Spontaneous Episodes Of Ventricular Tachycardia Research Articles

Electrophysiologic Response to Moricizine in Patients with Sustained Ventricular Arrhythmias

To assess the short-term efficacy and safety of moricizine in patients receiving electrophysiologically guided therapy for sustained ventricular arrhythmias refractory to treatment with class IA antiarrhythmic agents. Uncontrolled clinical trial. Referral-based teaching medical center. Twenty-one patients (18 of whom had coronary artery disease) with a mean left ventricular ejection fraction of 32% +/- 11% who presented with sustained ventricular tachycardia (13 patients), syncope (4 patients), or cardiac arrest (4 patients). Moricizine, 743 +/- 85 mg daily. Electrophysiologic testing in the drug-free state and after administration of moricizine unless sustained arrhythmias occurred. Sustained ventricular tachycardia was inducible in the absence of antiarrhythmic drugs in 20 patients and was not suppressed by moricizine in any patient. Four patients had six episodes of spontaneous ventricular tachycardia while receiving moricizine. A probable proarrhythmic response occurred in four patients. In patients with compromised left ventricular function caused by coronary artery disease in whom class IA antiarrhythmics were ineffective, moricizine was ineffective in suppressing sustained ventricular arrhythmias and resulted in proarrhythmic effects in some patients.

Circadian variation of ventricular tachycardia in patients with coronary arterial disease

Sudden cardiac death and ischaemic cardiac events occur in a circadian pattern. Because ventricular tachycardia is thought to play an important role in sudden cardiac death, the episodes of spontaneous ventricular tachycardias (≥ 3 consecutive beats) ( n = 1314) were analysed from 24-hour long term electrocardiographic recordings in 34 patients with coronary arterial disease to determine whether circadian rhythm exists in spontaneous ventricular tachycardia. Twelve patients had suffered cardiac arrest, four patients had a history of syncope, and palpitation was the indication for electrocardiographic recordings in eighteen patients. Analysis using chronobiologic single cosinor method showed a significant circadian variation in the occurrence of ventricular tachycardia episodes with the peak occurring at 6 a.m. Similar circadian rhythm was also observed in the occurrence of the longest episode of ventricular tachycardia. Ischaemic ST-segment depression preceded the longest ventricular tachycardia episode only in one patient. Thus, a circadian rhythm occurs also in spontaneous episodes of ventricular tachycardia, a finding which is similar to that in sudden cardiac death.

Radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia: Results and long-term follow-up

Seven of 120 consecutive patients with inducible sustained ventricular tachycardia (from September 1, 1988 to January 1, 1991) had bundle branch reentrant tachycardia and underwent percutaneous radiofrequency ablation of the right bundle branch. The seven patients had been unsuccessfully treated with a mean of 3 ± 1 drugs. Four patients presented with syncope and three with aborted sudden death. The baseline electrocardiogram revealed a left bundle branch block pattern in three patients and an intraventricular conduction defect in four.The baseline HV interval was prolonged in each case (79 ± 2 ms). With use of programmed ventricular extrastimuli, sustained bundle branch reentrant tachycardia was inducible in all patients at a mean cycle length of 283 ± 17 ms (range 230 to 350). Bundle branch reentrant tachycardia characteristics included atrioventricular dissociation, a His deflection that preceded each QRS complex and spontaneous His to His variation that preceded changes in ventricular tachycardia cycle length.A quadripolar catheter was positioned across the tricuspid valve with the distal electrode tip of the catheter near the right bundle branch. One to three applications of continuous unmodulated radiofrequency current at 300 kHz between the distal electrode and a large posterior skin patch resulted in complete right bundle branch block in all patients, after which none had inducible bundle branch reentrant tachycardia on restudy. On restudy, three of the seven patients had ventricular tachycardia of myocardial origin (not bundle branch reentry). One patient required no therapy; drug or defibrillator therapy was used in the others. After a mean follow-up interval of 12 ± 3 months (range 6 to 29) complete right bundle branch block persisted, there were no spontaneous episodes of ventricular tachycardia and no patient required a permanent pacemaker.Radiofrequency catheter ablation of the right bundle branch is easily performed and is a safe and effective treatment for bundle branch reentrant tachycardia. It is probably the procedure of choice for these highly symptomatic patients.

Ninety‐Six Episodes of Spontaneous Ventricular Tachycardia in 1 Week: Success of Ramp Pacing by a Pacer‐Cardioverter‐Defibrillator

This case report describes the flexibility and usefulness of a pacer-cardioverter-defibrillator for the management of a 63-year-old patient with malignant ventricular tachyarrhythmias. Ninety of 96 episodes of ventricular tachycardia were terminated successfully with ramp pacing in a 1-week period. In those patients who have frequent episodes of ventricular tachycardia that respond to antitachycardia pacing, the multifunction device can add to the patient's comfort and increase acceptance of this type of device.

Experience with a third-generation implantable cardioverter-defibrillator

A Medtronic 7216A pacemaker cardioverter-defibrillator was implanted in 16 patients (mean age 56 years) with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) and organic heart disease with a mean left ventricular ejection fraction of 33%. Endocardial and epicardial defibrillation shock efficacy was evaluated before or at implant using 1 to 3 shock patterns, i.e., monophasic single, sequential or simultaneous shocks with dual and triple electrode configurations. Endocardial leads used a common right ventricular cathode and dual anodes, whereas epicardial leads used 2 or 3 helical coil patches. VT termination was evaluated using pacing or shock therapy, or both, whereas only shocks were used in VF. Programmable bradycardia pacing, individual zones for VT and VF detection and individualized pacing and shock therapy for VT and VF were used. Monophasic shocks had epicardial defibrillation thresholds ranging from 3 to 18 (mean 10) J and were comparable for sequential and simultaneous shocks (p > 0.2). VT detection rates ranged from 340 to 470 ms and VF detection rates from 270 to 330 ms. VT or VF induction, or both, was performed noninvasively in 13 patients after implant and was reproducibly terminated by rapid pacing alone (5 patients), low-energy shocks (2 patients), high-energy shocks (3 patients) and combined therapy (3 patients). Intermediate or highenergy shocks terminated all induced VF episodes. During follow-up (2 to 12 months), there have been 2 noncardiac deaths. Electrical therapy was delivered in 7 patients, for VT (3 patients), VT and VF (3 patients) and indeterminate tachyarrhythmia (1 patient). All sol VT VF episodes were successfully terminated, with 78 of 96 (81%) spontaneous VT episodes terminated by pacing. Follow-up reprogramming was required n 5 patients. It is concluded that successful application of individualized electrical therapy prescriptions in patients with VT/VF is feasible. Pacing therapies, which are effective for induced VT, can be reliably used for effective long-term spontaneous VT termination in conjunction with shock therapy and can permit reduced patient exposure to shock therapy. Thus, a programmable hybrid pacemaker cardioverter-defibrillator system provides nonthoracotomy implantation, effective sol VT VF termination, demand ventricular pacing and noninvasive modes for arrhythmia induction, event monitoring and clinical troubleshooting.

Reduction in incidence of inducible ventricular tachycardia after myocardial infarction by treatment with streptokinase during infarct evolution

The aim of this study was to determine whether intravenous streptokinase administered with or without oral aspirin to patients with evolving myocardial infarction reduces the inducibility of ventricular tachycardia at electrophysiologic study and thus the risk of sudden death in infarct survivors. Of 159 patients randomized at Westmead Hospital to the multicenter Second International Study of Infarct Survival (ISIS-2) after streptokinase and aspirin in acute myocardial infarction, 87 underwent electrophysiologic testing 6 to 28 days after infarction to determine their risk of subsequent ventricular arrhythmias (streptokinase 20 patients; aspirin 25 patients; streptokinase and aspirin 21 patients; both placebos 21 patients). Patients who underwent electrophysiologic testing had similar clinical characteristics to those of patients who did not. The stimulation protocol comprised up to and including four extrastimuli applied to the right ventricular apex at twice diastolic threshold. An abnormal result was defined as ventricular tachycardia with a cycle length ≥ 230 ms lasting ≥ 10 s.Ventricular tachycardia was inducible at electrophysiologic study in 8 patients who received placebo streptokinase, but in no patient who received active streptokinase (8 of 46 versus 0 of 41; p = 0.005, Fisher's exact test). Ventricular tachycardia was inducible in 4 patients who received aspirin therapy and 4 who did not (4 of 41 versus 4 of 46; p = NS). During a mean follow-up period of 39 ± 9 months, there were no spontaneous episodes of ventricular tachycardia, ventricular fibrillation or witnessed sudden death in the streptokinase-treated group compared with three such events in the placebo-treated group (p = 0.13).When compared with placebo therapy, intravenous streptokinase substantially reduced the incidence of inducible ventricular tachycardia in infarct survivors. No similar benefit was attributable to aspirin therapy.

Electrophysiologic evaluation of antiarrhythmic therapy for ventricular tachyarrhythmias

The use of electrophysiologic studies has contributed significantly to our understanding of the mechanisms of ventricular tachyarrhythmias and enhanced our ability to assess objectively the efficacy of various therapeutic interventions in modifying or preventing their recurrence. The basis on which electrophysiologic testing techniques is founded is the ability reproducibly to initiate ventricular arrhythmias by programmed electrical stimulation in patients with a history of recurrent ventricular tachycardia or fibrillation. Ventricular tachycardia can be initiated by electrophysiologic studies in approximately 90% of patients with clinically documented recurrent, sustained ventricular tachycardia related to coronary artery disease and in 60% of patients with nonsustained ventricular tachycardia. Reports indicate that electrophysiologic testing is highly specific as well (99% for sustained monomorphic ventricular tachycardia). Studies in patients with recurrent ventricular tachycardia demonstrate that prevention by antiarrhythmic drugs of the ability to initiate tachycardias that were previously inducible by comparable stimulation techniques in the absence of therapy is highly predictive of freedom from recurrent episodes of spontaneous ventricular tachycardia and ventricular fibrillation. This end point can be achieved in 35 to 75% of patients. This wide range of success rates results from differences in the patient populations studied, as well as major differences in the programmed stimulation and antiarrhythmic drug protocols used among laboratories. The positive predictive value of this technique (defined as the percentage of patients in whom complete suppression of inducible ventricular tachycardia or ventricular fibrillation is achieved during electrophysiologic testing with antiarrhythmic drugs and in whom no spontaneous arrhythmia occurs at 1- to 2-year follow-up) ranges between 80 and 95%.

Prognosis following sustained ventricular tachycardia occurring early after myocardial infarction

Eighty-seven patients with sustained ventricular tachycardia (VT) between 3 and 90 days after acute myocardial infarction (AMI) were evaluated to define factors associated with a high risk of arrhythmia recurrence or death. Most patients had poor left ventricular function (mean ejection fraction 29 ± 12%), multivessel coronary artery disease (71%) and inducible sustained VT with programmed stimulation (87%). During a mean followup of 26 months, 36 patients (41%) died and 21 patients had arrhythmia recurrence (with 19 sudden deaths). Factors independently associated With mortality included: (1) treatment before 1981 (p < 0.01); (2) anterior AMI (p < 0.05); (3) short time from AMI to first episode of VT (p < 0.06); and (4) multivessel coronary artery disease (p < 0.07). Factors independently associated with arrhythmia recurrence were: (1) medical treatment (as opposed to surgical) (p < 0.01); (2) ≥3 episodes of spontaneous VT (p = 0.01); (3) multivessel coronary disease (p < 0.05); and (4) anterior AMI (p < 0.07). Medically and surgically treated patients did not differ significantly in overall survival (49 vs 61%, respectively), although short-term (6 month) surgical survival improved from 31% during the first half of the study to 96% in the latter half (p < 0.01). For patients with sustained VT early after AMI the risk of death and arrhythmia recurrence can be assessed based on clinical and angiographic characteristics; in addition, surgical treatment is associated with a lower incidence of arrhythmia recurrence than medical treatment. Given the recent improvement in short-term surgical survival, surgery may be the preferred option for high risk patients with multivessel coronary disease and frequent episodes of VT.

Anterior left ventricular aneurysm: Factors associated with the development of sustained ventricular tachycardia

Fifty patients with anteroapical left ventricular aneurysm secondary to prior myocardial infarction underwent aneurysmectomy, at which time endocardial sinus rhythm mapping was performed. Forty patients had a history of recurrent sustained monomorphic ventricular tachycardia, and 10 had an aneurysm hot no history of spontaneous sustained tachycardia. A comparison of the clinical, angiographic and sinus rhythm endocardial clectrographic characteristics of these two groups revealed that the patients without spontaneous ventricular tachycardia had more severe coronary artery disease (2.6 ± 0.5 versus 1.9 ± 0.8 coronary arteries having >70% stenosis; p < 0.03), underwent surgery earlier after infarction (3 ± 2 versus 46 ± 53 months; p < 0.003) and had less extensive wall motion abnormalities on contrast ventriculography (0 of 8 versus 13 of 35 patients assessed had an abnormally contracting ventriculographic segment length >60%; p < 0.04).During intraoperative programmed electrical stimulation, all 40 patients with and 4 of 10 without a history of spontaneous ventricular tachycardia had induciblc tachycardia. The patients with inducible tachycardia had a larger area of endocardium from which abnormal electrograms (duration >70 ms or amplitude <0.7 mV) were recorded (62 ± 17 versus 45 ± 20% of electrograms; p < 0.03) as well as fractionated (duration >90 ms, amplitude <0.3 mV) electrograms (20 ± 14 versus 9 ± 7% of electrograms; p < 0.04) than did patients without inducible tachycardia, but there were no angiographic diffirenres between groups.These data suggest that 1) differences between groups of patients with versus without either inducible or spontaneous ventricular tachycardia are more quantitative than qualitative; and 2) the pathophysiologic substrate for ventricular tachycardia may develop relatively early after infarc tion, but other factors determine the development of spontaneous episodes of tachycardia. In the absence of features that clearly identify those patients with an aneurysm who are at high risk for future episodes of spontaneous ventricular tachycardia, it may be reasonable to consider performing pre- or intraoperative stimulation or blind subendocardial resection in such patients at the time of elective aneurysmcctomy.

Subendocardial resection for ventricular tachycardia: predictors of surgical success.

We retrospectively evaluated the first 100 patients who underwent mapping-guided subendocardial resection (SER) at our hospital for drug-refractory sustained ventricular tachycardia caused by coronary artery disease. There were 91 survivors of surgery with 200 morphologically distinct types of ventricular tachycardia. Eighty-three patients (91%) were cured of ventricular tachycardia by SER alone (60 patients or 66%) or by SER in combination with antiarrhythmic drug therapy (23 patients or 25%) (mean follow-up, 28 +/- 19 months). There were four late sudden deaths and four patients continued to have rare episodes of spontaneous ventricular tachycardia after surgery despite receiving antiarrhythmic drugs. Factors associated with failure of SER alone to cure ventricular tachycardia were presence of disparate sites of ventricular tachycardia origin (greater than 5 cm between mapped sites of origin; 64% vs 30% failure rate) and presence of multiple morphologically distinct spontaneous tachycardias (47% vs 25% failure rate). A log-linear model of multivariate analysis identified disparate sites of origin of ventricular tachycardia and the absence of a discrete left ventricular aneurysm as the only independent variables associated with failure of surgery alone. Inferior wall site of origin (41% vs 12% failure) and right bundle branch block morphology of ventricular tachycardia (20% vs 7% failure) were also significantly associated with failure of surgery to cure ventricular tachycardia. Mapping-guided SER is a highly effective mode of treatment for drug-refractory ventricular tachycardia, despite the existence of subgroups of patients with higher-than-average surgical failure rates.

Clinical efficacy and electrophysiologic effects of cibenzoline therapy in patients with ventricular arrhythmias

Cibenzoline, a new antiarrhythmic agent, was tested in 26 patients who had symptomatic ventricular tachycardia (24 patients) or premature ventricular complexes (2 patients) unresponsive to conventional drugs. Cibenzoline was given orally every 8 hours to maximal doses of 65 mg in 2 patients, 81.25 mg in 22 patients and 97.5 mg in 2 patients. Cibenzoline abolished spontaneous episodes of ventricular tachycardia in 8 of 16 patients with ventricular tachycardia during a 72 hour control electrocardiographic recording, and 7 of 22 patients had greater than 83% decrease in premature ventricular complexes compared with control. The PR interval increased 14% (p less than 0.001), QRS duration increased 17% (p less than 0.001), QT interval did not change and mean ejection fraction in 10 patients did not change. Electrophysiologic studies were performed on 10 patients in the control period and during maximal cibenzoline dosage. Cibenzoline did not affect electrophysiologic properties of the atrium or atrioventricular (AV) node. It prolonged the ventricular effective (223 +/- 16 to 241 +/- 22 ms, p less than 0.02) and functional (247 +/- 18 to 264 +/- 25 ms, p less than 0.02) refractory periods. At control electrophysiologic studies, ventricular tachycardia was induced in 9 of 10 patients (mean cycle length 210 +/- 31 ms). Cibenzoline therapy prevented ventricular tachycardia induction in two patients, and in the other seven patients the mean ventricular tachycardia cycle length increased from 210 to 260 ms. The one patient with no ventricular arrhythmia induced during the control study still had no arrhythmia induced while receiving cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)

Induction of clinical ventricular tachycardia using programmed stimulation: Value of third and fourth extrastimuli

Initiation of ventricular tachycardia (VT) by right ventricular extrastimulation was analyzed in 142 consecutive patients, 53 with electrocardiographically documented episodes of spontaneous VT or ventricular fibrillation (VF) and 68 with no spontaneous VT or VF; 21 patients with a history of sudden death but no documented arrhythmia were excluded from further analysis, All patients received 1 to 4 extrastimuli (S 2, S 3, S 4 and S 5) during pacing at fixed cycle lengths of 600 or 500 msec at 1 or 2 right ventricular sites. Clinical VT was reproduced by extrastimulation in 28 of 43 patients (65%) with sustained VT and in 0 of 10 patients with nonsustained VT. Clinical VT was induced by S 2 or S 3 in 16 patients and by S 4 or S 5 in 12 patients. Ventricular burst pacing reproduced clinical VT in 3 other patients. Nonclinical VT, which was most often polymorphic and nonsustained, was induced in 24 of 121 patients (20%), In 11 by S 2 or S 3 and in 13 by S 4 or S 5. Ventricular burst pacing induced nonclinical VT in 4 other patients. In patients with spontaneous sustained VT, the use of S 4 and S 5 in the right ventricle increases the yield of inducible clinical VT compared with use of S 2 and S 3 alone, but at a cost of increased induction of nonclinical VT. Frequent induction of nonclinical VT limits the interpretation of the results of such stimulation in patients without previously documented VT.

Mexiletine for refractory-ventricular arrhythmias: Results using serial electrophysiologic testing

Mexiletine was administered during serial drug testing to 35 patients with electrically inducible ventricular arrhythmias and to 6 with recurrent ventricular tachycardia that could not be induced or terminated by programmed cardiac stimulation. All patients had arrhythmias resistant to all conventionally available agents. Electrically induced arrhythmias were completely suppressed during mexiletine therapy in 13 patients. In 12 patients no antiarrhythmic regimen was completely suppressive and in 7 of these mexiletine favorably modified the response to programmed stimulation. In four of six patients with frequent episodes of spontaneous ventricular tachycardia that were not inducible by programmed cardiac stimulation, arrhythmia was controlled by mexiletine. The presence of complete arrhythmia suppression with mexiletine during acute testing accurately predicted long-term freedom from recurrent arrhythmia in 16 of 17 patients over a mean follow-up period of 12.6 ± 6 months. Severe adverse neurologic effects were noted early during mexiletine therapy in three patients, but no patient discharged on such therapy experienced major adverse effects. The study demonstrates that mexiletine can provide well tolerated effective prophylaxis against recurrent ventricular arrhythmias in a significant proportion of patients resistant to conventional drugs.

Ventricular tachycardia and ventricular fibrillation in a young population.

In this study, we describe the findings in 18 young patients (age range 4 days to 24 years, mean 16.6 years) who had ventricular tachycardia and/or ventricular fibrillation and were followed for 4--70 months (mean 22.4 months). Patients had a variety of problems associated with their arrhythmia, including mitral valve prolapse, cardiomyopathy, myocarditis, prolonged QT syndrome and hypokalemia. Six patients had no clinically recognizable cardiac abnormality. The ventricular tachycardia showed a left bundle branch block contour in 10 of 17 patients, right bundle branch block in four, was multiform in two and had an indeterminate contour in one. Sustained ventricular tachycardia was initiated and terminated reproducibly by atrial and ventricular stimulation in three of seven patients who did not have spontaneous episodes of ventricular tachycardia during the electrophysiologic study. In one other patient, short bursts of ventricular tachycardia were induced. Patients who had ventricular fibrillation, those who died, and those who are still symptomatic with poorly controlled ventricular arrhythmias had significant heart disease. In one patient, a ventricular tachyarrhythmia that had required more than 100 electrical cardioversions spontaneously disappeared after requiring 1 year of antiarrhythmic therapy.

Electrophysiological studies in patients with chronic recurrent ventricular tachycardia.

Seventeen consecutive patients with chronic recurrent ventricular tachycardia (VT) were studied in an attempt to delineate the reproducibility and mechanism of this arrhythmia. Six patients had nonsustained and 11 had sustained VT. The following electrophysiological techniques were utilized in an attempt to reproduce VT: 1) rapid atrial and ventricular pacing (17 pts); 2) atrial extrastimulus technique (17 pts); 3) ventricular extrastimulus technique (17 pts); 4) V1V2V3 stimulation technique (5 pts); 5) ventricular pacing from two or more sites (5 pts). Ventricular tachycardia was induced in six of 11 (54%) patients with sustained VT. However, in four there was only a single induction and only in the remaining two patients could VT be repetitively induced. In the latter two patients ventricular tachycardia was induced with both atrial and ventricular stimulation. Ventricular tachycardia could not be induced in any patient with nonsustained VT, although three had spontaneous episodes of ventricular tachycardia during study. In conclusion, in the present series of patients with chronic recurrent VT, this rhythm could not be reproducibly induced in the majority of patients in the cardiac catheterization laboratory utilizing catheter stimulation techniques.