Incidence of ventricular tachyarrhythmias during permanent pacemaker therapy in low-risk patients results from the German multicentre EVENTS study.

AIMS: Current studies found an incidence of 12-31% ventricular tachyarrhythmias and sudden cardiac death during cardiac pacing months or even years after pacemaker insertion. MADIT(12) and MUSTT(13) demonstrated that patients with poor LV function after Myocardial infarction (MI) showing non-sustained ventricular tachycardia (nsVT) and inducibility during electrophysiologic testing benefit from an ICD. The present study was dedicated to assess the global incidence of non-sustained ventricular arrhythmias in a general population of pacemaker patients. Special regard was on patients with a potential ICD indication, e.g. those matching the MADIT/MUSTT criteria. METHODS AND RESULTS: Two hundred and thirty-one patients (72 +/- 11 years; 134 men) with an indication for dual chamber pacing entered the study. In all patients pacemaker systems capable of automatic storing of intracardiac electrocardiograms were implanted (Pulsar, Discovery, Guidant). Follow-up time was 15 months after inclusion. In 54 (25.7%) of 210 patients with at least one follow-up, episodes of nsVT were documented by stored electrocardiograms (up to >30 beats, >200 b.p.m.). Multiple-up to nine-episodes of ventricular tachycardia were retrieved in 31 of these patients. Three out of 14 patients with an LVEF <40% after MI presented nsVT during the follow-up. One of these patients received an ICD. CONCLUSION: A significant number of pacemaker patients present with ventricular tachycardia. Intracardiac electrocardiograms and alert functions from pacemakers may enhance physicians' awareness of the patient's intrinsic arrhythmic profile and help uncover underlying mechanisms of arrhythmias by storing the initiation of the arrhythmia.     

Markers of electrical instability in hypertensive patients with and without ventricular arrhythmias. Are they useful in identifying patients with different risk profiles?

BACKGROUND: Markers of electrical instability of the ventricular myocardium, namely abnormal repolarization and late potentials, are frequently observed in patients with hypertension when both ventricular arrhythmias and left ventricular hypertrophy are present. This information cannot be extrapolated to the population of hypertensive patients with ventricular arrhythmias but without left ventricular hypertrophy. OBJECTIVE: To evaluate QT duration, QT dispersion and the incidence of ventricular late potentials in patients with essential hypertension, already on anti-hypertensive therapy, both with and without non-sustained ventricular arrhythmia. DESIGN: The study population consisted of 49 patients with essential hypertension who were compared to 89 control normotensive subjects both with and without frequent (> 30 per h) ventricular ectopic beats (VPBs). Patients were divided into four groups: (1) hypertensive patients without VPBs (H, n = 19), (2) hypertensive patients with VPBs (HA, n = 30), (3) normotensive subjects without VPBs (C, n = 28), and (4) normotensive subjects with VPBs (CA, n=61). METHODS: Echocardiographic parameters, QT interval, QT dispersion and signal-averaged ECG were evaluated without withdrawing anti-hypertensive drugs. RESULTS: In no case was left ventricular hypertrophy documented. The number of VPBs during 24 h Holter recording (median 11 343 versus 7617) and the incidence of repetitive VPBs (37 versus 46% of patients) were similar in the two groups of patients (HA versus CA). Signal-averaged ECG parameters were normal and not different between the four groups. QT interval was longer in hypertensive patients compared to controls irrespective of the presence of VPBs. QT dispersion was slightly greater in subjects with VPBs, both hypertensive and normotensive, compared to subjects without arrhythmias. CONCLUSIONS: In patients with hypertension well-controlled by drug therapy and without left ventricular hypertrophy, frequent VPBs are not associated with markers indicating an electrophysiological substrate for re-entrant arrhythmias. However, QT prolongation suggests the persistence of a higher risk of cardiovascular mortality that is independent of the presence of VPBs.     

Prevalence and prognostic implications of non-sustained ventricular tachycardia in ST-segment elevation myocardial infarction after revascularization with either fibrinolysis or primary angioplasty.

AIMS: We compared the prevalence and prognostic implications of non-sustained ventricular tachycardia (nsVT) detected early after ST-segment elevation myocardial infarction (STEMI) in patients randomized to either fibrinolysis or primary angioplasty in the DANAMI-2 trial. METHODS AND RESULTS: Holter recordings were available in 1017 patients (fibrinolysis: n=501; primary angioplasty: n=516). Primary endpoint was all-cause mortality. The prevalence of nsVT was 8.8% in fibrinolysis-treated, and 8.1% in primary angioplasty-treated patients (P=0.71). During 4519 patient-years of follow-up (median 4.3 years), 116 patients died [fibrinolysis vs. angioplasty: HR=1.1 (95% CI, 0.8-1.6), P=0.47]. In univariate analysis, nsVT patients treated with fibrinolysis, had significantly higher mortality when compared with those without nsVT (P<0.001). However, after adjustment for other relevant prespecified risk factors, the association between nsVT and mortality did not remain statistically significant. In patients treated with primary angioplasty, nsVT was not associated with mortality in either univariate or multivariate analyses. CONCLUSION: Immediate revascularization with primary angioplasty for STEMI does not affect the subsequent prevalence of nsVT when compared with fibrinolysis. After adjustment for other relevant risk factors, the prognostic value of nsVT detected early after STEMI is limited, regardless of the chosen reperfusion strategy.     

Ambulatory ventricular tachycardia: Characteristics of the initiating beat

One hundred ten 24-hour Holter ECG recordings from 82 ambulatory patients with 341 episodes of ventricular tachycardia (VT) were analyzed. Most VT was precipitated by ventricular premature beats (VPBs) with prematurity indices (coupling interval/QT) between 1.0 and 2.0. However, a disproportionate number of VPBs initiating VT occurred early and late in the cardiac cycle compared with isolated VPBs. VT rate was not related to preceding heart rate, but faster basic rates appeared to protect against VT of extended duration. Approximately 80% of episodes of VT were initiated by VPB forms also seen in isolation. Of the 20% of VT initiated by a VPB of new morphology, one third occurred late in the cardiac cycle; almost none were early cycle.     

Fused TU complexes as a new electrocardiographic marker of poor prognosis after myocardial infraction

To date, the clinical significance of fused T and U waves, termed as TU complexes, has not been evaluated. The aim of the study was to present the clinical characteristics of the patients with TU complexes and to assess the value of this ECG abnormality in risk stratification after myocardial infarction. In the group of 330 postinfarction patients (mean age 61 +/- 10 years, 279 men and 51 women), 50 (15%) had TU complexes in one or more leads of a standard ECG. In patients with TU complexes, the decreased left ventricular ejection fraction, frequent (> or = 10/hour) ventricular premature beats and non-sustained ventricular tachycardia detected on 24-hours ECG monitoring, increased QT dispersion, ST-segment depression and ST-segment elevation on a routine ECG were more common than in patients without TU complexes. During a follow-up period of 43 +/- 17 months, 88 patients died from all causes. At univariate Cox analysis the presence of TU complexes (hazard ratio 3.30; 95% confidence interval 2.09-5.21) and left ventricular ejection fraction < 40% (hazard ratio 3.82; 95% confidence interval 2.51-5.82) were the best predictors of mortality among the 9 evaluated clinical and electrocardiographic variables. The multivariate, stepwise Cox analysis selected ejection fraction < 40% (hazard ratio 3.09; 95% confidence interval 2.00-4.80), TU complexes (hazard ratio 2.28; 95% confidence interval 1.42-3.69), RR interval < 800 ms (hazard ratio 1.62; 95% confidence interval 1.06-2.47), and age of patients > 65 years (hazard ratio 1.58; 95% confidence interval 1.03-2.42) as an independent predictors of all cause mortality. CONCLUSION: The presence of TU complexes on a routine ECG is associated with impaired left ventricular function, increased predisposition to ventricular arrhythmias and higher risk of mortality. TU complexes may be considered as a new electrocardiographic marker of poor prognosis in patients after myocardial infarction.     

Heart rate turbulence after ventricular and atrial premature beats in subjects without structural heart disease

INTRODUCTION: Studies assessing heart rate (HR) behavior after premature beats have focused on HR responses to ventricular premature beats (VBPs), but there is less information of HR behavior after atrial premature beats (APBs). METHODS AND RESULTS: HR turbulence after VPBs and APBs was first measured in response to ambient APBs and VPBs occurring during 24-hour ambulatory ECG recordings in 29 subjects without structural heart disease, and in response to programmed atrial (AE) and ventricular extrastimuli (VE) in 6 subjects undergoing electrophysiologic (EP) examination. Turbulence onset (TO) was more negative (-2.3 +/- 3.2% vs -0.9 +/- 2.8%, P < 0.01) and turbulence slope (TS) was steeper (11 +/- 11 vs 5.1 +/- 4.1 msec/R-R interval, P < 0.05) after VPBs than APBs. Compared to VPBs, the acceleration of HR after APBs was delayed by one beat, and APBs were associated with a short R-R interval preceding the APB, resulting in a blunted TO. Studies of patients undergoing an EP test confirmed the one-beat delay of HR acceleration and the blunted TO after programmed AE compared to VE (P < 0.05). TO and TS after VPBs were related to baroreflex sensitivity. TO also was related to 24-hour standard deviation of N-N intervals (SDNN). However, the TO or TS following APBs was not related to either SDNN or baroreflex sensitivity. CONCLUSION: HR behavior is different in response to APBs and VBPs among subjects without structural heart disease. Different definitions and calculation formulas should be used in the analysis of HR turbulence after APBs and VPBs.     

Prediction of sudden cardiac death after myocardial infarction in the beta-blocking era

OBJECTIVES: This study assessed the predictive power of arrhythmia risk markers after an acute myocardial infarction (AMI). BACKGROUND: Several risk variables have been suggested to predict the occurrence of sudden cardiac death (SCD), but the utility of these variables has not been well established among patients using medical therapy according to contemporary guidelines. METHODS: A consecutive series of 700 patients with AMI was studied. The end points were total mortality, SCD, and nonsudden cardiac death (non-SCD). Nonsustained ventricular tachycardia (nsVT), ejection fraction (EF), heart rate variability, baroreflex sensitivity, signal-averaged electrocardiogram (SAECG), QT dispersion, and QRS duration were analyzed (n = 675). Beta-blocking therapy was used by 97% of the patients at discharge and by 95% at one and two years after AMI. RESULTS: During a mean (+/-SD) follow-up of 43 +/- 15 months, 37 non-SCDs (5.5%) and 22 SCDs (3.2%) occurred. All arrhythmia risk variables differed between the survivors and those with non-SCD (e.g., the standard deviation of N-N intervals was 98 +/- 32 vs. 74 +/- 21 ms [p < 0.001] and the QRS duration was 103 +/- 22 vs.89 +/- 16 ms [p < 0.001]). Sudden cardiac death was weakly predicted only by reduced EF (<0.40; p < 0.05), nsVT (p < 0.05), and abnormal SAECG (p < 0.05), but not by autonomic markers or standard ECG variables. The positive predictive accuracy of EF, nsVT, and abnormal SAECG as predictors of SCD was relatively low (8%, 12%, and 13%, respectively). CONCLUSIONS: The common arrhythmia risk variables, particularly the autonomic and standard ECG markers, have limited predictive power in identifying patients at risk of SCD after AMI in the beta-blocking era.     

Chronic hemodynamic effects after radiofrequency catheter ablation of frequent monomorphic ventricular premature beats

INTRODUCTION: Radiofrequency catheter ablation (RFCA) of severely symptomatic monomorphic ventricular premature beats (VPBs) is reported to be a safe and effective treatment option. However, the chronic hemodynamic effects of these VPBs have not been precisely evaluated. METHODS AND RESULTS: We sought to investigate chronic effects after decreasing the number of VPBs by RFCA. A total of 47 patients who had no underlying heart disease and frequent monomorphic VPBs, consisting of more than 10,000 beats per day (24,194 +/- 12,516 beats per day), were enrolled. Patients were treated with RFCA and followed up over 6 months as outpatients. Echocardiography and serum B-type natriuretic peptide (BNP) level were repeatedly checked before and after RFCA. In 38 patients, whose VPBs were dramatically decreased to less than 1,000 beats per day by successful RFCA, left ventricular (LV) end-diastolic dimension (LVEDd) and end-systolic dimension (LVESd) measured by echocardiography decreased significantly (LVEDd: 50 +/- 5 to 48 +/- 5 mm, P < 0.01; LVESd: 33 +/- 7 to 30 +/- 6 mm, P < 0.01) in association with improvement of BNP level (39.9 +/- 34.1 to 16.8 +/- 10.3 pg/mL, P = 0.0001). In nine patients, whose VPBs were treated unsuccessfully by RFCA or that recurred, LV dimensions and BNP level did not change during the follow-up period. CONCLUSION: Significant improvement in LV dimensions and serum BNP level appeared to indicate that RFCA of VPBs ameliorated occult cardiac dysfunction induced by frequent VPBs.     

1- and 7-year risk of cardiac events in relation to Holter monitoring in patients admitted with chest pain in whom AMI is not confirmed

The prognostic value of ventricular premature beats (VPBs) was evaluated in 198 patients with chest pain (non-AMI patients) in whom the diagnosis of acute myocardial infarction was ruled out after admission to hospital. VPBs were registered at the time of discharge during a 24-hour Holter monitoring. The amount of cardiac events (CEs) were analyzed after 1 and 7 years follow-up. After 1 year, CEs were seen in 9% of the non-acute myocardial infarction (AMI) patients. After 7 years, 51 CEs (20 nonfatal AMIs and 31 cardiac deaths) had occurred (25%). After 1 year, only pairs of VPBs were associated with an increased risk of CEs. CEs were seen in 25% of the patients with pairs of VPBs and in 6% of the patients without pairs (p<0.01). The occurrence of CEs after 7 years was related to the presence of pairs of VPBs and multiform VPBs. Fifty-five percent of the patients with pairs of VPBs had CEs during the long-term follow-up, compared with 22.5% without pairs (p<0.0005). CE was seen in 48.9% of the patients with multiform VPBs, compared with 19.0% without multiform VPBs (p< 0.0001). Thus, Holter monitoring seems to be of better value for predicting long-term prognosis than for predicting short-term prognosis in non-AMI patients. The presence of multiform VPBs or pairs of VPBs is strongly associated with an increased risk of CE after 7 years. Non-AMI patients with pairs of VPBs or multiform VPBs should be considered as high-risk patients.Presented at The 35th World Congress, International College of Angiology, Copenhagen, Denmark, July 1993     

Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.

AIMS: Intravenous amiodarone has recently emerged as an important drug for the acute treatment of ventricular tachyarrhythmias. However, electrophysiological actions and the efficacy of the drug in the suppression of ventricular tachycardia inducibility have not yet been fully established. The present study was designed to address these issues. METHODS AND RESULTS: The study group consisted of 18 patients (all males, mean age 75 +/- 14 years), who underwent electrophysiological study due to a history of sustained ventricular tachyarrhythmia or syncope with non-sustained ventricular tachycardia detected on ambulatory ECG monitoring. The effects of 5 mg.kg(-1) or 10 mg.kg(-1) of intravenous amiodarone on (1) ventricular refractoriness (QTc interval, right ventricular effective refractory period and monophasic action potential duration), (2) intraventricular conduction (paced-QRS and signal-averaged QRS duration), and (3) ventricular tachycardia inducibility, were examined. The drug had no significant effect on ventricular refractoriness. However, a relatively small but significant slowing of intraventricular conduction was seen (paced-QRS duration: 182 +/- 27 ms vs 191 +/- 28 ms, P<0.0007; 183 +/- 32 ms vs 195 +/- 33 ms, P<0.0007; and 177 +/- 21 ms vs 192 +/- 24 ms, P<0.003, at the cycle lengths of 600, 500 and 400 ms, respectively). This effect was more evident during extrasystolic beats than during stable pacing (for example, at the cycle length of 600 ms, the magnitude of amiodarone-induced lengthening of QRS duration was 23.9 +/- 17.6 ms vs 9.7 +/- 7.2 ms, P<0.009, respectively). Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion. CONCLUSION: Intravenous amiodarone does not prolong ventricular refractoriness, slows intraventricular conduction and may facilitate inducibility of sustained ventricular arrhythmias.     

Risk Stratification Using Heart Rate Turbulence and Ventricular Arrhythmia in MADIT II: Usefulness and Limitations of a 10‐Minute Holter Recording

Background: We evaluated the usefulness of heart rate turbulence (HRT) parameters and frequency of ventricular premature beats (VPBs) for risk‐stratifying postinfarction patients with depressed left ventricular function enrolled in Multicenter Automatic Defibrillator Trial II (MADIT II). Methods: In 884 MADIT II patients, 10‐minute Holter monitoring at enrollment was used to evaluate HRT parameters and frequency of VPBs. The primary endpoints were defined as all‐cause mortality in patients randomized to conventional treatment and as appropriate therapy for ventricular tachycardia or fibrillation in patients randomized to implantable cardioverter defibrillator (ICD) therapy. Results: The median turbulence slope was lower in patients who died in comparison to survivors in the conventional arm (2.3 vs 4.5 ms/RR; P < 0.05); but it was not a significant predictor of mortality after adjustment for clinical covariates (age, ejection fraction, beta‐blocker use, and BUN levels). There was no association between HRT parameters and arrhythmic events in ICD patients. Conventionally treated patients who died and ICD patients who had appropriate ICD therapy had significantly more frequent VPBs than those without such adverse events. After adjustment for clinical covariates, frequent VPBs>3/10 min were associated with death in the conventional arm (HR = 1.63; P = 0.070) and were predictive for appropriate ICD therapy in the ICD arm (HR = 1.75; P = 0.003). Conclusion: In postinfarction patients with severe left ventricular dysfunction, frequent VPBs are associated with increased risk of mortality and with appropriate ICD therapy. HRT obtained from 10‐min Holter ECG showed a trend toward the association with mortality in univariate analysis but HRT parameters were not predictive of the outcome in multivariate analyses.     

Relationship of ventricular ectopy in men without apparent heart disease to occurrence of ischemic heart disease and sudden death

The purpose of this investigation was to determine whether ventricular ectopic beats, or ventricular premature beats (VPBs), on routine electrocardiograms in men without apparent heart disease predict the later occurrence of clinical manifestations of ischemic heart disease (IHD). The Manitoba Study cohort consisted of 3983 men predominantly between 25 and 34 years of age and free of IHD at entry. During the 29-year observation period, 401 persons without clinical evidence of heart disease had VPBs on an electrocardiogram at a routine examination. They were followed 10.8 ± 0.5 (SEM) years and 13.5% (54 men) later manifested IHD. Age-specific total IHD incidence was significantly (p < 0.05) greater for men 40 to 59 years of age at VPB occurrence compared to men of the same age without VPBs. The clinical manifestation with the strongest association with VPBs was sudden death. VPB characteristics of frequency, configuration, coupling interval, and postextrasystolic T-wave change did not distinguish those who developed IHD. Prematurity index ($\text{R-R′}\text{QT}$) showed a trend toward an association of late coupled ectopic beats ($\text{R-R′}\text{QT}\text{> 1.6}$) and IHD risk. However, faster basic ventricular rate plus VPBs significantly correlated with greater IHD probability. Thus ventricular ectopic beats on a routine electrocardiogram in men over 40 years of age without apparent heart disease identify those at high risk for a clinical IHD event, especially sudden death.     

Spontaneous and inducible ventricular arrhythmias in a canine model of chronic heart failure: relation to haemodynamics and sympathoadrenergic activation.

The relationship between the incidence, frequency and complexity of spontaneous ventricular arrhythmias and the extent of haemodynamic compromise and sympathoadrenergic hyperactivity was evaluated in a canine model of chronic heart failure produced by multiple sequential intracoronary microembolizations. Ambulatory ECG Holter monitoring recorded during chronic heart failure in 18 dogs revealed spontaneous ventricular arrhythmias ranging from single ventricular premature beats (VPBs) to non-sustained episodes of ventricular tachycardia (VT). Single VPBs were present in 94% of dogs, couplets in 67%, triplets in 28% and spontaneous episodes of non-sustained VT in 33%. Dogs with > 28 VPBs.h-1 (n = 9) had a markedly higher plasma norepinephrine (PNE) concentration (1001 +/- 185 vs 561 +/- 31 pg.ml-1) (P < 0.03), and a higher pulmonary artery wedge pressure (PAWP) (18 +/- 2 vs 12 +/- 1 mmHg) (P < 0.03) than dogs with < or = 28 VPBs.h-1 (n = 9). Dogs that developed spontaneous episodes of VT also had significantly higher PNE levels (1119 +/- 247 pg.ml-1) compared to dogs that did not develop VT (612 +/- 64 pg.ml-1) (P < 0.02). Programmed ventricular stimulation performed in seven of 18 dogs resulted in the development of sustained monomorphic VT in three and ventricular fibrillation in three dogs each (43%, 43%). Dogs with inducible sustained monomorphic VT had a significantly higher number of ambient arrhythmias and higher PAWP compared to dogs that did not develop sustained VT. The observed complexity, frequency and incidence of spontaneous and inducible ventricular arrhythmias in this canine model are similar to those described in patients with chronic heart failure.     

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.     

Effects of oral flecainide treatment of refractory tachyarrhythmias

Oral flecainide treatment was given to five patients who were refractory to conventional antiarrhythmic agents. The five patients included one with atrioventricular reentrant tachycardia (AVRT), one with non-sustained ventricular tachycardia (nsVT) and three with sustained VT (sVT). Flecainide produced favorable responses in patients of AVRT, nsVT and sVT with arrhythmogenic right ventricular dysplasia (ARVD). In the case of AVRT, flecainide exhibited a preventive effect on tachycardia induced by programmed electrical stimulation (PES). In the case of nsVT, flecainide markedly reduced the number of VPC and abolished the VT on the Holter ECG. In the case of sVT with ARVD, sVT was not induced by PES after the flecainide. Long-term treatment with flecainide on these three cases produced complete prevention of tachycardias. As an adverse effect of flecainide, an aggravation of congestive heart failure was recognized in one case with cardiac sarcoidosis. PQ interval and QRS interval in all the cases were prolonged after flecainide. The results indicate that flecainide is a useful antiarrhythmic agent for tachyarrhythmias refractory to treatment with conventional drugs.     

Cardiac arrhythmias during theophylline toxicity. A prospective continuous electrocardiographic study

To examine the effects of theophylline toxicity on cardiac rhythm, patients underwent continuous ambulatory ECG recording during acute theophylline toxicity and recovery. The patients, who were recruited form inpatient wards, intensive care units, and emergency departments of a University Medical Center and a Veterans Administration Medical Center, had serum theophylline concentrations (STC) greater than 30 mg/L. There were 14 men and two women with a mean age of 66 years. Fourteen patients had COPD and developed toxicity following long-term theophylline overmedication. Two patients had asthma and ingested an intentional overdose. The STC at the onset of ECG recording ranged from 23 to 67 mg/L. The principal rhythm was sinus in 15 patients; one patient had atrial fibrillation. Sinus tachycardia (heart rate greater than 100/min) was common, and heart rate fell in proportion to STC as toxicity resolved. Supraventricular ectopic beats (SVEs) were noted in seven patients with multiple runs of SVE being present in four. One patient developed multifocal atrial tachycardia (MAT) during toxicity that resolved spontaneously. During the 11 +/- 8 hours of recording during toxicity (STC greater than 20 mg/L), 80 percent of patients had ventricular premature beats (VPBs), 44 percent had paired VPBs, and 25 percent had ventricular runs. One elderly patient with heart disease developed sustained ventricular tachycardia (VT) when STC = 66 mg/L. No other patient had ventricular ectopy that required intervention. During the 10 +/- 6 hours of recording during the "recovery phase" (STC less than 20 mg/L), all patients with VPBs continued to have ectopy; however, the number of VPBs declined significantly. A follow-up 24-hour ECG recording obtained one week after recovery from toxicity in the patient with sustained VT demonstrated marked reduction in the frequency and complexity of VPBs. Patients with frequent (greater than 10/h) or repetitive VPBs were older (p less than 0.05) than those without complex ectopy. There was a trend (p = 0.07) suggesting patients with underlying heart disease were at risk for having complex ventricular ectopy. We conclude that sinus tachycardia, SVE, and VPBs are common among patients with theophylline toxicity; however, sustained ventricular or supraventricular tachyarrhythmias that require antiarrhythmic therapy are uncommon.     

Outpatient evaluation and management of patients with ventricular premature beats or non-sustained ventricular tachycardia

In this survey, European physicians who deal with arrhythmia patients gave their opinions about diagnostic work up when they see patients with ventricular premature beats (VPBs) or non-sustained ventricular tachycardia (NSVT). In general, similar work-up regimens were used for these two arrhythmias except for coronary angiography, which was considered by one in four physicians when dealing with NSVT but by almost none for VPBs. The majority of physicians believe that it is acceptable to abstain from pharmacological therapy in an asymptomatic patient with VPBs. When considering second-line therapy almost half of the respondents would consider amiodarone in patients with NSVT whereas almost none would when dealing with VPBs. When the effect of therapy was evaluated, its influence on symptoms and arrhythmia burden were ranked highest.     

Ventricular arrhythmias in patients with COPD are associated with QT dispersion

STUDY OBJECTIVE: QT dispersion (QTd) and late potentials derived from signal-averaged ECG (SAECG) have been proposed as noninvasive predictors of cardiac arrhythmias that occur in patients with COPD. In this study, we aimed to investigate QTd and SAECG in patients with COPD. DESIGN: Cross-sectional study. SETTING: Teaching chest disease hospital and cardiology center in a university hospital. PATIENTS: Thirty patients with COPD (28 men and 2 women; mean +/- SD age, 60 +/- 9 years) and 31 age- and sex-matched control subjects (28 men and 3 women; mean age, 57 +/- 7 years) were included. Measurements and results: Respiratory function tests, arterial blood gas analyses, echocardiographic examinations, rhythm Holter recordings, and heart rate variability (HRV) analyses were performed in addition to the measurements of QT intervals and SAECG. Patients with COPD had higher rate of ventricular premature beats (VPBs) as compared to control subjects (924 +/- 493 beats vs 35 +/- 23 beats, p = 0.009). Eight patients with COPD (27%) had nonsustained runs of ventricular tachycardia (VT). QTd rates were significantly increased in patients with COPD as compared to control subjects (57.7 +/- 9.9 ms vs 37.5 +/- 8.2 ms, p < 0.001). On comparing patients with COPD with and without runs of VT, patients with VT had longer QTd (67 +/- 10 ms vs 55 +/- 8 ms, p = 0.001). However no difference in any HRV and late potential parameters were found between patients with COPD with and without runs of VT. VPB rates were strongly correlated with QTd in patients with COPD (r = 0.61, p < 0.001). On SAECG analysis, patients with COPD had significantly increased total QRS duration as compared to control subjects. Nine of the 30 patients with COPD (30%) had positive late potentials. However, QTd and VPB rates were also similar between patients with COPD with and without late potentials. CONCLUSIONS: The development of ventricular arrhythmia in patients with COPD was associated with increased QTd. Increased QTd may be associated with autonomic changes seen in patients with COPD.     

Morphology of ventricular premature beats as an aid in the electrocardiographic diagnosis of myocardial infarction

To determine whether morphologic analysis of ventricular premature beats (VPBs) can aid in the electrocardiographic diagnosis of myocardial infarction (MI), 12-lead electrocardiograms were evaluated in 760 consecutive patients who underwent cardiac catheterization, and 2-minute multiple-lead rhythm strips were evaluated in 515 of these patients. VPBs occurred in 58 patients; 21 had prior MI diagnosed by regional akinesia or dyskinesia on left ventricular cineangiography. Standard criteria were used to diagnose prior MI from the sinus beats of the electrocardiogram. Infarction was diagnosed from the morphology of a VPB when it had a QR or QRS pattern with Q wave greater than or equal to 0.04 second. Morphologic analysis of VPBs had a low sensitivity (29%) but high specificity (97%) and high predictive value (86%) for the diagnosis of MI. Sinus beats diagnosed MI with higher sensitivity (52%, and 69% if patients with left bundle branch block and left ventricular hypertrophy were excluded from analysis) than VPB morphologic analysis (p less than 0.05), but with similar specificity (97%) and predictive value (92%). Two patients with angiographic MI had no MI according to standard electrocardiographic criteria, but did have an MI manifest by VPB morphologic analysis. Despite low sensitivity, analysis of the morphology of VPBs may be useful for the diagnosis of MI when the morphology of sinus beats is not diagnostic. Therefore, VPB analysis is complementary to the standard electrocardiographic diagnosis of MI.     

Increased left ventricular dimensions in patients with frequent nonsustained ventricular arrhythmia and no evidence of underlying heart disease

INTRODUCTION: To test the hypothesis that frequent nonsustained ventricular premature beats (VPBs) in patients without underlying heart disease are the first marker of mild systolic dysfunction of the left ventricle, we evaluated whether a subclinical abnormality of left ventricular function and/or an intraventricular conduction defect was present at the first clinical documentation of the arrhythmia. METHODS AND RESULTS: We compared 57 patients (mean age 46 +/- 14 years) with > 30 VPBs/hour and no heart disease (A) to 32 healthy volunteers (mean age 42 +/- 12 years) without arrhythmia (B). Left ventricular echocardiographic parameters and signal-averaged ECG were evaluated. Filtered QRS duration (98 +/- 10 msec in A vs 98 +/- 7 msec in B) was similar in the two groups. End-diastolic left ventricular diameter (EDLVD) was 50 +/- 6 mm in A versus 47 +/- 3 mm in B (P < 0.005); 15 patients (26%) and none of the controls had EDLVD > or = 55 mm (P < 0.005). Filtered QRS interval was longer in the subgroup of patients (n = 15) with increased EDLVD (> or = 55 mm) compared with the subgroup (n = 42) with EDLVD < 55 mm (106 +/- 9 msec vs 95 +/- 9 msec; P < 0.001) and was related to greater left ventricular mass. CONCLUSION: We documented a subclinical but significant increase of left ventricular dimensions that suggests that frequent VPBs may be an initial marker of mild systolic dysfunction of the left ventricle. However, an effect of VPBs per se in modifying left ventricular dimensions cannot be excluded.