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Background Patients with Brugada syndrome and aborted sudden cardiac death or syncope have higher risks for ventricular arrhythmias (VAs) and should undergo implantable cardioverter-defibrillator (ICD) placement. Device-based management of asymptomatic patients is controversial. ICD therapy is associated with high rates of inappropriate shocks and device-related complications. Objectives The objective of this study was to investigate clinical features, management, and long-term follow-up of ICD therapy in patients with Brugada syndrome. Methods Patients presenting with spontaneous or drug-induced Brugada type 1 electrocardiographic findings, who underwent ICD implantation and continuous follow-up at a single institution, were eligible for this study. Results A total of 176 consecutive patients were included. During a mean follow-up period of 83.8 ± 57.3 months, spontaneous sustained VAs occurred in 30 patients (17%). Eight patients (4.5%) died. Appropriate ICD shocks occurred in 28 patients (15.9%), and 33 patients (18.7%) had inappropriate shocks. Electrical storm occurred in 4 subjects (2.3%). Twenty-eight patients (15.9%) experienced device-related complications. In multivariate Cox regression analysis, aborted sudden cardiac death and VA inducibility on electrophysiologic studies were independent predictors of appropriate shock occurrence. Conclusions ICD therapy was an effective strategy in Brugada syndrome, treating potentially lethal arrhythmias in 17% of patients during long-term follow-up. Appropriate shocks were significantly associated with the presence of aborted sudden cardiac death but also occurred in 13% of asymptomatic patients. Risk stratification by electrophysiologic study may identify asymptomatic patients at risk for arrhythmic events and could be helpful in investigating syncope not related to VAs. ICD placement is frequently associated with device-related complications, and rates of inappropriate shocks remain high regardless of careful device programming.

Objectives: The goal of this study was to investigate the clinical features, management, and long-term follow-up of children with drug-induced Brugada syndrome (BS).Background: Patients with BS

A proband of Brugada syndrome (BrS) is the first patient diagnosed in a family. There are no data regarding this specific, high-risk population.This study sought to investigate the Brugada probands diagnosed from 1986 through the next 28 years.We included 447 probands belonging to families with a diagnostic type 1 electrocardiogram Brugada pattern. The database was divided into 2 periods: the first period identified patients who were part of the initial cohort that became the consensus document on BrS in 2002 (early group); the second period reflected patients first diagnosed from 2003 to January 2014 (latter group).There were 165 probands in the early group and 282 in the latter group. Aborted sudden death as the first manifestation of the disease occurred in 12.1% of the early group versus 4.6% of the latter group (p = 0.005). Inducibility during programmed electrical stimulation was achieved in 34.4% and 19.2% of patients, respectively (p 0.001). A spontaneous type 1 electrocardiogram pattern at diagnosis was present in 50.3% early versus 26.2% latter patients (p = 0.0002). Early group patients had a higher probability of a recurrent arrhythmia during follow-up (19%) than those of the latter group (5%) (p = 0.007). The clinical suspicion and use of a sodium-channel blocker to unmask BrS has allowed earlier diagnoses in many patients.Since being first described, the presentation of BrS has changed. There has been a decrease in aborted sudden cardiac death as the first manifestation of the disease among patients who were more recently diagnosed. These variations in initial presentation have important clinical consequences. In this setting, the value of inducibility to stratify individuals with BrS has changed.

An intriguing new clinical entity characterized by ST-segment elevation in the right precordial electrocardiographic leads and a high incidence of sudden death in individuals with structurally normal hearts was described by Pedro and Josep Brugada in 1992. The past decade has witnessed an exponential rise in the number of reported cases and a dramatic proliferation of papers serving to define the clinical, genetic, cellular, ionic, and molecular aspects of this disease. The purpose of this brief review is to chronicle the historical highlights that have brought us to our present understanding of Brugada syndrome.

Patients with Brugada syndrome and aborted sudden cardiac death or syncope have higher risks for ventricular arrhythmias (VAs) and should undergo implantable cardioverter-defibrillator (ICD) placement. Device-based management of asymptomatic patients is controversial. ICD therapy is associated with high rates of inappropriate shocks and device-related complications.The objective of this study was to investigate clinical features, management, and long-term follow-up of ICD therapy in patients with Brugada syndrome.Patients presenting with spontaneous or drug-induced Brugada type 1 electrocardiographic findings, who underwent ICD implantation and continuous follow-up at a single institution, were eligible for this study.A total of 176 consecutive patients were included. During a mean follow-up period of 83.8 ± 57.3 months, spontaneous sustained VAs occurred in 30 patients (17%). Eight patients (4.5%) died. Appropriate ICD shocks occurred in 28 patients (15.9%), and 33 patients (18.7%) had inappropriate shocks. Electrical storm occurred in 4 subjects (2.3%). Twenty-eight patients (15.9%) experienced device-related complications. In multivariate Cox regression analysis, aborted sudden cardiac death and VA inducibility on electrophysiologic studies were independent predictors of appropriate shock occurrence.ICD therapy was an effective strategy in Brugada syndrome, treating potentially lethal arrhythmias in 17% of patients during long-term follow-up. Appropriate shocks were significantly associated with the presence of aborted sudden cardiac death but also occurred in 13% of asymptomatic patients. Risk stratification by electrophysiologic study may identify asymptomatic patients at risk for arrhythmic events and could be helpful in investigating syncope not related to VAs. ICD placement is frequently associated with device-related complications, and rates of inappropriate shocks remain high regardless of careful device programming.

The goal of this study was to investigate the clinical features, management, and long-term follow-up of children with drug-induced Brugada syndrome (BS).Patients with BS12 years of age with a spontaneous type I electrocardiogram have a higher risk of arrhythmic events. Data on drug-induced BS in patients12 years of age are lacking.Among 505 patients with ajmaline-induced BS, subjects ≤12 years of age at the time of diagnosis were considered as children and eligible for this study.Forty children (60% male; age 8 ± 2.8 years) were included. Twenty-four children (60%) had a family history of sudden death. Two (5%) had a previous episode of aborted sudden death, and 8 (20%) had syncope. Children experienced more frequent episodes of sinus node dysfunction (SND) compared with older subjects (7.5% vs. 1.5%; p = 0.04) and had a comparable incidence of atrial tachyarrhythmias. Children more frequently experienced episodes of ajmaline-induced sustained ventricular arrhythmias (VAs) compared with older patients (10.0% vs. 1.3%; p = 0.005). Twelve children (30%) received an implantable cardioverter-defibrillator (ICD). After a mean follow-up time of 83 ± 51 months, none of the children died suddenly. Spontaneous sustained VAs were documented in 1 child (2%). Among children with ICD, 1 (8%) experienced an appropriate shock, 4 (33%) had inappropriate ICD shocks, and 4 (33%) experienced device-related complications.Drug-induced BS is associated with atrial arrhythmias and SND. Children are at higher risk of ajmaline-induced VAs. The rate of device-related complications, leading to lead replacement or inappropriate shocks, is considerable and even higher than with appropriate interventions. Based on these findings, the optimal management of BS in childhood should remain individualized, taking into consideration the patient's clinical history and family's wishes.

We thank Drs. Steinfurt and Odening for their thoughtful comments on our recent publication [(1)][1]. Apart from the coved-type ST-segment elevation in the right precordial leads, the heterogeneity of Brugada syndrome (BS) can lead to additional electrocardiographic (ECG) repolarization

Objectives. We report the occurrence of cardiac events during long-term follow-up in patients with hypertrophic cardiomyopathy (HCM) after cardioverter-defibrillator implantation.Background. The identification of patients at high risk for sudden death and the prevention of recurrence of sudden death in HCM represents a difficult problem.Methods. We retrospectively analyzed the occurrence of cardiac events during follow-up of 13 patients with HCM who received an implantable cardioverter-defibrillator (ICD) because of aborted sudden death (n = 10) or sustained ventricular tachycardia (n = 3) (group I). Findings were compared with those in 215 patients with an ICD and other structural heart disease or idiopathic ventricular fibrillation (group II).Results. After a mean (±SD) follow-up period of 26 ± 18 months, 2 of 13 patients in group I received appropriate shocks. The calculated cumulative incidence of shocks was 21% in group I and 66% in group II after 40 months (p < 0.05). We observed a low incidence of recurrence of ventricular tachycardia/fibrillation during follow-up in patients with HCM. No deaths occurred.Conclusions. Our data suggest that ventricular tachyarrhythmias may not always be the primary mechanism of syncope and sudden death in patients with HCM. The ICD seems to have a less important impact on prognosis in patients with HCM than in patients with other etiologies of aborted sudden death.

Objectives. The objectives of this study were to present data on eight patients with recurrent episodes of aborted sudden death unexplainable by currently known diseases whose common clinic...

[Figure][1] Bidirectional ventricular tachycardia is a hallmark of severe digitalis toxicity. The 12-lead electrocardiogram obtained from a 54-year-old man with acute heart failure and digitoxin intoxication shows typical features of this potentially life-threatening arrhythmia: a regular

Seven of 17 patients with incessant supraventricular tachycardia caused by an accessory pathway with a long retrograde conduction time were seen with symptoms or echocardiographic signs of a tachycardia-induced cardiomyopathy. Three patients were in New York Heart Association functional class II with dyspnea and four were in class III. Eight patients (six with tachycardia-induced cardiomyopathy) underwent surgery because of failure of medical treatment (including one patient in functional class I) and one underwent direct current catheter ablation of the atrioventricular (AV) node. In six patients echocardiograms recorded before and after the procedure were available. Before surgery or direct current ablation the mean left ventricular ejection fraction was 36.3 +/- 8.7%, the left ventricular end-diastolic diameter 55.7 +/- 7.6 mm and the left ventricular end-systolic diameter 44.3 +/- 7.8 mm. A mean of 21.6 +/- 6.8 months after the procedure the mean left ventricular ejection fraction increased to 58.6 +/- 8.0%, the left ventricular end-diastolic diameter decreased to 49.0 +/- 3.6 mm and the left ventricular end-systolic diameter decreased to 32.2 +/- 2.7 mm; all six patients were in functional class I. These results confirm that control of incessant tachycardia leads to a regression of symptoms and signs of cardiomyopathy and progressive normalization of the dimensions of the heart. Because of these findings, surgery should be considered early in patients with an accessory AV pathway and incessant tachycardia. The presence of a tachycardia-induced cardiomyopathy should therefore be an indication for surgery rather than a contraindication.

In a multicenter study, 390 patients with sustained symptomatic ventricular tachycardia or ventricular fibrillation late after acute myocardial infarction were prospectively followed up to assess determinants of mortality and recurrence of arrhythmic events. Patients were given standard antiarrhythmic treatment, which consisted primarily of drug therapy. During a mean follow-up period of 1.9 years, 133 patients (34%) died; arrhythmic events and heart failure were the most common cause of death (41 patients [11%] died suddenly, 31 [8%] died of recurrent ventricular tachycardia or ventricular fibrillation and 23 [6%] died of heart failure). One hundred ninety-two patients (49%) had at least one recurrent arrhythmic event; 85% of first recurrent arrhythmic events were nonfatal.Multivariate analysis of data from patients who developed the arrhythmia 70 years (risk ratio 4.5); 2) Killip class III or IV in the subacute phase of infarction (risk ratio 3.5); 3) cardiac arrest during the index arrhythmia (risk ratio 1.7); 4) anterior infarction (risk ratio 2.2); and 5) multiple previous infarctions (risk ratio 1.6). Multivariate analysis of data from patients developing the arrhythmia >6 weeks after infarction identified four variables as independently predictive of total mortality: 1) Q wave infarction (risk ratio 2.1); 2) cardiac arrest during the index arrhythmia (risk ratio 1.7); 3) Killip class III or IV in the subacute phase of infarction (risk ratio 1.7); and 4) multiple previous infarctions (risk ratio 1.4).The results of the two multivariate analyses were used in a model for prediction of mortality at 1 year. The average predicted mortality rate varied considerably according to the model: for 243 patients (62%) with the lowest risk, it was 13%, corresponding to an observed mortality rate of 12%; for 92 patients (24%) with intermediate risk, it was 27%, corresponding to an observed rate of 28%; for 55 patients (14%) with the risk, it was 64%, corresponding to an observed rate of 54%.This study shows that patients with symptomatic ventricular tachycardia or ventricular fibrillation late after myocardial infarction who are given standard antiarrhythmic treatment have a high mortality rate. The predictive model presented identifies patients at low, intermediate and high risk of death and can be of help in designing the appropriate diagnostic and therapeutic strategy for the individual patient.

The 12 lead electrocardiographic (ECG) findings were reviewed in 17 patients having two or more accessory pathways as documented during electrophysiologic study in all 17 patients and by intraoperative mapping in 8.Twelve patients had findings suggesting the presence of more than one atrioventricular (AV) pathway. These were 1) more than one P wave configuration during orthodromic circus movement tachycardia (four patients); 2) a “mismatch” between the location of the ventricular and atrial ends of the accessory pathway as assessed when comparing exclusive AV and ventriculoatrial conduction over the accessory pathway during antidromic and orthodromic circus movement tachycardia, respectively (seven patients); 3) atrial fibrillation showing more than one pre-excitation pattern (six patients); 4) a spontaneous change from orthodromic to antidromic circus movement tachycardia and vice versa (two patients); 5) a spontaneous change from one type of antidromic tachycardia to another (two patients); and 6) a change in pre-excitation pattern after administration of a drug that prolongs the anterograde refractory period of the accessory pathway (three patients).The retrospective nature of this study does not allow conclusions as to the true value of the ECG in predicting the presence of more than one accessory pathway. This issue needs to be evaluated in a prospective study.

An intriguing new clinical entity characterized by ST-segment elevation in the right precordial electrocardiographic leads and a high incidence of sudden death in individuals with structurally normal hearts was described by Pedro and Josep Brugada in 1992. The past decade has witnessed an exponential rise in the number of reported cases and a dramatic proliferation of papers serving to define the clinical, genetic, cellular, ionic, and molecular aspects of this disease. The purpose of this brief review is to chronicle the historical highlights that have brought us to our present understanding of Brugada syndrome.

In 1924, Willem Einthoven received the Nobel Prize for physiology or medicine “for his discovery of the mechanism of the electrocardiogram.” His colleague Sir Thomas Lewis, regarded by many as another father of clinical electrocardiography, was born in 1881, 21 years after Einthoven, and it is

Objectives We recently described a syndrome characterized by an electrocardiographic (ECG) pattern of right bundle branch block and persistent ST segment elevation in leads Vl to V3 in 8 patients (pts) suffering from aborted sudden death without structural heart disease. The objectives of the present study are to present new observations on this syndrome. Methods A total of 22 pts (mean age 40 ± 12 years) have been identified with the described ECG pattern. Of them, 17 were symptomatic with syncope and aborted sudden cardiac death. The other 5 pts were asymptomatic when first seen, however, 1 died suddenly after 6 years of follow-up without treatment and another received an implantable defibrillator after syncope. Subsequently, several episodes of ventricular fibrillation were terminated by the defibrillator in this pt. The other 3 pts remain asymptomatic without treatment. In 4 of 22 pts the ECG transiently normalized during follow–up. Conclusions The present observations demonstrate that there exist asymptomatic pts with this syndrome. These pts may become symptomatic during follow-up. It is difficult to set a therapeutic strategy for these asymptomatic pts at present. Our observations also show that the ECG can transiently normalize, suggesting that the disease is not based on a permanent structural cardiac abnormality, but rather on functional alterations of the electrical activity of the heart.

To investigate how the electrophysiologic properties of the accessory pathway affect the occurrence of atrial fibrillation in the Wolff-Parkinson-White syndrome, programmed stimulation data of 57 patients with overt pre-excitation and 33 patients with a concealed accessory pathway with documented circus movement tachycardia were reviewed. Atrial fibrillation had occurred spontaneously in 31 (54%) of the 57 patients with the Wolff-Parkinson-White syndrome and in 1 (3%) of the 33 with a concealed accessory pathway (p less than 0.001). Sustained atrial fibrillation was induced in 23 of 31 patients with the Wolff-Parkinson-White syndrome and spontaneous atrial fibrillation (Group A), in 7 of 26 patients with the Wolff-Parkinson-White syndrome without spontaneous atrial fibrillation (Group B) and in 5 of 33 patients with a concealed accessory pathway (Group C). The anterograde effective refractory period of the accessory pathway was shorter in Group A than in Group B (252 versus 297 ms, p less than 0.001). There were no differences among groups in PA interval, right to left atrium conduction time, cycle length of tachycardia and atrial and retrograde accessory pathway effective refractory period. Atrial fibrillation is more frequent in patients with the Wolff-Parkinson-White syndrome than in those with a concealed accessory pathway. Patients with overt pre-excitation and atrial fibrillation have a shorter anterograde accessory pathway refractory period. It seems therefore that the anterograde rather than the retrograde conduction properties of the accessory pathway are the critical determinants of atrial fibrillation in the Wolff-Parkinson-White syndrome.

Data on the correlation of left ventricular segmental wall motion and electrocardiographic findings are, except for Q waves and ST segment elevation, still controversial. Therefore, in addition to Q waves and ST segment elevation, eight features of the electrocardiogram were studied in 265 patients, 61 with normal coronary arteries and 204 with coronary artery disease. Patients with a QRS duration of 0.12 second or greater were excluded.Left ventricular wall motion was assessed in the 30° right anterior oblique and the 60° left anterior oblique projections and analyzed by the Stanford method and a modification of that method, respectively. Asynergy of a particular segment correlated well with the presence of Q waves in the corresponding electrocardiographic lead or leads, but was also found in other segments. There was a significant (p < 0.001) correlation between the number of leads with Q waves and the degree of extension of asynergy. The R/S ratio in lead V1and Q waves in lead V6appeared to be the most informative about the posterior wall. Loss of R wave voltage had a lower predictive value for segmental asynergy than did Q waves in the same lead. Among patients with electrocardiographic findings of an infarct, asynergy was found in 83 to 94%. Patients having Q waves in combination with ST segment elevation manifested more severe asynergy than did patients whose Q waves were not associated with ST elevation. New data are presented for lateral and posterior infarction. Patients having left-axis deviation, low voltage and QRS notching had severe asynergy. ST segment depression and negative T waves gave only limited additional information on wall motion.It is concluded that certain QRS abnormalities correlate highly with asynergy. ST segment elevation is the most important non-QRS abnormality in predicting asynergy.

Although uncommon, incessant supraventricular tachycardia (the daily presence of supraventricular tachycardia for more than 50% of the day) is a major therapeutic problem. Using programmed electrical stimulation of the heart, long-term electrocardiographic monitoring and exercise testing, the effect of intravenous and oral encainide for termination and prevention of incessant supraventricular tachycardia was assessed in 11 patients (aged 25 to 58 years). All patients had received 3 to 12 drugs (mean 6) without control of their arrhythmia. Eight patients suffered from incessant supraventricular tachycardia using an accessory pathway in retrograde direction (three with overt Wolff-Parkinson-White syndrome, one with a concealed accessory atrioventricular [AV] pathway of the fast type, three with a concealed accessory AV pathway of the slow type and one with a nodo-ventricular accessory pathway). Three patients had incessant atrial tachycardia, one of whom also had the Wolff-Parkinson-White syndrome. Intravenous encainide (1.5 mg/kg in 15 minutes) terminated incessant supraventricular tachycardia in seven of nine patients. In four of nine patients, supraventricular tachycardia could thereafter still be reinitiated by pacing. Oral encainide (100 to 325 mg/day, mean 180) completely suppressed the incessant supraventricular tachycardia in eight patients in a follow-up period of 5 to 20 months (mean 11). In two patients, episodes of tachycardia were markedly reduced with the administration of encainide in combination with sotalol (one patient) and amiodarone (one patient). Encainide failed to control incessant tachycardia in one patient. Mild central nervous system side effects developed in two patients, but both could continue taking oral encainide. Encainide proved to be a very useful agent to control incessant supraventricular tachycardia resistant to other antiarrhythmic agents.

The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway) was studied using atrial and ventricular pacing in 18 patients with paroxysmal AV node tachycardia. Transient entrainment occurred in all patients. During atrial pacing, localized block in the AV node for one beat followed by anterograde conduction over the fast pathway was observed in three patients. During ventricular pacing, localized block for one beat followed by retrograde conduction over the slow pathway was not observed in any patient. Neither atrial nor ventricular fusion beats were observed during entrainment. These observations indicate in a way not previously shown that reentry involving two functionally dissociated pathways in the AV node is the underlying mechanism of paroxysmal AV node tachycardia. The inability to demonstrate atrial or ventricular fusion beats during entrainment suggests a true intranodal location of the reentrant circuit. Finally, the ability to transiently entrain intranodal tachycardia demonstrates that this electrophysiologic phenomenon is not exclusively limited to macroreentrant circuits.

In the differential diagnosis of tachycardias showing a wide QRS complex and having a 1 to 1 relation between ventricular and atrial events, a supraventricular tachycardia with anterograde conduction over an accessory pathway and retrograde conduction by way of the specific conduction system must be considered. Five patients showing this type of circus movement tachycardia were studied by programmed electrical stimulation of the heart. Sudden changes in the tachycardia cycle length were observed in these patients that were based on changes in the VH interval. This finding suggested a change in the reentrant circuit with anterograde conduction over the accessory pathway but retrograde conduction sometimes occurring over the right bundle branch and at other times over one of the two divisions of the left bundle branch system. Characteristically, the tachycardia cycle length changed suddenly depending on the bundle branch used in retrograde direction. In one patient, an important difference was also observed between the anterograde effective refractory period of the accessory bypass (280 ms) and the shortest RR interval between preexcited QRS complexes during atrial fibrillation (measuring 190 ms). It is postulated that the short RR intervals during atrial fibrillation in the Wolff-Parkinson-White syndrome could result from bundle branch reentry after activation of the ventricles over the accessory pathway.

To assess the value of lead V4R during exercise testing for predicting proximal stenosis of the right coronary artery, 107 patients were studied. In all patients, a Bruce exercise test with the simultaneous recording of leads I, II, V4R, V1, V4 and V6 was followed by coronary angiography. Apart from registering ST segment changes in the conventional leads, all patients were classified according to absence or presence of an ST segment deviation of 1 mm or greater in lead V4R. Seventy-nine of the 107 patients were studied because of inadequate control of angina pectoris. Seven patients had had myocardial infarction before 40 years of age. Twenty-one patients were analyzed because of severe cardiac arrhythmias. In the 46 patients who had a previous myocardial infarction, the infarct location was inferior in 28 and anterior in 18. Seven of the 14 patients without myocardial infarction and significant proximal stenosis in the right coronary artery showed an ST segment deviation of 1 mm or greater in lead V4R during exercise. This was also observed in 11 of 18 patients with an old inferior wall infarction and proximal occlusion of the right coronary artery. None of the 53 patients without significant proximal stenosis in the right coronary artery showed exercise-related ST segment changes in lead V4R. Exercise-related ST segment deviation in lead V4R had a sensitivity of 56%, a specificity of 96% and a predictive accuracy of 84% in recognizing proximal stenosis in the right coronary artery. These observations indicate that the recording of lead V4R is of value for predicting or excluding proximal stenosis in the right coronary artery.

Paroxysmal atrioventricular (AV) block was induced by exercise in an otherwise healthy young man. The only abnormalities demonstrated at comprehensive cardiac evaluation were: 1) angiographic systolic narrowing of the left anterior descending coronary artery, and 2) reversible radionuclide hypoperfusion of the septum during exercise. It is postulated that ischemia of the conduction system due to systolic milking of the left anterior descending coronary artery was responsible for the paroxysmal AV block in this patient.

To detect right ventricular involvement, lead V4R was recorded within 10 hours of the onset of chest pain in 42 consecutive patients admitted with acute inferior wall myocardial infarction. One week after the acute infarction, multigated equilibrium radionuclide ventriculography was performed to assess right and left ventricular ejection fraction. Two weeks after the acute infarction, coronary angiography was performed to determine the site and location of the obstruction leading to the infarction. Seventeen patients had an obstruction in the right coronary artery proximal to the first branch to the right ventricular free wall (group 1); all of these had ST segment elevation in lead V4R. Fourteen patients had an obstruction in the right coronary artery distal to the first branch to the right ventricular free wall (group 2); only two of these patients had ST segment elevation in lead V4R. In 11 patients, the obstruction was located in the circumflex coronary artery (group 3); none of these had ST segment elevation in lead V4R. Nineteen patients had ST segment elevation of 1 mm or greater in lead V4R (group 4). Left ventricular ejection fraction was not different among the four groups of patients, although the right ventricular ejection fraction was significantly lower in group 1 and group 4 patients. It is concluded that ST segment elevation in lead V4R reliably identifies the group of patients with inferior wall myocardial infarction with depressed right ventricular function. This phenomenon persists for at least 1 week after infarction.

Information from programmed electrical stimulation of the heart has improved our ability to diagnose the site of origin and mechanism of a tachycardia from the 12 lead electrocardiogram. To test this hypothesis, the 12 lead electrocardiograms of a 12 year old girl with the Wolff-Parkinson-White syndrome showing four different types of tachycardia were sent for interpretation to 30 leading electrocardiologists , 22 of whom responded. A correct diagnosis of all four tachycardias was made by 13. Three or two of the tachycardias were correctly diagnosed by four and five cardiologists, respectively. The outcome of our study indicates that the pathway and mechanism of tachycardia can frequently be predicted from the 12 lead electrocardiogram alone.

in five patients with chronic re•current ventricular tachycardia demonstrating that the ar•rhythmia could be reproducibly initiated and terminated dur•ing programmed stimulation of the heart, a very large and important body of information dealing with this subject has appeared. While the application of programmed cardiac stimulation to assist in the management of patients with ventricular tachycardia continues to develop, and some as•pects of its application remain controversial, there is now a body of consistent observations that make it possible to consider what a minimally acceptable clinical electrophys•iologic study should be. Because of the important and ex•panding use of electrophysiologic testing in patients, the North American Society of Pacing and Electrophysiology thought it timely to recommend minimal standards for elec•trophysiologic studies in patients who present with ventric•ular tachycardia, Therefore, the Society held a policy con•ference on this subject in Toronto, Canada on May

Objectives. This prospective, multicenter trial was aimed at defining efficacy and safety of low energy shocks during atrial fibrillation in a diverse cohort of patients.Background. Experimental studies in sheep and preliminary data in humans have suggested that low energy internal shocks delivered between right atrial and coronary sinus electrode catheters may terminate atrial fibrillation.Methods. Biphasic 3/3-ms R wave synchronous shocks were delivered between two electrode catheters in the right atrium and coronary sinus. The defibrillation protocol started with a test shock of 20 V, and shocks increased in 40-V steps until restoration of sinus rhythm or a maximum of 400 V. Shock delivery was withheld after short RR intervals. In 141 patients with atrial fibrillation, the protocol was carried out under sedation in case the shock was associated with discomfort. The atrial arrhythmia was paroxysmal (≤7 days) in 50 patients, chronic (>30 days) in 53, intermediate (>7 days, ≤30 days) in 18 and induced in 20. Underlying heart disease was present in 88 patients (62%).Results. Paroxysmal atrial fibrillation was successfully terminated in 46 (92%) of 50 patients, chronic atrial fibrillation in 37 (70%) of 53, intermediate in 16 (89%) of 18 and induced in 16 (80%) of 20. Mean conversion threshold was 1.8 J (213 V) in the induced group, 2.0 J (229 V) in the paroxysmal group, 2.8 J (272 V) in the intermediate group and 3.6 J (311 V) in the chronic group. The conversion voltage was significantly (p < 0.001) higher in the chronic group than in the other groups of atrial fibrillation and increased significantly with the duration of atrial fibrillation and with left atrial size (p < 0.05). Of 1,779 R wave synchronized shocks delivered with a mean (±SD) preceding RR interval of 676 ± 149 ms, no ventricular arrhythmia was induced. The latter may occur after unsynchronized shocks.Conclusions. Low energy transvenous shocks in patients with atrial fibrillation are effective and safe, provided that shocks are properly synchronized to R waves with preceding RR intervals that meet appropriate cycle length criteria. This study provides data that may be useful in the development of an implanted atrial defibrillator.(J Am Coll Cardiol 1997;29:750–5)

observed that a critical rate of pacing was requiredto terminate atrial flutter. At the lower rates of pacing,continuation of the arrhythmia occurred immediately aftercessation of pacing. Their observations had important clin­ical implications, including the recommendation for system­atic prophylactic implantation of electrodes during cardiacsurgical procedures to terminate arrhythmias by rapid pacing(3,4), A more complicated issue is the value of the rapidpacing technique to study mechanisms of arrhythmias. Waldoet al. (5) also suggested that the demonstration of transiententrainment supports reentry as the underlying mechanismof the arrhythmia. In this issue of the Journal. Waldo et al.(6) offer us a study of a unique case of ventricular tachy­cardia that could be transiently entrained and terminated byatrial pacing. Most important, the reentrant circuit could bereversed by rapid atrial pacing. In this article, we wouldlike to discuss some aspects of the phenomenon of entrain­ment and some of its implications.

Findings are described in six patients with no clinical evidence of heart disease who had documented ventricular fibrillation (five patients) or ventricular flutter (one patient). The mean age of the six patients, all men, was 34 years (range 26 to 43). Cardiovascular collapse occurred in all and was followed by successful cardioversion. No patient had electrolyte or QT abnormalities. One patient had slight right ventricular enlargement on M-mode echocardiography, and another had a left ventricular pressure gradient at rest of 30 mm Hg with a normal two-dimensional echocardiogram. Holter electrocardiographic monitoring revealed incessant ventricular tachycardia in one patient and nonsustained ventricular tachycardia in three others. Exercise testing revealed nonsustained ventricular tachycardia in one patient.Ventricular fibrillation was induced at the time of programmed electrical stimulation in four of the six patients. Documented recurrence of ventricular fibrillation or ventricular flutter occurred in three patients, but in only one patient receiving antiarrhythmic drugs. Four patients were treated with amiodarone and one received an automatic implantable cardioverter-defibrillator. All patients are alive after a mean follow-up period of 78 months after the first documentation of their arrhythmia and 37 months after programmed electrical stimulation.Ventricular fibrillation can occur in the apparently structurally normal human heart. Antiarrhythmic treatment can provide effective control of this malignant arrhythmia.

The effect of different modes of pacing on interval and configuration of the first postpacing QRS complex was studied during digitalis-induced ventricular tachycardia in the conscious dog. The effect of overdrive pacing was related to pacing rate; the longest pacing intervals resulted in prolongation of the first postpacing interval, while increasing the rate of overdrive pacing led to a progressive shortening of the first postpacing interval. When extrastimuli were introduced during fixed rate pacing, the duration of the first postpacing interval was found to be predominantly effected by the extrastimulus coupling interval. The importance of the last paced interval to the duration of the first postpacing cycle length was also observed when only a single or two extrastimuli were given. The duration of the first postpacing interval was found to be independent of the site site of stimulation. In contrast, the configuration of the first postpacing QRS complex was found to be related to the site of pacing; the first postpacing QRS complex originated close to the site of stimulation independent of the configuration of the tachycardia. In conclusion, it was found that during digitalis-induced ventricular tachycardia 1) the first postpacing interval is mainly, dependent on the interval of the last paced beat, 2) the length of the first postpacing interval is independent of the site of stimulation, but 3) the configuration of the first postpacing QRS complex is related to the site of stimulation. These findings may facilitate the understanding of complex ventricular arrhythmias observed during severe digitalis intoxication in human beings.