Nonsustained Polymorphic Ventricular Tachycardia Research Articles

Pulmonary Valve Replacement in Adult Patients With a Severely Dilated Right Ventricle and Refractory Arrhythmias After Repair of Tetralogy of Fallot

Refractory arrhythmias caused by right ventricular (RV) volume overload resulting from pulmonary regurgitation are the main concern in adult patients after repair of tetralogy of Fallot (TOF). Early pulmonary valve replacement (PVR) may prevent irreversible RV dysfunction and refractory arrhythmias, so the present study evaluated the PVR outcomes in adult patients with a severely dilated RV (d-RV) and refractory arrhythmias after TOF repair. Three TOF patients with a d-RV and tachyarrhythmias underwent PVR between the ages of 28 and 38 years. All had a d-RV (RV end-diastolic volume index (RVEDVI) >200 ml/m(2)) with a polymorphic nonsustained ventricular tachycardia (NSVT). Atrial tachycardia (AT) was identified in 2 patients and they underwent radiofrequency catheter ablation. The arrhythmias in all 3 were refractory to antiarrhythmic drugs. One year after PVR, the RVEDVI, left ventricular ejection fraction, right atrial pressure, cardiac index, cardiothoracic ratio, brain natriuretic peptide levels, and peak VO(2) improved in all, but without normalization. During the 2.6-3.8 year follow-up, all experienced tachyarrhythmias (NSVT or AT), which were controlled with medication. PVR may be beneficial for refractory arrhythmias, even in TOF patients with a d-RV, but it is difficult to completely normalize the hemodynamics and resolve the arrhythmogenicity.

Ibutilide Therapy for Atrial Fibrillation

Many institutions restrict the use of ibutilide because of the potential risk of polymorphic ventricular tachycardia (PMVT). Over a 5-year period from June 2000 to May 2005, 238 patients, 151 men and 87 women, with a mean age of 67.1 years (range, 22-94 years), received intravenous ibutilide at our institution. Ibutilide was administered by nurses or physicians in 4 clinical settings: emergency department (n = 80), intensive care unit (n = 11), patient room on telemetry (n = 107), and in the cardiac catheterization/electrophysiology laboratory (n = 40). Conversion to sinus rhythm occurred in 59% of patients outside the catheterization/electrophysiology laboratory. The incidence of PMVT was 1.7%. Three patients had brief nonsustained PMVT and 1 patient had a sustained PMVT. There was no difference in outcome whether a physician was present at the time of ibutilide administration. Our data suggest that ibutilide is a safe and efficacious drug when ordered by experienced physicians in properly selected patients in a variety of monitored settings.

Challenges of Diagnosis of Long‐QT Syndrome in Children

We describe the clinical and genetic characteristics of the family, in which the diagnosis of LQT1 had been made. The electrocardiogram (ECG) characteristics of this patient indicated the likelihood of LQTS1. Polymorphic ventricular extrasystolies and episodes of polymorphic non-sustained ventricular tachycardia were confirmed by Holter ECG monitoring. On the exertional electrocardiogram polymorphic ventricular tachycardia (torsade de pointes) was recorded. Direct sequencing of both DNA strands revealed the absence of mutations or polymorphisms in the KCNQ1, HERG, and SCN5A genes.

Preventing Torsades de Pointes by Careful Cardiac Monitoring in Hospital Settings

In the electrocardiogram, the QT interval represents the time it takes the ventricular myocardium to repolarize. Prolongation of the QT interval indicates congenital or acquired abnormality of cardiac membrane channels. In the critical care setting, acquired long QT interval most commonly results from administration of common pharmacologic agents, including some antiarrhythmics and antibiotics. Patients with prolonged QT interval may be at risk for developing torsades de pointes and cardiac arrest. Furthermore, new-onset bradyarrhythmias and electrolyte disorders may increase this risk. Warning signs of impending sustained torsades de pointes include occurrence of polymorphic ventricular ectopic complexes, T-wave alternans, and nonsustained polymorphic ventricular tachycardia. Measurement and documentation of the QT interval, corrected for heart rate (QTc), is an important component of cardiac monitoring in the critical care setting. When prolonged QTc occurs in patients at risk, specific clinical interventions must be implemented to prevent the occurrence of torsades de pointes.

Development of torsade de pointes caused by exacerbation of QT prolongation during clipping of cerebral artery aneurysm in a patient with subarachnoid haemorrhage

We report the case of a 79-yr-old woman with subarachnoid haemorrhage (SAH) in whom torsade de pointes (TdP) caused by worsening the QT prolongation occurred during clipping of cerebral artery aneurysm. This patient shows a potential risk of occurrence of life-threatening tachyarrhythmia, TdP by prolonging the QT interval during surgery in patients with SAH even with no additional factors that predispose to TdP. Therefore, a proper monitoring of the QT interval is necessary as a predictor of TdP. When ventricular tachyarrhythmia occurs, recognition of TdP is important because antiarrhythmic drug therapy for TdP is different from that for ventricular tachyarrhythmias that is not TdP.

Malignant Entity of Idiopathic Ventricular Fibrillation and Polymorphic Ventricular Tachycardia Initiated by Premature Extrasystoles Originating From the Right Ventricular Outflow Tract

The aim of this study was to assess the clinical characteristics and the efficacy of radiofrequency catheter ablation (RFCA) for idiopathic ventricular fibrillation (VF) and/or polymorphic ventricular tachycardia initiated by ventricular extrasystoles originating from the right ventricular outflow tract (RVOT). Ventricular fibrillation and/or polymorphic ventricular tachycardia are occasionally initiated by ventricular extrasystoles originating from the RVOT in patients without structural heart disease. Among 101 patients without structural heart disease in whom RFCA was conducted for idiopathic ventricular tachyarrhythmias arising from the RVOT, we examined the clinical characteristics and the efficacy of RFCA in 16 patients with spontaneous VF and/or polymorphic ventricular tachycardia initiated by the ventricular extrasystoles originating from the RVOT. Among 16 patients, spontaneous episodes of VF were documented in 5 patients, and 11 patients had prior episodes of syncope. Holter recordings showed frequent isolated ventricular extrasystoles with the same morphology as that of initiating ventricular extrasystoles, and non-sustained polymorphic ventricular tachycardia with short cycle length (mean of 245 +/- 28 ms) in all 16 patients. Radiofrequency catheter ablation by targeting the initiating ventricular extrasystoles eliminated episodes of syncope, VF, and cardiac arrest in all patients during follow-up periods of 54 +/- 39 months. Our data suggest that the malignant entity of idiopathic VF and/or polymorphic ventricular tachycardia was occasionally present in patients with idiopathic ventricular arrhythmias arising from the RVOT. Radiofrequency catheter ablation was effective as a treatment option for this entity.

Ventricular arrhythmias triggered by alerting stimuli in conscious rabbits pre-treated with dofetilide.

We tested whether normally benign alerting/arousing stimuli provoke cardiac arrhythmias in conscious rabbits with electrically unstable myocardium. Alerting stimuli (loud sound, tapping and moving the cage, pinprick, inhalation of formaldehyde vapour) were presented before and after administration of dofetilide to conscious unrestrained rabbits (New Zealand White). Dofetilide (0.28-3.0 mg/kg i. v.) caused prolongation of QT interval (from 131 +/- 9 to 217 +/- 11 ms; p < 0.01, n = 6) and Tpeak-Tend interval (from 34 +/- 5 to 81 +/- 9 ms; p < 0.01, n = 6), altered ventricular conductance, and caused appearance of spontaneous ventricular ectopic beats. Alerting stimuli elicited ventricular ectopic beats in 18/30 trials in all dofetilide-treated animals, with a short latency (3.1 +/- 0.4 s). Formaldehyde vapour, in addition, elicited profound bradycardia, and precipitated non-sustained polymorphic ventricular tachycardia (torsades de points) lasting 0.6-8.5 s in 5/6 animals. These arrhythmias occurred also with a short latency (mean 8.7 +/- 1.6 s). Betaadrenergic blockade with propranolol (1.5 mg/kg i. v.) abolished spontaneous ventricular ectopy, suppressed torsades de points precipitated by formaldehyde, and significantly (p < 0.05) reduced the number of ventricular ectopic beats triggered by alerting stimuli. In predisposed hearts, alerting stimuli precipitate arrhythmias by producing transient increases in sympathetic discharge in the ventricular myocardium. Vagally induced bradycardia with concurrent ventricular beta-adrenoreceptor activation may underlie development of torsades de points in patients with long QT syndrome precipitated by swimming, diving or facial immersion.

Evidence that nonsustained polymorphic ventricular tachycardia causes syncope (data from implantable cardioverter defibrillators)

Patients with syncope account for ≅6% of hospital admissions and 3% of emergency room visits. 1 Kapoor W.N. Evaluation and management of syncope. JAMA. 1992; 268: 2553-2560 Crossref PubMed Scopus (245) Google Scholar Whether and how often nonsustained ventricular fibrillation (VF) or nonsustained polymorphic ventricular tachycardia (NSPMVT) can cause syncope is not entirely clear. In patients with the long QT syndrome, nonsustained Torsades de Pointes causing syncope is well described. Other reports, generally in patients with normal hearts, have occasionally described the association of NSPMVT and syncope. 2 Viskin S. Belhassen B. Idiopathic ventricular fibrillation. Am Heart J. 1990; 120: 661-671 Abstract Full Text PDF PubMed Scopus (188) Google Scholar , 3 Schwartz S.P. Studies on transient ventricular fibrillation. IV. Observations on clinical and graphic manifestations following revival of the heart from transient ventricular fibrillation. Am J Med Sci. 1936; 192: 808-815 Crossref Google Scholar , 4 Dubner S.J. Gimeno G.M. Elencwajg B. Leguizamon J. Tronge J.E. Quintero R. Ventricular fibrillation with spontaneous reversion on ambulatory electrocardiogram in the absence of heart disease. Am Heart J. 1983; 105: 691-693 Abstract Full Text PDF PubMed Scopus (33) Google Scholar , 5 Patt M.V. Podrid P.J. Friedman P.L. Lown B. Spontaneous reversion of ventricular fibrillation. Am Heart J. 1988; 115: 919-921 Abstract Full Text PDF PubMed Scopus (23) Google Scholar , 6 Masrani K. Cowley C. Bekheit S. El-Sherif N. Recurrent syncope for over a decade due to idiopathic ventricular fibrillation. Chest. 1994; 106: 1601-1603 Crossref PubMed Scopus (15) Google Scholar However, it is generally believed that VF is a sustained tachyarrhythmia that results in death 7 Olshansky B. Syncope overview and approach to management. in: Olshansky B. Syncope Mechanisms and Management. Futura Publishing Co, Inc, Armonk, NY1998: 15-71 Google Scholar and that NSPMVT is unusual as a cause of syncope. The current generation of implantable cardioverter defibrillators (ICDs) with intracardiac electrogram storage offer an opportunity to evaluate the incidence of NSPMVT relative to sustained VF and to document the association of syncope and presyncopal symptoms with these arrhythmias.

Altered response to ibutilide in a heart failure model.

Despite the frequent use of anti-arrhythmic drugs in the general population, the electrophysiologic effects of these agents have not been elucidated in congestive heart failure (CHF). To examine the impact of left ventricular dysfunction on actions of type III anti-arrhythmic drugs, we evaluated the actions of ibutilide in a canine model of pacing-induced dilated cardiomyopathy. Following ablation of the atrioventricular node, effects on action potential duration at 90% (APD(90)) were compared in vivo, between eight CHF animals and seven controls. Monophasic action potential recordings were obtained from right and left ventricular endocardium/epicardium during and after three doses of ibutilide (0. 01, 0.02 and 0.05 mg/kg), at pacing cycle lengths of 300-1000 ms. APD(90) prolongation with ibutilide (0.01 mg/kg) was significantly greater in CHF vs. controls (P=0.0026, ANOVA). However, plasma ibutilide levels at this dose, were not significantly different between the two groups. In CHF, maximal effects were observed at the lowest dose, whereas effects were gradual and dose-dependent in controls. With ibutilide administration (0.01 mg/kg), an increased dispersion of left-right ventricular APD(90) was observed in CHF, but not in controls (P=0.03). A trend was observed, for increased incidence of non-sustained polymorphic ventricular tachycardia in CHF. In the presence of CHF, the actions of ibutilide are altered significantly. These findings may reflect altered tissue effects, as a consequence of myocardial electrical remodeling in CHF.

49-Year-Old Woman With Chest Pain

49-Year-Old Woman With Chest Pain

Conversion efficacy and safety of repeated doses of ibutilide in patients with atrial flutter and atrial fibrillation

Background A study was conducted to determine the efficacy and safety of ibutilide fumarate versus placebo in the acute termination of atrial flutter and fibrillation. Methods and Results Two hundred sixty-two patients aged 28 to 88 years with atrial flutter or fibrillation duration of 3 hours to 90 days were randomly assigned in a 5:1 ratio (ibutilide:placebo) to receive two 10-minute infusions, 10 minutes apart, of ibutilide (1 mg) or placebo. Patients were hospitalized and monitored by telemetry for 24 hours, with follow-up 72 hours later. Seventy-three (34.9%) of 209 evaluable ibutilide recipients had termination of atrial flutter or fibrillation within 1.5 hours compared with 0 (0%) of 41 placebo recipients. Those with atrial flutter had a higher success rate. At hour 24, 86.3% remained in normal or alternative sinus rhythm. Of the patients who received ibutilide, 2.3% experienced drug-related sustained polymorphic or monomorphic ventricular tachycardia and recovered after intervention. Additionally, 7.3% experienced nonsustained polymorphic or monomorphic ventricular tachycardia. Other frequent medical events in ibutilide recipients were generally also noted in the placebo group. Conclusions Ibutilide is effective and safe for acute termination of atrial fibrillation or atrial flutter. (Am Heart J 1998;136:632-42.)

Torsade de Pointes During Orthotopic Liver Transplantation

Torsade de Pointes During Orthotopic Liver Transplantation

Elucidating the mechanism of cesium-induced sustained monomorphic ventricular tachycardia in rabbits.

The mechanisms of sustained ventricular tachycardia (VT) induced by large cumulative dose of cesium chloride (Cs) remains unclear. Seven anesthetized rabbits were intravenously injected with Cs (1 mmol/kg) 3 times at 20-min intervals. The surface ECG and monophasic action potential of the left ventricular endocardium were simultaneously recorded. In another 12 rabbits, transmembrane action potentials of right ventricular muscles were recorded with glass microelectrodes. In experiments in vivo, sustained monomorphic VT was induced after the third injection of Cs, whereas the early afterdepolarization (EAD)-related nonsustained polymorphic VT was induced after the second injection. Overdrive pacing during the sustained VT resulted in postdrive acceleration. The pacing and recovery cycle lengths showed an inverse relation. In experiments in vitro, preparations were superfused with Tyrode's solution containing 7.5 mM Cs. Cs initially induced EADs. Additional exposure to Cs depolarized the membrane potential, which consequently attained threshold, producing spontaneous activities. Further exposure resulted in an induction of sustained rhythms that were accelerated by overdrive pacing. Our results indicate that the sustained rhythms at low membrane potential induced by a long exposure to Cs in vitro may underlie an electrophysiologic mechanism for the sustained VT induced after large cumulative dose of Cs in vivo.

Ibutilide. A review of its pharmacological properties and clinical potential in the acute management of atrial flutter and fibrillation.

Ibutilide is the first 'pure' class III antiarrhythmic drug to become available. Its predominant action is prolongation of the myocardial action potential duration. This appears to be achieved by a unique ionic mechanism of action that involves activation of a late inward sodium current and possibly blockade of the rapidly activating component of the cardiac delayed rectifier potassium current. Intravenous ibutilide 0.01 to 0.025 mg/kg or 1 to 2 mg successfully converted atrial flutter or fibrillation to sinus rhythm in 33 to 49% of patients in 2 placebo-controlled trials involving 439 patients with sustained arrhythmia. In a third trial in 300 patients who developed atrial flutter or fibrillation after cardiac surgery, ibutilide 2 mg successfully converted the arrhythmia in 57% of patients. The mean times to conversion were < or = 30 minutes in these trials. In 3 comparative trials, ibutilide was significantly more effective than racemic sotalol or procainamide in terminating atrial flutter or fibrillation. The pretreatment duration of the arrhythmia is an important predictor of the success of ibutilide treatment; the greatest conversion rates are achieved when the arrhythmia is of recent onset (i.e. < or = 30 days' duration). Ibutilide is more effective in terminating atrial flutter than atrial fibrillation. Adverse events associated with ibutilide are predominantly cardiovascular. Sustained polymorphic ventricular tachycardia developed in 1.7%, and non-sustained polymorphic ventricular tachycardia in 2.7%, of 586 patients treated with ibutilide in clinical trials. However, no proarrhythmia-related deaths have been reported with the use of ibutilide. The drug has minimal haemodynamic effects and is associated with few noncardiovascular adverse events. Thus, ibutilide is a useful agent for the pharmacological cardioversion of recent-onset atrial fibrillation or flutter, provided that adequate steps are taken to monitor for proarrhythmic events. The drug causes few noncardiovascular adverse events and has minimal haemodynamic effects. Furthermore, it appears to be more effective than procainamide (especially in patients with atrial flutter) and racemic sotalol.

Discrepant drug action of disopyramide on ECG abnormalities and induction of ventricular arrhythmias in a patient with Brugada syndrome

An electrophysiologic study was attempted in a patient who experienced cardiac arrest. Programmed electrical stimulation from the right ventricle, without the use of any drugs, induced ventricular fibrillation (VF) twice. Disopyramide prevented the induction of ventricular arrhythmia by rendering VF to a nonsustained polymorphic ventricular tachycardia when administered at 300 mg/day, and noninducible at 400 mg/day. However, ST-segment elevation and the rSr′ pattern in leads V 1–3 characteristic of Brugada syndrome became exaggerated by disopyramide. Disopyramide exerted discrepant action on the electrocardiographic (ECG) abnormalities and induction of VF in this patient, suggesting the efficacy of antiarrhythmic drugs assessed by an electrophysiologic study may be unrelated to ECG abnormalities in cases of Brugada syndrome.

Efficacy of intravenous ibutilide for rapid termination of atrial fibrillation and atrial flutter: A dose-response study

Objectives. Currently available antiarrhythmic drugs have limited efficacy for short-term, rapid termination of atrial fibrillation and atrial flutter.Background. Ibutilide fumarate is an investigational class III antiarrhythmic agent that prolongs repolarization by increasing the slow inward sodium current and by blocking the delayed rectifier current. It can be administered intravenously and has a rapid onset of electrophysiologic effects.Methods. The efficacy and safety of ibutilide were studied in 200 patients with atrial flutter >3 b in duration or atrial fibrillation 3 h to 90 days in duration. Patients were randomized to receive a single intravenous dose of placebo or an infusion of ibutilide fumarate at 0.005, 0.010, 0.015, or 0.025 mg/kg body weight over 10 min. Conversion was defined as termination of the atrial arrhythmia during or within 60 min after infusion. Forty-one patients received placebo and 159 received ibutilide (0.005 mg/kg [n = 41], 0.010 mg/kg [n = 40], 0.015 mg/kg [n = 38] or 0.025 mg/kg [n = 40]).Results. The arrhythmia terminated in 34% of drug-treated patients. The rates of successful arrhythmia termination were 3% for placebo and 12%, 33%, 45% and 46%, respectively, for 0.005-, 0.010-, 0.015- and 0.025-mg/kg ibutilide. The placebo and 0.005-mg/kg ibutilide groups had lower success rates than all other dose groups (p < 0.05). The mean time to termination of the arrhythmia was 19 min (range 3 to 70) from the start of infusion. Successful arrhythmia termination was not affected by enlarged left atrial diameter, decreased ejection fractions, presence of valvular heart disease or the use of concomitan medications (beta-adrenergic blocking agents, calcium channel blocking agents or digoxin). Arrhythmia termination was not predicted by the magnitude of corrected QT interval prolongation but was associated with a shorter duration of atrial arrhythmia. The most frequent adverse events in ibutilide-treated patients were sustained and nonsustained polymorphic ventricular tachycardia (3.6%). All patients with sustained polymorphic ventricular tachycardia were successfully treated with direct current cardioversion and had no recurrence. The occurrence of proarrhythmia did not correlate with ibutilide plasma concentration.Conclusions. These data demonstrate that ibutilide is able to rapidly terminate atrial fibrillation and atrial flutter.

Hypomagnesemia: Characterization of a model of sudden cardiac death

Objectives. We sought to compare the incidence of sudden death in rats treated with magnesium-deficient and control diets and to address the electrophysiologic characteristics associated with these end points.Background. Although magnesium deficiency is associated with an increased incidence of sudden cardiac death in patients, there has been no clear cause and effect relation because of a number of covariables, including diuretic use, hypokalemia, digitalis use and left ventricular dysfunction.Methods. Hypomagnesemic rats and their paired control rats underwent in vivo electrophysiologic studies and measurements of the total calcium and magnesium content of their cardiac ventricles.Results. Serum magnesium levels were 0.5 ± 0.3 mEq/liter (mean ± SD) in hypomagnesemic animals and 1.2 ± 0.9 mEq/liter in control animals. A modest but significant prolongation of the repolarization time was seen at the apical epicardial site (83 ± 8 ms in hypomagnesemic rats vs. 68 ± 13 ms in control rats, p < 0.05), but not at the other sites studied. Bradyarrhythmias and tachyrrhytmias were observed in 82% of the hypomagnesemic rats during the in vivo electrophysiologic studies, compared with 0% in the control group. During these studies, sudden, unexpected asystolic deaths were observed in 4 of 11 hypomagnesemic rats and 0 of 8 control rats. Polymorphic nonsustained ventricular tachycardia was provoked by rapid pacing in 5 of 11 hypomagnesemic rats and 0 of 8 control rats. Three of six hypomagnesemic rats exposed to auditory stimuli developed seizures, followed immediately by sudden deaths—two due to asystole and one due to ventricular fibrillation—although no end points occurred in the control animals.Conclusions. In this model, magnesium deficiency results in sudden cardiac death. The presence of startle induction of sudden death preceded by seizures suggests that sudden cardiac death results from a neurologic trigger.

Evaluation and treatment of nonsustained ventricular tachycardia.

The clinical significance of nonsustained ventricular tachycardia continues to undergo reevaluation as clinicians attempt to optimize screening strategies for identifying high-risk patients and to evaluate the efficacy of therapeutic interventions. The utility of ambulatory monitoring and programmed stimulation as screening tools in the patient who has suffered an infarction remains unsettled; ongoing clinical trials may help resolve these issues. New data suggest that the survival benefit associated with angiotensin-converting enzyme inhibition is unrelated to effects on spontaneous arrhythmias, similar to results previously reported for beta-blockers. Randomized clinical trials of prophylactic amiodarone in patients with congestive heart failure and nonsustained ventricular tachycardia have produced conflicting results. A strong relationship between polymorphic nonsustained ventricular tachycardia and sudden death in patients without structural heart disease or QT prolongation has been reported. The significance of nonsustained ventricular tachycardia in dilated cardiomyopathy and hypertrophic cardiomyopathy has also been reassessed.

960-90 Ventricular Fibrillation Induction Efficacy of Low Energy T-Wave Synchronized Shocks in Patients with Nonthoracotomy ICDs

Incremental ventricular pacing or alternating current have been traditionally used to induce ventricular fibrillation (VF) while testing defibrillating function of the ICD. The available data are limited on ventricular fibrillation induction efficacy of the low energy T-wave shocks. To determine this, we analyzed data in 14 patients with Medtronic ICDs (7219C 9 pts, 7219D 2 pts, PCD 3 pts) who had undergone a total of 110 VF induction attempts either at time of ICD implant or during follow-up noninvasive EPS. The underlying heart disease was coronary in all patients with prior myocardial infarction in 10 patients. The LV ejection fraction was 30 ± 12% (range 15–64%). QT interval 440 ± 57 ms (range 360–560 ms) and QTc interval 449 ± 49 ms (range 336–520 ms) The low energy synchronized shocks (0.2–2 J) were delivered to the T wave of last of the 8 beat paced train at 400 ms with S l -T delays ranging between 290–340 ms. Of 110 attempts with T wave shocks, the inducible arrhythmia was VF in 69%. nonsustained polymorphic ventricular tachycardia (VT) in 15%, monomorphic VT in 2% and none in 14%. The VF induction efficacy was 75% (69 of 92 attempts) for T-wave shock energy of &gt;0.6 J compared with 50% (9 of 18 attempts) for T-wave shock energy of ≤ 0.6 J (P &lt; 0.05). In contrast, the VF induction efficacy was unaffected by S 1 -T delays ranging from 290–330 ms. It was 80% 14/5) at S 1 -T delay of 290 ms, 80% (4/5) at S 1 -T delay of 300 ms, 70% (44/66) at S 1 -T delay of 310 ms, 78% (7/9) at S 1 -Tdelay of 320 ms, 74% (17/23) at S 1 -T delay of 330 ms and 0% (0/2) at S 1 -T delay of 340 ms. In no patients incremental ventricular pacing or alternating current had to be used to induce VF. We conclude that a low energy (1–2 J) shock, when synchronized to the paced-T wave withS 1 -T delays of 290–330 ms, induces VF in over 70–80% of the attempts. This precludes the need for prolonged ventricular bursts or the use of alternating current and should, thus, be the preferred modality of choice while inducing VF to check ICD function.

The value of electrophysiologic testing in patients resuscitated from documented ventricular fibrillation.

Electrophysiologic testing is performed in patients resuscitated from ventricular fibrillation (VF) on the assumption that sustained monomorphic ventricular tachycardia (VT) may be a precursor to VF, with the former amenable to assessment by serial drug testing. We assessed the usefulness of this strategy by analyzing clinical and electrophysiologic data of 42 survivors (29 men and 13 women; mean age 54 +/- 14 years) of VF without a reversible cause. All patients had VF documented on ECG and required defibrillation. Underlying heart diseases included coronary disease in 28, dilated cardiomyopathy in 3, arrhythmogenic right ventricular dysplasia in 1, and no apparent structural heart disease in 10 patients. Only 2 (4.7%) patients had a prior history of documented VT. The electrophysiologic study was performed 7 to 30 days after VF. Programmed stimulation at the right ventricular apex using at least two drive cycle lengths and up to three extrastimuli induced sustained monomorphic VT in 4 (9.5%), sustained polymorphic VT in 3 (7.1%), nonsustained monomorphic VT in 1 (2.3%), nonsustained polymorphic VT in 5 (11.9%), and VF in 13 (30.9%) patients. Two patients with documented prior VT and coronary disease had sustained VT induced during the electrophysiologic study. On the other hand, sustained monomorphic VT was induced in 53 of the 59 (90%) patients (45 men and 14 women; mean age 57 +/- 16 years) with clinically documented VT concurrently studied using the same stimulation protocol. We conclude that reproducible induction of sustained monomorphic VT in survivors of documented VF is uncommon. It may be more cost effective to proceed directly to treatment with implantable cardioverter defibrillators in these patients.