Artery

Identifying the Tachycardia-Related Coronary Artery. Introduction: Transcatheter chemical ablation is a new treatment option for patients with ventricular tachycardia. Availability of a safe, simple, and sensitive method to identify the ventricular tachycardia-related artery is required for successful intracoronary chemical ablation for ventricular tachycardia. The purpose of this study was to compare bolus intracoronary iced saline injection to bolus intracoronary antiarrhythmic drug injection as methods for identifying the ventricular tachycardia-related coronary artery. Methods and Results: Patient selection was limited to eight individuals with recurrent sustained monomorphic ventricular tachycardia, coronary artery disease, remote myocardial infarction, and in whom programmed stimulation could reproducihiy induce the clinical arrhythmia. An infusion catheter was positioned in the putative ventricular tachycardia-related artery and ventricular tachycardia was provoked hy programmed stimulation. In four patients the putative ventricular tachycardia-related artery was a patent infarct-related vessel and in the other four patients was a vessel supplying collateral flow to an occluded infarct-related artery. The effects of selective intracoronary iced saline bolus injection (10 mL), and then of selective intracoronary bolus antiarrhythmic drug injection (2.5 mg lidocaine in one patient, procainamide 1.0–9.0 mg in seven patients) were observed. Bolus intracoronary iced saline injection did not alter ventricular tachycardia in any patient. Bolus intracoronary antiarrhythmic drug injection, however, led to ventricular tachycardia cycle length prolongation in two patients and arrhythmia termination in four patients. In two of these individuals, infusion of ethanol into the tachycardia-related vessel previously identified by intracoronary drug injection resulted in ablation of the ventricular tachycardia. Conclusions: In the present study, selective intracoronary antiarrhythmic drug injection appeared to be more effective than intracoronary iced saline for identifying the ventricular Uchycardia-related coronary artery, (J Cardiovasc Electrophysiol, Vol. 3, pp. 199–208 June 1992)     

Antidromic atrioventricular reentrant tachycardia mimicking ventricular tachycardia in the setting of previous myocardial infarction

The differentiation between ventricular tachycardia and broad-complex supraventricular tachycardia can be extremely difficult, particularly in emergency situations. We report a case of hemodynamically compromising broad-complex tachycardia in a 63-year-old man. The patient had previously sustained an anteroseptal myocardial infarction and had subsequently undergone coronary artery bypass surgery because of triple-vessel coronary artery disease. Intravenous treatment with ajmalin terminated the tachycardia and revealed preexcited QRS complexes compatible with the presence of a left-sided atrioventricular accessory pathway. An antidromic atrioventricular reentrant tachycardia (identical to the clinical tachycardia) was induced during an electrophysiologic study. In conclusion, there are several causes of broad-complex tachycardia, even in patients with previous myocardial infarction, and, where doubt exists, electrophysiologic studies should be performed.     

Ventricular Tachycardia After Myocardial Infarction: From Arrhythmia Surgery to Catheter Ablation

Ablation of Ventricular Tachycardia. Ventricular tachycardia due to prior myocardial infarction is caused by reentry. Intraoperative mapping at the time of arrhythmia surgery has shown that the reentry circuits arc diverse in size and location. Many circuits are large, extending over several square centimeters. Endocardial excision guided by activation sequence mapping, fractionated sinus rhythm electrograms, or visual identification of scarred subendo-cardium renders 69% to 95% of patients free from inducible ventricular tachycardia, but with an operative mortality that exceeds 8%, at most centers. Catheter ablation is difficult due to limitations of catheter mapping, relatively small size of lesions produced with current techniques, and limited access to intramural and epicardial portions of the reentry circuits. Many problems need to be overcome for catheter ablation to achieve success comparable to that of surgery. At present, only hemodynamically tolerated ventricular tachycardias can he mapped. Progress is being made, and it is likely that catheter ablation will become a viable therapy for subgroups of patients with postmyocardial infarction ventricular tachycardia.     

Intracoronary ethanol ablation for the treatment of recurrent sustained ventricular tachycardia.

The selective infusion of ethanol into the coronary circulation supplying the site of origin of incessant ventricular tachycardia has been demonstrated to abolish this arrhythmia in selected patients. The present study was designed to evaluate the efficacy and safety of the intracoronary ethanol ablation technique in patients with paroxysmal ventricular tachycardia related to prior myocardial infarction. Twenty-three patients with sustained monomorphic ventricular tachycardia that was refractory to conventional antiarrhythmic drug therapy were prospectively studied. After induction of ventricular tachycardia by programmed electrical stimulation, the response of the arrhythmia to the infusion of radiographic contrast medium or saline solution into the ostia of the native coronary arteries and coronary artery bypass grafts was assessed. If ventricular tachycardia was reliably interrupted by injections into the proximal coronary artery or bypass graft, the vessel was cannulated with a steerable guide wire and 2.7F infusion catheter to determine the smallest arterial branch that would result in termination of the arrhythmia with selective injections. If reliable interruption of ventricular tachycardia was observed with saline or contrast injections, ethanol (2 ml) was then delivered through the infusion catheter. Ventricular tachycardia could be terminated by injections of saline solution or contrast medium in 11 of 21 patients in whom the protocol could be completed. Ethanol was infused in 10 of these patients. Ventricular tachycardia was inducible in only 1 of 10 patients immediately after ethanol infusion. At a follow-up electrophysiologic study performed 5 to 7 days after ablation, ventricular tachycardia became inducible in two other patients, in one of whom the arrhythmia substrate was successfully ablated after three sessions. The mean left ventricular ejection fraction was 0.33 +/- 0.1 before and 0.35 +/- 0.11 after ablation. Complications of the procedure included complete atrioventricular block in four patients and pericarditis in one patient. Thus, intracoronary ethanol ablation is associated with a moderate degree of efficacy but the potential for important complications. Despite these limitations, this technique may provide effective long-term control of ventricular tachycardia for some patients.     

A Comparison of the QT and QTc Dispersion Among Patients with Sustained Ventricular Tachyarrhythmias and Different Etiologies of Heart Disease

Objectives: To determine if etiology of heart disease is associated with differences in QT and QTc dispersion among patients with ventricular tachyarrhythmias. Methods: This study was undertaken in 145 patients undergoing electrophysiological testing for sustained ventricular tachycardia or ventricular fibrillation. Patients were divided into groups based on etiology of heart disease determined by history, ECG, coronary angiography, and echocardiography. The groups included patients with: dilated cardiomyopathy (n = 29), myocardial infarction (n = 90), established coronary artery disease without a myocardial infarction (n = 11), or hypertension induced left ventricular hypertrophy (n = 15). The QT intervals on a 12—lead ECG were determined and Bazett's formula was used to derive the QTc intervals. The QT and QTc dispersion were determined by subtracting the shortest QT(c) interval from the longest on each 12‐lead recording. Results: The patients with dilated cardiomyopathy had significantly higher QT and QTc dispersion values as compared to any of the other three groups (P < 0.05 for both). No other differences in electrocardiographic variables were found between groups. Conclusions: In a group of patients with a history of ventricular tachycardia or ventricular fibrillation, QT and QTc dispersion are significantly greater among patients with dilated cardiomyopathy than for patients with a previous myocardial infarction, established coronary artery disease without a myocardial infarction, or hypertensive left ventricular hypertrophy. A.N.E. 2001;6(4):319–322     

Ventricular Tachycardia Originating from the Posterior Papillary Muscle in the Left Ventricle A Distinct Clinical Svndrome

1．focal mechanism通常出现在有关地震学研究中,译为“震源机制”。在有关心律失常机制研究的文献中,focal mechanism是指一种有别于折返（reentry）机制的机制,确切的机制尚不完全清楚,认为与自律性异常、促发活动和微折返（microreentry）有关,通译为“局灶机制”。     

Epicardial idiopathic ventricular tachycardia originating within the left main coronary artery ostium area: identification using the LocaLisa nonfluoroscopic catheter navigation system

Idiopathic ventricular tachycardia (IVT) in patients without structural heart disease commonly arises from the right or left outflow tracts, but there remain arrhythmias that can only be ablated by an epicardial approach. We report a case of an epicardial ventricular tachycardia originating within the left main coronary artery ostium area, as identified using the LocaLisa nonfluoroscopic catheter navigation system. Due to the high risk of coronary artery thrombosis, ventricular tachycardia was successfully ablated by a transthoracic surgical approach using cryoenergy. Ventricular ectopy disappeared and ventricular tachycardia did not recur during long-term follow-up.     

Catheter ablation and antiarrhythmic drugs for haemodynamically tolerated post-infarction ventricular tachycardia; long-term outcome in relation to acute electrophysiological findings.

AIMS: Radiofrequency catheter ablation is effective at terminating ventricular tachycardia, but the overall clinical role of the technique in patients with a prior myocardial infarction is still debated, due to the uncertainties of the long-term reliability of the procedure. The purpose of this study was to prospectively investigate the relationship between acute results obtained by catheter ablation and long-term outcome in a homogeneous population of patients with post-myocardial infarction ventricular tachycardia. METHODS AND RESULTS: One hundred and twenty-four consecutive patients with recurrent, drug-refractory, haemodynamically tolerated ventricular tachycardia were included in the study. This population accounted for 30% of the patients with post-myocardial infarction ventricular tachycardia admitted between April 1992 and September 1997 to the investigating centres. The ablation was successful in eliminating sustained ventricular tachycardia in 91 of them (73%); a partial result was obtained in 21 (17%) and failure in 12 (10%). Low dose amiodarone and/or beta-blockers were maintained in 86% of the patients. Over a median follow-up of 41.5 months (interquartile range 30.5-59.5 months), there were 15 deaths (12%), three of which were sudden (2.4%); the 12 remaining patients died of heart failure. Event-free survival analysis showed a significantly lower ventricular tachycardia recurrence rate in patients with a successful procedure as compared to those with failure or a partial result (19% vs 53% at one year and 27% vs 60% at 3 years, P=0.003). A repeat procedure was performed in 15 patients with early recurrences and was followed in all by long-term success. Of those who submitted to a second procedure, 93/124 patients (75%) are free of ventricular tachycardia recurrences. An implantable cardioverter-defibrillator (ICD), following procedure failure, was implanted in 13 patients (11%) of the study population. CONCLUSIONS: Radiofrequency catheter ablation is effective in a wide population of patients with recurrent tolerated ventricular tachycardia, with very low sudden death and cardiac mortality rates over the long-term. Persistent ventricular tachycardia inducibility after catheter ablation requires an ICD implant and/or repeat ablation.     

Inducible ventricular flutter and fibrillation predict for arrhythmia occurrence in coronary artery disease patients presenting with syncope of unknown origin

INTRODUCTION: Ventricular fibrillation and ventricular flutter (cycle length < or = 230 msec) induced at electrophysiologic studies are thought to be nonspecific findings in patients presenting with syncope of unknown origin. However, there are limited data on the prognosis of these patients in long-term follow-up. METHODS AND RESULTS: We followed 274 consecutive patients with coronary artery disease presenting with syncope or presyncope who underwent electrophysiologic studies from January 1992 to June 1999 and assessed the risk of subsequent arrhythmias stratified by the electrophysiologic result at the time of their presentation with syncope. Ventricular fibrillation was induced in 23 patients (8%); ventricular flutter in 24 (9%), sustained ventricular tachycardia in 41 (15%); and nonsustained ventricular tachycardia 42 (15%). In 37 +/- 25 months of follow-up, there have been ventricular arrhythmias in 34 patients, including 3 (13%) of 23 who had induced ventricular fibrillation, and 7 (30%) of 24 with induced ventricular flutter, compared to 13 (32%) of 41 with sustained ventricular tachycardia, 7 (17%) of 42 with nonsustained ventricular tachycardia, and only 4 (3%) of 144 noninducible patients (P < 0.001 for induced ventricular fibrillation and ventricular flutter vs noninducible patients). The inducibility of ventricular fibrillation and ventricular flutter were independent risk factors for arrhythmia occurrence in follow-up. CONCLUSION: Ventricular fibrillation and ventricular flutter induced at electrophysiologic studies have prognostic significance for arrhythmia occurrence in patients presenting with syncope. These induced arrhythmias may not be as nonspecific as previously thought and treatment should be considered for these patients.     

Short-term effect of coronary artery bypass grafting on the signal-averaged electrocardiogram

Ventricular late potentials at the end of the QRS can be detected on the body surface during sinus rhythm by recording a signal-averaged electrocardiogram (SAECG). In patients with coronary artery disease, these late potentials have been shown to be markers for spontaneous or inducible ventricular tachycardia, or both. The short-term (before and 10 +/- 4 days after coronary revascularization) influence of coronary artery bypass grafting (CABG) on the quantitative SAECG variables was studied in 40 patients with chronic coronary artery disease. Twenty-five of these patients had a previous myocardial infarction. In the 15 patients without previous myocardial infarction, no abnormal SAECG indexes were recorded before CABG and no change in the quantitative SAECG variables was observed after surgery. In the patients with a previous myocardial infarction, 7 (28%) had a late potential before CABG. After CABG, 5 (71%) patients remained late potential-positive, whereas the other 2 (29%) lost their late potential. The mean values of their SAECG variables improved after coronary revascularization. In the entire group of postmyocardial infarction patients, the high-frequency QRS duration had shortened (p less than 0.01) after CABG (the other SAECG indexes did not change). The postoperative arrhythmic complications (transient atrial fibrillation, new onset of ventricular couplets) tended to be more frequent in the postmyocardial infarction group and in patients with late potentials. Our findings suggest that the reported increase in ventricular arrhythmias after CABG is probably not related to a change in the arrhythmogenic substrate for ventricular reentry but is associated with changes in the arrhythmogenic milieu.     

Bundle Branch Reentrant Ventricular Tachycardia:

Sustained Bundle Branch Reentrant Tachycardia. introduction: The clinical, electrophysiologic features and follow-up of 48 patients with inducible bundle branch reentrant (BBR) tachycardia are presented. Methods and Results: Forty-eight patients were identified in whom a diagnosis of BBR tachycardia was made during electrophysiologic evaluation. The clinical presentation was syncope or sudden death in 38 patients, and sustained palpitations during wide QRS complex tachycardia in 5 patients. Electrophysiologic studies were performed in 5 additional patients for various other reasons. Structural heart disease was present in 45 patients. Idiopathic dilated cardiomyopathy and coronary artery disease were the anatomical substrates in 19 (39%) and 24 (50%) patients, respectively, severe aortic regurgitation was present in 2 patients, and no organic heart disease was identified in 3. All 48 patients had evidence of His-Purkinje system disease. BBR tachycardia with left and right bundle branch block morphologies was induced in 46 and 5 patients, respectively, and interfascicular BBR tachycardia was initiated in 2 patients. Ventricular tachycardia of a myocardial origin was induced in 11 patients. Management of BBR tachycardia included transcatheter bundle branch ablation in 28 patients, and antiarrhythmic drug therapy in 16 patients. Four patients were treated with implantablc defibrillators. After a mean follow-up of 15.8 months in 42 patients, there were 13 deaths due to congestive heart failure, 4 sudden cardiac deaths, 3 nonsudden cardiac deaths, and 3 noncardiac related deaths. Conclusion: Sustained BBR, a form of monomorphic ventricular tachycardia, is a highly malignant arrhythmia usually seen in patients with structural heart disease. Three different types of BBR tachycardia are described. If distinguished from ventricular tachycardia of a myocardial origin, catheter ablation of the right bundle branch can be easily performed and effectively eliminates BBR. During follow-up, congestive heart failure is the most common cause of death in this population.     

The nature of ventricular arrhythmias during ergonovine-induced vasospastic angina pectoris

The peak incidence of ventricular fibrillation in acute myocardial infarction usually occurs during the first hours after the onset. Electrophysiological changes immediately after the onset have been studied in animal models, but are still incompletely understood in humans. For clarification of the characteristic features of ventricular arrhythmias during acute myocardial ischemia, ventricular arrhythmias were studied in 81 patients with vasospastic angina pectoris induced by ergonovine. Ventricular arrhythmias occurred in 45 of these patients, including ventricular tachycardia in 15, and ventricular fibrillation requiring repeated DC defibrillation in two patients. Most ventricular extrasystoles occurred before the ST segment reached maximum elevation, while reperfusion arrhythmias were less common. In many patients the coupling intervals varied, and the configuration was multiform. It is concluded that ventricular arrhythmias occurring during ergonovine-induced coronary spasm show different characteristics from those occurring during chronic ischemia. As the arrhythmias in this study seem, in some ways, to resemble arrhythmias occurring at the onset of myocardial infarction, the results might provide useful information on ventricular arrhythmias in myocardial ischemia in humans.     

Catheter Ablation of Recurrent Scar-Related Ventricular Tachycardia Using Electroanatomical Mapping and Irrigated Ablation Technology: Results of the Prospective Multicenter Euro-VT-Study

Catheter Ablation of Ventricular Tachycardia.   Introduction: Ventricular tachycardia (VT) late after myocardial infarction is an important contributor to morbidity and mortality. This prospective multicenter study assessed the efficacy and safety of electroanatomical mapping in combination with open-saline irrigated ablation technology for ablation of chronic recurrent mappable and unmappable VT in remote myocardial infarction.
Methods and Results: In 8 European institutions, 63 patients (89% males) were enrolled in the study. All patients had remote myocardial infarction and presented with a median number of 17 (range 1–380) VTs in the preceding 6 months. Incessant VT was present in 14 patients (22%). Left ventricular ejection fraction measured 30 ± 13%. A mean of 3 VTs were targeted per patient and 22% of all patients had only unmappable VT. The mean follow-up period was 12 ± 3 months. A total of 164 VTs were targeted during catheter ablation. Ablation was acutely successful in 51 patients (81%). One patient (1.5%) experienced a major complication with degeneration of VT into ventricular fibrillation necessitating cardiopulmonary resuscitation maneuvers. However, no death occurred acutely or within the first 30 days after catheter ablation. During the follow-up, 19 of the initially successful ablated patients (37%) and 31 of all ablated patients (49%) developed some type of VT recurrence.
Conclusions: The results of this multicenter study demonstrate the high acute success rate and a low complication rate of irrigated tip catheter ablation of all clinical relevant VTs in remote myocardial infarction. However, during the follow-up a relevant number of recurrences occurred. (J Cardiovasc Electrophysiol, Vol. 21, pp. 47–53, January 2010)     

Elevated troponin level is not synonymous with myocardial infarction

BACKGROUND: Elevated troponin I in the absence of angiographically visible coronary lesions is seen in up to 10-15% of those undergoing angiography for suspected coronary artery disease. This study aims to elucidate the etiology of elevated cardiac troponin I in patients with normal coronary arteries on angiography. METHODS: We identified 1551 (8.6%) patients with normal coronary arteries from our catheterization database of 17,950 patients from Jan 2000 to Jun 2004. Elevated troponin I levels were found in 217 (14%) of 1551 patients with normal coronary arteries. Of these 217 patients, 73 surgical patients were excluded, and the remaining 144 patients formed the study population. The study population was compared with age and gender matched patients with myocardial infarction and coronary artery disease (Group II). RESULTS: The patients with elevated cardiac troponin I (cTnI) with normal coronary arteries had significantly lower prevalence of atherosclerotic risk factors and significantly higher left ventricular ejection fractions. The cTnI in patients with normal coronary arteries was elevated due to a number of causes including tachycardia, myocarditis, pericarditis, severe aortic stenosis, gastrointestinal bleeding, sepsis, left ventricular hypertrophy, severe congestive heart failure, cerebrovascular accident, electrical trauma, myocardial contusion, hypertensive emergency, myocardial bridging, pulmonary embolism, diabetic ketoacidosis, chronic obstructive pulmonary disease exacerbation and coronary spasm. CONCLUSIONS: Cardiac troponin I could be elevated in a number of conditions, apart from acute myocardial infarction, and could reflect myonecrosis. Acute myocardial infarction is a clinical diagnosis as the laboratory is an aide to, not a replacement for, informed decision making.     

Ventricular Fibrillation Induced with Programmed Stimulation: Clinical Substrate and Prognosis

The implications of ventricular fibrillation induced during elect rophysiologic testing are unclear. To determine the profile of patients in whom this arrhythmia occurs and to determine whether it has any prognostic value, follow-up data were obtained on all patients in whom this arrhythmia was in duced in our laboratory during a ventricular stimulation protocol over an 18-month period. Of 836 patients tested, 29 (27 men and 2 women) had inducible ventricular fibrillation. Most (52%) had coronary disease and 12 (41%) had suffered a prior myocardial infarction. All but 3 had some form of heart disease. Sixteen (55%) had abnormal left ventricular function. Eleven (38%) presented with spontaneous sustained ventricular tachycardia or ventricular fibrillation. Eight others had a history of nonsustained ventricular tachycardia.Follow-up was obtained for a mean of 12 months.
In spite of therapy, 2 patients died an arrhythmic death, 1 was resuscitated from ventricular fibrillation, 1 had spontaneous sustained ventricular tachycardia, 4 had inducible sustained ventricular tachycardia, 2 continued to have inducible ventricular fibrillation at second study, and 1 had recurrent syncope. Five patients had ventricular fibrillation induced on multiple occasions.
Ventricular fibrillation induced during electraphysiologic study was found primarily in patients with structural heart disease and appeared reasonably reproducible. When reproducible, ventricular fibrillation appears to indicate a poor prognosis rather than an aspecific finding. The clinical profile of our poor prognosis group includes a history of prior ventricular tachycardia or ventricular fibrillation and the presence of coronary artery disease.     

Catheter Ablation of Ventricular Tachycardia Induced by Injection of Acetylcholine in the Right Coronary Artery

Ventricular Tachycardia Induced by Acetylcholine. We report the case of a patient who suffered from early morning nonsustained ventricular tachycardia. Clinical ventricular tachycardia without coronary spasm was reproducibly induced only by injection of acetylcholine in the right coronary artery. A good pace mapping site with 30 ms early ventricular activity was present in the right ventricular free wall. After radiofrequency ablation based on electroanatomical mapping, the tachycardia could no longer be induced by intracoronary injection of acetylcholine. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1410‐1412, December 2010)