Incidence of nonsustained and sustained ventricular tachyarrhythmias in patients with an implantable cardioverter defibrillator

INTRODUCTION: Nonsustained ventricular tachycardia (NSVT) is a frequent phenomenon in some patients with heart disease, but its association with sustained ventricular tachycardias (ventricular tachycardia [VT]/ventricular fibrillation [VF]) is still not clear. The aim of this study was to determine whether NSVT incidence was associated with sustained VT/VF in patients with an implantable cardioverter defibrillator (ICD). METHODS AND RESULTS: Retrospective data analysis was conducted in 923 ICD patients with a mean follow-up of 4 months. NSVT and sustained VT/VF were defined as device-detected tachycardias. The incidence rates of NSVT and sustained VT/VF as well as ICD therapies were determined as episodes per patient. The NSVT index was defined as the product of NSVT episodes/day times the mean number of beats per episode, i.e., total beats/day. The NSVT index peak was defined as the highest value on or prior to the day with sustained VT/VF episodes. Patients (n = 393) with NSVT experienced a higher incidence of sustained VT/VF (17.2 +/- 63.0 episodes/patient) and ICD therapies (15.2 +/- 61.4 episodes/patient) than patients (n = 530) without NSVT (sustained VT/VF: 0.5 +/- 6.6 and therapies: 0.5 +/- 5.6; P < 0.0001). Approximately 74% of NSVT index peaks occurred on the same day or <3 days prior to sustained VT/VF episodes. The index was higher for peaks < or =3 days prior to the day with sustained VT/VF (94.3 +/- 140.1 total beats/day) than for peaks >3 days prior to the day with sustained VT/VF (32.7 +/- 55.9 total beats/day; P < 0.0001). CONCLUSION: ICD patients with NSVT represent a population more likely to experience sustained VT/VF episodes with a temporal association between an NSVT surge and sustained VT/VF occurrence.     

Efficacy and tolerance of intravenous flecainide in patients with chronic high frequency ventricular arrhythmias

The effectiveness and safety of intravenous flecainide was evaluatedin 33 patients with chronic high frequency premature ventricularcomplexes (mean value of PVCs 23.7 min^–1). Flecainidewas injected intravenously at a rate of 20 mg per 2 min untilcomplete disappearance of ventricular arrhythmias or up to atotal dose not exceeding 200 mg. Total suppression of PVCs occurredin 31 out of 33 patients at the end of the injection (mean dose132 mg). The overall reduction of PVCs was 94 per cent (P>0.001)at the end of infusion and 74 per cent (P>0.001) 1 h later.The mean plasma drug level attained 1 h after administrationwas 287 ng ml^–1 (range 82–984). Heart rate and bloodpressure did not change, but a significant increase (P>0.001)in PR (+12%), QRS (+13%) and QTc (+4%) duration occurred afterdrug administration. Flecainide was well tolerated. An idioventriculartachycardia was induced in one patient and two patients experiencedside effects of the central nervous type: dizziness, blurringof vision and a sensation of warmth. In view of its activityflecainide appears to be a valuable addition to the antiarrhythmicarmamentarium.     

Efficacy of phenytoin in suppressing inducible ventricular tachyarrhythmias

Summary We examined the efficacy of phenytoin in 69 of 87 consecutive patients undergoing serial electrophysiologic studies for inducible sustained ventricular tachycardia or fibrillation (VT/VF). In general, during the initial session lidocaine and procainamide were tested immediately after baseline electrophysiologic evaluation, followed by phenytoin and quinidine during the next two sessions, and then by additional drugs as needed. Once a successful drug was identified, all testing was stopped. Drugs that had failed in prior empiric trials were not tested. Twenty-five of the 87 patients (28.7%) had success in 258 serial drug tests. Sixty-nine patients were tested on phenytoin (mean serum level 13.4 ± 5.0 mg/L), 52 after oral loading, and 17 after intravenous loading; the remaining 18 had either had prior successful testing with other drugs (9 patients) or had prior empiric failures with phenytoin (9 patients). Nine of the 69 phenytoin trials were successful (13.0%), compared to 8 of 57 trials (14.0%) with procainamide, 4 of 37 trials (10.8%) with quinidine, and 0 of 41 trials (0%) with lidocaine. All nine patients who had successful phenytoin trials tolerated chronic doses adequate to maintain serum phenytoin levels equivalent to those measured during successful drug testing.For the 25 patients with successful drug trials, the mean follow-up was 14.5 ± 9.8 months, and the actuarial incidence or recurrent VT/VF was 7 ± 5% at 12 months. For the nine patients who had success with phenytoin the mean follow-up was 18.4 ± 11.7 months, and the 12-month actuarial recurrence was 0%. Phenytoin is a well tolerated drug whose efficacy appears similar to most standard antiarrhythmic agents. If our results are confirmed in a larger, randomized study, routine testing with phenytoin should be considered.     

Obesity as a risk factor for sustained ventricular tachyarrhythmias in MADIT II patients

Background: Obesity, as defined by body mass index ≥30 kg/m², has been shown to be a risk factor for cardiovascular disease. However, data on the relationship between body mass index (BMI) and the risk of ventricular arrhythmias and sudden cardiac death are limited. The aim of this study was to evaluate the risk of ventricular tachyarrhythmias and sudden death by BMI in patients after myocardial infarction with severe left ventricular dysfunction.
Methods : The risk of appropriate defibrillator therapy for ventricular tachycardia or ventricular fibrillation (VT/VF) by BMI status was analyzed in 476 nondiabetic patients with left ventricular dysfunction who received an implantable cardioverter defibrillator (ICD) in the Multicenter Automatic Defibrillator Implantation Trial-II (MADIT II).
Results : Mean BMI was 27 ± 5 kg/m². Obese patients comprised 25% of the study population. After 2 years of follow-up, the cumulative rates of appropriate ICD therapy for VT/VF were 39% in obese and 24% in nonobese patients, respectively (P = 0.014). In multivariate analysis, there was a significant 64% increase in the risk for appropriate ICD therapy among obese patients as compared with nonobese patients, which was attributed mainly to an 86% increase in the risk of appropriate ICD shocks (P = 0.006). Consistent with these results, the risk of the combined endpoint of appropriate VT/VF therapy or sudden cardiac death (SCD) was also significantly increased among obese patients (Hazard Ratio 1.59; P = 0.01).
Conclusions : Our findings suggest that in nondiabetic patients with ischemic left ventricular dysfunction, a BMI ≥30 kg/m² is an independent risk factor for ventricular tachyarrhythmias.     

Effect of flecainide on left ventricular ejection fraction

Antiarrhythmic agents may depress cardiac contractility andworsen heart failure. Flecainide is an effective antiarrhythmicdrug, but when administered orally in patients with left ventricular(LV) dysfunction, its effect on LV function is unknown. To assessthe effects of flecainide on cardiac function, LV ejection fraction(LVEF) was measured by radionuclide ventriculography in 36 patientswith LV dysfunction (LVEF 40%), prior to and 7 days after drugtherapy was initiated. To analyse the possibility of a dose-dependenteffect on LVEF, 18 patients received 200 mg day^–1 of flecainideand 18 patients with an identical initial LVEF (27±8vs 27±9) (NS) received 300 mg day^–1. The studywas stopped in 7 patients because of severe cardiac adverseeffects; in these patients the LVEF was significantly lower(15±7) than that of the 29 patients who completed theprotocol (27±8) (P<0.01). In patients who completedthe protocol, there was no significant change in LVEF eitherwith a daily dosage of flecainide of 200 mg day^–1 (27±8vs 27±8) or with 300 mg day^–1 (27±9 vs 28±13).Thus, in the patients with LV dysfunction studied, oral flecainidedid not significantly affect LV function either with a low orwith the ususal daily dosage. However in patients with severeimpairment of LV function (LVEF<30%) flecainide must be usedcarefully owing to a higher incidence of adverse effects oncardiac rhythm.     

Myocardial ischemia and induction of sustained ventricular tachyarrhythmias: evaluation using dobutamine stress echocardiography-electrophysiologic testing

INTRODUCTION: This study examined the relationship between dobutamine facilitation of ventricular tachyarrhythmia (VT) inducibility with programmed electrical stimulation (PES) and dobutamine stress-induced myocardial ischemia. METHODS AND RESULTS: Twenty patients with prior myocardial infarction and cardiac arrest or sustained VT but no sustained VT induced at baseline electrophysiologic testing underwent repeat PES during dobutamine infusion. Ischemia (new or worsened wall-motion abnormality) was documented by echocardiography performed in conjunction with PES. Eight patients were receiving Class I or III antiarrhythmic drugs and seven beta-blockers. Dobutamine facilitated induction of sustained VT in 16 patients (80%) and provoked ischemia in 13 patients (65%). Induction of VT was associated with ischemia in 9 patients (56%). VTs associated with ischemia were induced at higher dobutamine doses (26 +/- 11 vs 11 +/- 10 microg/kg per min, P = 0.02) than were VTs without ischemia (n = 7). Among 13 patients with provoked ischemia, 9 (69%) had VTs induced and 4 remained noninducible. The onset of ischemia occurred at the same dose as induction of VT in 5 patients and at a lower dose in 4 patients. Monomorphic VT (318 +/- 59 ms) was induced in 13 patients, of whom 8 (62%) had ischemia. The ECG morphology of VT suggested an origin in a myocardial segment that demonstrated initial viability at low doses then ischemic dysfunction at higher doses preceding VT induction in 7 (88%) of 8 patients. CONCLUSION: Dobutamine enhances inducibility of sustained VTs during PES. The temporal and anatomic association of dobutamine-induced ischemia and VT suggests that at high dobutamine doses, ischemia may contribute to ventricular arrhythmia inducibility in some patients.     

Comparison of the long-term efficacy of implantable defibrillators and sotalol for documented spontaneous sustained ventricular tachyarrhythmias secondary to coronary artery disease

Background: The relative efficacy of antitachycardia pacing implantable cardioverter defibrillators (ATPICD) and sotalol in the treatment of ventricular tachyarrhythmias is controversial. Aim: To compare the mortality in patients treated with ATPICD and sotalol for documented spontaneous sustained ventricular tachyarrhythmias occurring late after previous myocardial infarction. Methods: In this non-randomised retrospective study of 139 consecutive patients all patients had inducible ventricular tachycardia at baseline electrophysiological studies. Before the availability of ATPICD, 22 patients were treated with sotalol as part of a randomised study comparing the efficacy of sotalol to amiodarone. After ATPICD became available sotalol was used in 49 patients in whom intravenous testing predicted sotalol to be effective and ATPICD were implanted in 68 patients in whom sotalol was predicted to be ineffective at electrophysiological testing. Thus, 68 patients were treated with an ATPICD and 71 with sotalol. Results: The two groups were well-matched for age, type of presenting arrhythmia, severity of coronary artery disease and ventricular function. At 36 months Kaplan-Meier estimates of mortality from ventricular tachyarrhythmia were 0% with ATPICD and 15% with sotalol (p=0.03). Kaplan-Meier estimates of total mortality at 36 months were 12% with ATPICD and 25% with sotalol (p=0.09). Multivariate analysis showed hazard ratio of 7.9 (p=0.06) for death from ventricular tachyarrhythmia in patients treated with sotalol compared to ATPICD. Conclusions: While no difference in total mortality was demonstrated, treatment with ATPICD is probably superior to sotalol for preventing deaths due to ventricular tachyarrhythmia. (Aust NZ J Med 1999; 29: 331–341.)     

Transmural dispersion of repolarization and ventricular tachyarrhythmias

BACKGROUND: Myocardial transmural dispersion of repolarization (TDR) has been associated with reentrant arrhythmias in animal studies but a clinical association has not yet to been demonstrated. The present study examines the relationship between TDR and ventricular tachyarrhythmias in human subjects. METHODS: This study consisted of 65 patients with non-sustained ventricular tachycardia, sustained ventricular tachycardia, ventricular fibrillation or unexplained syncope with organic heart disease. The control group included 65 patients with paroxysmal supraventricular tachycardia. The 12 ECG was recorded at a recording rate of 100 mm/sec. The interval from the peak to the end of the T wave in the precordial (ECG), referred to as TpTe was assumed to be representative of TDR. RESULTS: Patients were divided into three groups based on the ability to induce VT at the time of electrophysiologic study: VT inducible group (n=37), VT non-inducible group (n=25) and control group (n=65). V4 TpTe/ radical RR was significantly prolonged in the VT inducible group, as compared to the VT non-inducible group (n=25) and the control group (118.9 +/- 26.1 vs. 103.9 +/- 25.7, 104.1 +/- 22.6 ms, P<.05). Patients who develop VT spontaneously (n=13) during a mean follow-up period of 25 months, displayed significantly prolonged V3 TpTe/ radical RR, compared to patients who did not develop VT spontaneously or the control group (132.5 +/- 37.4 vs. 109.8 +/- 26.3, 107.1 +/- 24.1 ms, P <.05). CONCLUSION: Prolonged TDR is associated with inducibility as well as spontaneous development of VT in higher risk patients. TDR may be a useful index for predicting ventricular tachyarrhythmias.     

Idiopathic verapamil-sensitive sustained left ventricular tachycardia

Idiopathic verapamil-sensitive left ventricular tachycardia (VT) has characteristic QRS configurations during VT: right bundle-branch block with either left axis or right axis (less common) deviation. QRS duration is relatively narrow (0.13-0.16s) and frequently endocardial activation prior to QRS is recorded during VT, which is the basis of its being called fascicular tachycardia. The mechanism is probably reentry, but the nature of the slow conduction necessary for the occurrence of reentry is quite different from that of other sustained monomorphic VT associated with structural heart disease. Chronic oral verapamil therapy is the drug of choice for alleviation of symptoms. Long-term prognosis is good.     

急性心肌梗死非持续和持续室性心动过速的Q—T离散度

为研究急眭心肌梗死伴持续和非持续室性心动过速患者间Q-T离散度和其它心电图参数之间的关系。比较14例急性心肌梗死伴持续室性心动过速和26例伴非持续室性心动过速患者的心室Q-T离散度、Q-T和Q-T_c间期。结果显示持续和非持续室性心动过速患者之间的Q-T离散度以及相邻胸导联Q-T离散度差异有显著意义(110.1±7.80对80.8±4.4,105.9±6.9对67.6±4.0,P<0.01)。我们认为相邻导联Q-T离散度增大极易出现室性心动过速,Q-T离散度大于110ms有发生持续室性心动过速的危险。而Q-T离散度在80—110ms之间有非持续室性心动过速的可能性。     

Antiarrhythmic effects of oral indecainide in patients with ventricular tachyarrhythmias

In order to assess the efficacy and safety of oral indecainide in patients with serious ventricular arrhythmias we studied 11 patients with high-grade ventricular ectopy and ventricular tachycardia (VT) which were refractory to therapy with at least one standard antiarrhythmic drug. Spontaneous arrhythmias were quantitated by 24-h Holter monitor before and during therapy with indecainide. Spontaneous VT was sustained in 4 patients and nonsustained in 7. Ten patients underwent baseline electrophysiologic study (EPS) and VT was induced in 9. The mean ejection fraction was 25 +/- 14%. Indecainide was given orally at a dose of 211 +/- 118 mg/day. The frequency of ventricular premature beats (VPBs) was significantly (greater than 85%) decreased in 90% of patients, while ventricular couplets frequency decreased in 78%. Spontaneous VT was abolished in 5 of 11 (45%). Sustained VT was induced in 5 of 7 (71%) patients who underwent follow-up EPS. The QRS duration was significantly prolonged during therapy (0.13 +/- 0.04 s) compared to control (0.10 +/- 0.02 s). The PR, QTc, and JTc intervals were not significantly changed. Indecainide was well tolerated, but 2 patients died of ventricular tachyarrhythmias while receiving the drug. Indecainide suppressed VPBs in a high percentage of patients, but was much less successful in controlling VT. Caution is necessary when using this drug because of its potential for exacerbation of arrhythmia.     

Cardiac autonomic tone and its relation to nonsustained ventricular tachyarrhythmias in idiopathic dilated cardiomyopathy

BACKGROUND: In contrast to postinfarct patients, little is known about cardiac autonomic tone and its relation to spontaneous ventricular tachyarrhythmias in idiopathic dilated cardiomyopathy (IDC). Both heart rate variability (HRV) and baroreflex sensitivity (BRS) are indices of autonomic innervation of the heart. HYPOTHESIS: The aim of the present study was to determine the relation between cardiac autonomic tone assessed by HRV and BRS and spontaneous nonsustained ventricular tachycardia (NSVT) on Holter in a large patient population with IDC. METHODS: 24-h digital Holter recordings including HRV analysis and BRS testing were prospectively performed in 137 patients with IDC and preserved sinus rhythm. Mean age was 48 +/- 12 years, and mean left ventricular (LV) ejection fraction was 32 +/- 9%. The HRV analysis on Holter included the mean RR interval (RRm), the standard deviation of all normal RR intervals (SDNN), the square root of the mean of the squared differences between adjacent normal RR intervals (rMSSD), and the proportion of adjacent normal RR intervals differing more than 50 ms (pNN50). Testing for BRS was performed noninvasively using the phenylephrine method. RESULTS: Of 137 study patients, 42 (31%) had spontaneous NSVT on 24-h Holter. Compared with patients without NSVT, patients with NSVT on Holter had a higher New York Heart Association (NYHA) functional class (NYHA III: 40 vs. 18%, p < 0.01), a lower ejection fraction (29 +/- 9 vs. 34 +/- 9%, p = 0.01), and an increased LV end-diastolic diameter (69 +/- 8 mm vs. 66 +/- 7 mm, p = 0.03). The HRV variables rMSSD, pNN50, RRm, and BRS did not differ significantly between patients with and without spontaneous NSVT. Only SDNN on Holter was slightly lower in patients with versus without NSVT (106 +/- 45 vs. 121 +/- 46 ms, p = 0.08). CONCLUSIONS: Patients with IDC and spontaneous NSVT on Holter are characterized by a higher NYHA functional class, a lower LV ejection fraction, an increased LV end-diastolic diameter, and a tendency toward a lower SDNN value compared with patients without NSVT. The remaining measures of HRV including rMSSD and pNN50 reflecting primarily tonic vagal activity, as well as BRS reflecting predominantly reflex vagal activity, were similar in patients with and without NSVT. The prognostic significance of these findings in patients with IDC is currently under investigation in the Marburg Cardiomyopathy Study (MACAS) at our institution.     

Implantable defibrillator event rates in patients with unexplained syncope and inducible sustained ventricular tachyarrhythmias: a comparison with patients known to have sustained ventricular tachycardia

OBJECTIVES

To assess the clinical significance of inducible ventricular tachyarrhythmias among patients with unexplained syncope.

BACKGROUND

Induction of sustained ventricular arrhythmias at electrophysiology study in patients with unexplained syncope and structural heart disease is usually assigned diagnostic significance. However, the true frequency of subsequent spontaneous ventricular tachyarrhythmias in the absence of antiarrhythmic medications is unknown.

METHODS

In a retrospective case-control study, the incidence of implantable cardiac defibrillator (ICD) therapies for sustained ventricular arrhythmias among patients with unexplained syncope or near syncope (syncope group, n = 22) was compared with that of a control group of patients (n = 32) with clinically documented sustained ventricular tachycardia (VT). Sustained ventricular arrhythmias were inducible in both groups and neither group received antiarrhythmic medications. All ICDs had stored electrograms or RR intervals. Clinical variables were similar between groups except that congestive cardiac failure was more common in the syncope group.

RESULTS

Kaplan-Meier analysis of the time to first appropriate ICD therapy for syncope and control groups produced overlapping curves (p = 0.9), with 57 ± 11% and 50 ± 9%, respectively, receiving ICD therapy by one year. In both groups, the induced arrhythmia was significantly faster than spontaneous arrhythmias, but the cycle lengths of induced and spontaneous arrhythmias were positively correlated (R = 0.6, p < 0.0001). During follow-up, three cardiac transplantations and seven deaths occurred in the syncope group, and two transplantations and five deaths occurred in the control group (36-month survival without transplant 52 ± 11% and 83 ± 7%, respectively, p = 0.03).

CONCLUSIONS

In patients with unexplained syncope, structural heart disease and inducible sustained ventricular arrhythmias, spontaneous sustained ventricular arrhythmias occur commonly and at a similar rate to patients with documented sustained VT. Thus, electrophysiologic testing in unexplained syncope can identify those at risk of potentially life-threatening tachyarrhythmias, and aggressive treatment of these patients is warranted.     

Objective features of the surface electrocardiogram during ventricular tachyarrhythmias

The aim of this study was to quantify the electrocardiographicsignal characteristics of three types of ventricular arrhythmia;monomorphic ventricular tachycardia, polymorphic ventriculartachycardia and ventricular fibrillation. Patients in a coronarycare unit were monitored using a single bipolar ECG lead. Thirtyepisodes of ventricular tachyarrhythmia (ten from each group)were recorded automatically by computer. Frequency analysisof ten consecutive 1 s epochs from each recording gave 100 spectrafor each tachyarrhythmia group. Each spectrum was characterisedby the frequency, width and proportional size of the dominantpeak. Despite a qualitative similarity in spectral appearance,there were significant differrences in all characteristics betweenthe tachyarrhythmia groups (P<0·025). Ventricularfibrillation had a higher mean dominant frequency (4·8Hz) than polymorphic ventricular tachycardia (3·7 Hz)and monomorphic ventricular tachycardia (3·8 Hz). Thedominant frequency of ventricular fibrillation was also morevariable than that of monomorphic ventricular tachycardia (P<0·01).Mean peak size was largest for monomorphic ventricular tachycardia(0·78) and smallest for ventricular fibrillation (0·64).The single spectral peaks seen throughout this study indicatethat all three tachyarrhythmias have an underlying periodicmechanism. The difference in spectral characteristics show thatvarying degrees of myocardial electrical organisation can bequantified from surface ECG features.     

Multicentre randomized trial of sotalol vs amiodarone for chronic malignant ventricular tachyarrhythmias

Sotalol was compared with amiodarone in this open randomizedmulticentre study of patients with ventricular tachycardia orfibrillation not associated with acute myocardial infarctionrefractory to or intolerant of Class I drugs. 16 of 30 patientstreated with amiodarone completed 12 months on therapy, fivewere withdrawn because of recurrent ventricular tachycardiaand nine because of presumed adverse drug reactions, complianceproblems or protocol violation. Four of those who were withdrawndied within 12 months. Sixteen of 29 patients completed 12 months on sotalol, one waswithdrawn because of ventricular tachycardia and nine becauseof presumed adverse drug reactions, poor compliance or the needfor coronary artery surgery. Three died on treatment and twoafter withdrawal but within 12 months of entering the study. When the results are analysed by intention to treat there wasno significant difference in antiarrhythmic efficacy or in theincidence of side-effects severe enough to warrant withdrawalfrom the trial. There was an increase in left ventricular ejectionfraction in those treated with sotalol, which, because of itspharmacokine-tics, is an attractive alternative to amiodaronefor patients with malignant ventricular arrhythmias who cantolerate ß-adrenergic blockade.     

Clinical electrophysiologic effects of flecainide acetate

Summary Flecainide acetate depresses the rate of depolarization of action potential (V_max), the so-called membrane stablizing action. In the intact heart it has a unique profile of substantial effect on conduction with modest effect on refractoriness. After intravenous administration, clinical electrophysiologic studies show that conduction through atrial myocardium, atrioventricular (AV) node, His-Purkinje system, and ventricular myocardium is depressed, the most prominent effect being on the His-Purkinje system. Refractorines of the normal atrial and AV nodal myocardium is not prolonged while that of the ventricular muscle is slightly increased. Atrial fibrillation (60% to 70%), atrial tachycardia (90% to 100%), and nodal and AV tachycardia (80% to 90%) are generally terminated, while flutter is usually slowed, but in a small proportion of patients (10% to 20%) might be terminated by the intravenous use of flecainide acetate. This drug has also been shown to be effective in terminating stable ventricular tachycardia (70%). However, it appears to be slightly less effective in suppressing inducibility of ventricular arrhythmias. Administered orally, flecainide is very effective in decreasing ventricular ectopic activity (80% to 95%) and nonsustained ventricular tachycardia. Thus, flecainide has a wide range of antiarrhythmic properties, making it a useful agent in the management of a variety of supraventricular and ventricular arrhythmias. In a small proportion of patients, however, its use can lead to apparent arrhythmogenic effects, the most dangerous being exacerbation of ventricular tachycardia.     

Transition from purkinje fiber-related rapid polymorphic ventricular tachycardia to sustained monomorphic ventricular tachycardia in a patient with a structurally normal heart: a case report

We describe a 17-year-old woman with a structurally normal heart in which short-sustained rapid polymorphic ventricular tachycardias (VTs) were repetitively provoked by an antiarrhythmic agent, pilsicainide, and spontaneously changed into a sustained monomorphic VT. The latter was terminated by verapamil and was shown to be due to reentry by entrainment. Those two VTs originated from the Purkinje fibers in the left ventricular septum. Radiofrequency catheter ablation guided by the diastolic double potentials eliminated both VTs. Neither tachycardia recurred over a 5-month follow-up period or during antiarrhythmic drug challenge tests at 1 week, 1 month, and 3 months after the ablation.     

Sotalol in patients with life-threatening ventricular tachyarrhythmias

Summary To assess the antiarrhythmic efficacy of oral d,l-sotalol, 68 patients with sustained monomorphic ventricular tachycardia (SMVT) (n=62) or ventricular fibrillation (VF) (n=6) were studied by programmed ventricular stimulation (PVS). Fifty-one patients had coronary artery disease with a previous myocardial infarction and there were 17 patients without coronary disease: 11 patients had right and/or left ventricular dysplasia, one patient an aortic-valve replacement, and five patients had no visible heart disease. Prior to sotalol patients were treated with a mean of 3.6±1.3 antiarrhythmic class I drugs. None of these drugs prevented SMVT or VF. During control PVS (PVS 1), VF was induced in 8 patients (12%), SMVT in 47 patients (69%), and nonsustained ventricular tachycardia (NSVT) in 13 patients (19%). After loading with oral d,l-sotalol (320 mg/day), PVS (PVS 2) was repeated 4.2±3.3 weeks after PVS 1. In one of the patients (1%) VF was inducible, in 15 patients (22%) SMVT was induced, and in 18 patients (26%) NSVT was induced. In 34 patients (50%) either no or a short ventricular response was inducible. Our data show that oral d,l-sotalol is an effective antiarrhythmic agent in patients with SMVT or VF.