Value of non-invasive and invasive studies in patients with bundle branch block, syncope and history of myocardial infarction.

The prognosis of patients with bundle branch block (BBB) and myocardial infarction (MI) is poor, particularly for patients suffering from syncope. The purpose of this study was to investigate the diagnostic value of some techniques for the evaluation of the mechanism of syncope in patients with MI and BBB and their prognosis. METHODS: We prospectively obtained the results of clinical history, 24 h Holter monitoring, left ventricular ejection fraction (LVEF), signal-averaged ECG (SAECG) and programmed ventricular stimulation in 130 patients with syncope, MI and BBB. 81 of them had right (R)BBB and 49-left (L)BBB. RESULTS: Ventricular tachycardia (VT) was identified as the main cause of syncope in patients with MI and BBB: 68% of them had inducible VT. The sensitivity (se) and specificity (sp) of non sustained VT on Holter monitoring for the detection of VT were respectively 42.5 and 47% in patients with RBBB, 62 and 36% in those with LBBB; se and sp of LVEF <40% were 67.5% and 65% in patients with RBBB, 85 and 9% in those with LBBB; se and sp of the combination of 2 of the 3 SAECG criteria, QRS duration > 155 ms, LAS duration >30 ms and RMS 40 < 17 microV were respectively 50 and 57% in patients with RBBB; se and sp of the combination of 2 of the 3 criteria QRS duration >165 ms, LAS duration >40 ms and RMS 40 <17 microV were 73 and 55.5%) in patients with LBBB. During the follow-up (4.7 years +/- 2.5), 12 patients died suddenly and 12 patients died from heart failure. Univariate and multivariate analysis revealed than only the induction of VT was a significant predictor of sudden death. A long QRS duration (> 165 ms) and induction of VT were independent predictors of total cardiac mortality. CONCLUSION: Among noninvasive studies, only the determination of filtered QRS duration was a significant predictor of cardiac mortality in the case of a prolongation (> 165 ms). Sudden death was only predicted by the induction of sustained VT. Because of the high incidence of inducible sustained VT, the low value of Holter monitoring and decreased LVEF for the prediction of ventricular arrhythmias and the poor prognosis of patients with inducible VT and low LVEF, systematic programmed ventricular stimulation is indicated in patients with MI, syncope and BBB, whatever the non-invasive studies results.     

Impact of diabetes mellitus on the improvement in signal-averaged electrocardiography after coronary artery bypass grafting.

BACKGROUND: Although it has been reported that coronary artery bypass grafting (CABG) for multivessel disease markedly improves several parameters of signal-averaged electrocardiography (SAECG), its beneficial effect on SAECG is variable. The hypothesis of the present study was that the presence of diabetes mellitus (DM) affects the improvement in SAECG after CABG. METHODS AND RESULTS: Pre- and post-operative SAECGs were recorded in 100 consecutive patients who underwent complete surgical revascularization. Changes in the following parameters were compared between the diabetic (n=43) and non-diabetic (n=57) patients: filtered QRS duration (dQRS), root mean square voltage in the terminal 40 s of the QRS complex (RMS40), and duration of the terminal low-amplitude signal lower than 40 microV (LAS40). Although baseline characteristics and the occurrence of late potentials were similar in both groups, quantitative improvements in the SAECG parameters after CABG were significantly greater in non-diabetic than in diabetic patients (dQRS: 109 +/- 22 ms vs 102 +/- 19 ms in diabetics and 106 +/- 21 ms vs 88 +/- 11 ms in non-diabetics; p=0.028, RMS40: 55 +/- 46 microV vs 65 +/- 38 microV in diabetics and 50 +/- 37 microV vs 76 +/- 37 microV in non-diabetics; p=0.037, LAS40: 31 +/- 20 ms vs 26 +/- 17 ms in diabetics and 32 +/- 12 ms vs 17 +/- 8 ms in non-diabetics; p=0.007, respectively). CONCLUSIONS: The presence of DM limits the CABG-induced improvement in SAECG. In diabetic patients, therefore, perioperative changes of the SAECG must be interpreted with caution.     

Quantitative improvement in signal-averaged electrocardiography after coronary artery bypass grafting.

Abnormal signal-averaged electrocardiography (SAECG) reflects slow and heterogeneous myocardial conduction, predicting ventricular arrhythmia and sudden cardiac death in patients with ischemic heart disease. The purpose of this study was to investigate the quantitative effect of coronary artery bypass grafting (CABG) on SAECG, which is still controversial, and to identify the factors that are related to it. Pre- and postoperative SAECGs were recorded in 100 patients who underwent CABG. Compared parameters included filtered QRS duration (dQRS), root mean square voltage in the terminal 40 ms of the QRS complex (RMS40), and duration of the terminal low-amplitude signal less than 40 microV (LAS40). All 3 parameters in SAECG improved significantly after CABG (dQRS: 105+/-21 ms-->99+/-18 ms, RMS40: 55+/-45 microV-->65+/-41 microV, LAS40: 29+/-19 ms-->25+/-12 ms). The improvements in SAECG were greater in patients who underwent complete revascularization and in those without prior myocardial infarction. In conclusion, CABG improved SAECG quantitatively, even in patients with normal SAECG. However, this improving effect was variable and closely related to the presence of prior myocardial infarction and the completeness of revascularization.     

Electrophysiologic testing: predictive of amiodarone efficacy in recurrent sustained ventricular tachycardia?

The role of programmed ventricular stimulation (PVS) was evaluated in 12 patients with recurrent sustained ventricular tachycardia (VT) who were treated with amiodarone as the sole antiarrhythmic agent. At control PVS, sustained VT was induced in 11 patients and nonsustained VT was induced in one patient, as compared with late PVS (mean, 8.6 weeks) when sustained VT was induced in six patients and nonsustained VT was induced in five. Amiodarone significantly prolonged the patients' RR, PR, QRS, and QTc intervals, VT cycle length, and right ventricular effective refractory period. During a mean follow-up of 16 +/- 13.6 months, two patients had recurrent clinical VT. In the patients in whom amiodarone therapy failed (1) sustained VT was induced during late PVS, (2) VT cycle length and symptoms during late PVS and during recurrent clinical VT were similar, and (3) the QTc failed to be prolonged significantly (32.5 +/- 1.6 ms in amiodarone failure vs. 84.1 +/- 27.1 ms in amiodarone success, P<0.05). It is concluded that (1) amiodarone in high-risk patients is clinically effective (88.3%), (2) patients with noninducible VT or nonsustained VT during late PVS did not have recurrent clinical VT, (3) late PVS is probably predictive of electrophysiologic and hemodynamic consequences in patients with recurrent spontaneous VT, and (4) failure of the QTc interval to be prolonged substantially is probably predictive of clinical recurrence of VT.     

Oral amiodarone loading therapy. I. The effect on serial signal-averaged electrocardiographic recordings and the QTc in patients with ventricular tachyarrhythmias

The effect of amiodarone loading (1400 mg/day for 7 days) and maintenance therapy (400 mg/day) on the signal-averaged electrocardiogram (SAECG) and the QTc were evaluated in 14 patients. Daily recordings were taken for the first 7 days of loading and on the ninth, twelfth, fourteenth, and twenty-first day of maintenance therapy. All patients had inducible sustained ventricular tachycardia (VT), 10 of them had late potential (LP) positive recording, and four were LP negative during control measurements. Amiodarone loading significantly changed all SAECG indices and prolonged the QTc. Changes induced by amiodarone were present within 24 hours of administration. The time to reach peak effect varied from 6 to 9 days. The maximum increase in late potential duration (LPD) was threefold greater than the increase in filtered QRS duration or QTc (61% vs 18% vs 14%, respectively), suggesting a more pronounced effect on the reentrant pathway than on the remaining myocardium. Of the four LP negative patients, three became LP positive while receiving amiodarone. In conclusion, amiodarone affects all SAECG indices. However, the magnitude of the changes varies, being most pronounced on the LPD. Amiodarone affects the SAECG and the QTc within the first 24 hours. The time of onset of the peak effect varies from 6 to 9 days. LP negative patients with inducible VT frequently became LP positive during amiodarone therapy.     

Spectral and bidirectional filters give different results for signal-averaged ECG analysis in patients with postmyocardial infarction. GISSI-3 Arrhythmias Substudy Investigators

This study aims at assessing the specific effects of bidirectional filters (BF) and spectral filters (SF) on signal-averaged ECG (SAECG) analysis. The GISSI-3 Arrhythmias Substudy collected SAECGs of 598 patients 10 +/- 4 days after myocardial infarction (MI) from 20 Italian coronary care units. BF and SF were applied on 340 and 258 patients, respectively. QRS duration (QRSD), low amplitude signal duration (LAS40), and root mean-square-voltage (RMS40) were measured with filters set at 40 to 250 Hz. For ventricular late potentials (VLP) detection filter-specific criteria were adopted: QRSD > 114 ms, LAS40 > 38 ms, RMS40 < 20 microV for BF and QRSD > 120 ms, LAS40 > 38 ms, RMS40 < 20 microV for SF. VLP were considered present if any 2 of the criteria were met. The QRSD obtained by BF (100.6 +/- 13 ms) was shorter (P < .0001) than that obtained by SF (109.1 +/- 12 ms). Nevertheless, a higher prevalence of VLP for patients with BF than for patients with SF was found (23.8% vs 16.7%; P < .04). Indeed, filter-specific criteria were able to avoid any differences in the prevalence of abnormal QRSD and LAS40, but not of RMS40 (25.6% vs 17.1%, P < .02). Finally, the difference of VLP prevalence was mainly owing to the higher number of abnormal pairs of RMS40 + LAS40 (58% vs 44%) for BF than for SF. This multicentric study suggests that after MI, BF and SF produce discordant results on low-amplitude signals of filtered QRS that are not avoided by adopting filter-specific criteria. On the contrary, specific criteria seem to be suitable for comparison of QRSD between different SAECG devices in post-MI patients.     

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.     

Flecainide-related alterations in the signal-averaged electrocardiogram: similarity between patients with or without ventricular tachycardia.

The signal-averaged electrocardiogram (SAECG) identifies patients at risk of sustained ventricular tachycardia (VT), but the influence of anti-arrhythmic agents on the SAECG is not yet established. We have evaluated the effects of flecainide on the SAECG (XYZ leads, high-pass filters 25 Hz and 40 Hz, noise level 0.2 microV-0.4 microV, Model 1200 EPX, ART) in 25 patients: 15 (VT group) had documented sustained VT (nine post-MI, two dilated cardiomyopathy, four normal hearts) and 10 (control group) had supraventricular arrhythmias and structurally normal hearts. The SAECG was recorded in all patients prior to, and 5 min following a flecainide infusion (2 mg.kg-1 over 10 min). Before flecainide administration an abnormal SAECG was recorded in six patients from the VT group and in no control patient. Following flecainide, 13 patients from the VT group and eight control subjects demonstrated abnormal SAECG. Flecainide produced similar significant percentage changes in all SAECG indices in both the VT and control groups: total QRS duration was prolonged by 26.0 +/- 10.4% vs 26.7 +/- 15.7%, late potential duration under 40 microV was prolonged by 55.5 +/- 62.0% vs 106.1 +/- 61.4%, and the root mean square voltage of the last 40 ms of the QRS was reduced by 42.1 +/- 34.9% vs 55.3 +/- 24.4%, respectively. We conclude that flecainide significantly changes the SAECG parameters in patients with and without a history of VT, irrespective of the underlying disease.     

Effect of complete bundle-branch block on the averaged signal of high amplification electrocardiogram

Intraventricular conduction defects delay ventricular activation and change the appearances of the signal averaged electrocardiogram. The aim of this study was to determine criteria capable of identifying patients with bundle branch block at high risk of ventricular tachycardia (VT). Two hundred and twenty four patients were studied by Simson's method. One hundred and twenty eight patients (Group I control) had narrow QRS complexes and sequellae of previous myocardial infarction. Eighty four patients had no clinical or inducible VT; 44 had clinical and/or inducible VT with programmed stimulation. Forty six patients (Group II) had complete right bundle branch block (RBBB); 30 had no VT and 16 had VT. Twenty seven patients (Group III) had complete left bundle branch block of whom 18 had no VT and 9 had VT. Twenty three patients (Group IV) had RBBB with operated tetralogy of Fallot; 16 had no VT and 7 had VT. In the control group, the results of signal averaged ECG were the same as those reported in the literature: prolongation of the duration of the averaged QRS (136 +/- 35 ms vs 104 +/- 14 ms), decrease in amplitude of the last 40 ms (11 +/- 15 microV vs 43 +/- 28 microV) and an increase in the duration of less than 40 microV terminal activity (53 +/- 30 ms vs 28 +/- 11 ms) in those subjects with VT compared to those without VT. In Groups II, III and IV no significant difference was found in the amplitude of the last 40 ms or duration of less than 40 microV activity between patients with and without VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Quantitative analysis of ventricular late potentials in healthy subjects

Signal averaging is a technique that improves the signal-to-noise ratio. Obscuring random noise, it allows the detection of low-amplitude wave forms in the terminal portion of the QRS complex, also known as ventricular late potentials. A higher incidence of arrhythmic events has been found in patients with abnormal ventricular late potentials after an acute myocardial infarction. Few studies have been conducted in healthy subjects to assess normal values. Sixty-one healthy subjects were enrolled in our study (33 men and 28 women). The results (mean +/- standard deviation) are as follows: duration of the filtered QRS (QRS duration) was 95 +/- 10 ms; duration of the low-amplitude signals in the terminal portion of QRS less than 40 microV (LAS less than 40) was 32 +/- 8 ms; and root-mean-square voltage in the last 40 ms (RMS - 40) was 33 +/- 16 microV. A significant difference was noted in QRS duration between men and women (98 +/- 11 vs 92 +/- 6 ms, p = 0.006); no difference was found in LAS less than 40 (31 +/- 8 vs 34 +/- 8 ms) and in RMS-40 (36 +/- 17 vs 30 +/- 13 microV). QRS duration confidence limits of 95% were less than or equal to 114 ms for the total group, less than or equal to 120 ms for men and less than or equal to 104 ms for women. Normalization of QRS duration for height (normal value less than 66 ms/m) eliminated any difference between men and women.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison between QRS duration at standard ECG and signal-averaging ECG for arrhythmic risk stratification after surgical repair of tetralogy of fallot

INTRODUCTION: Surgical repair of tetralogy of Fallot is complicated by the occurrence of ventricular tachycardia (VT). Among different indexes proposed to assess prognosis of these patients, the study of QRS and repolarization provided useful information. Controversial results come from the analysis of signal-averaging ECG (SAECG). The aim of our study was to identify patients operated for tetralogy of Fallot at higher risk of sudden death by means of SAECG. METHODS AND RESULTS: Sixty-six consecutive patients, mean age 26 +/- 10 years, were studied 17.7 +/- 5.8 years after total correction for tetralogy of Fallot using standard ECG, 24-hour Holter recordings, SAECG, and echocardiography. The following variables were measured: standard QRS duration, filtered QRS duration (fQRS), high-frequency and low-amplitude signal duration (HFLA), root mean square of the mean voltage in the terminal portion of filtered QRS (RMS), left and right end-diastolic volumes, and ejection fractions. During a mean follow-up period of 7.3 +/- 3.1 years, 12 patients had episodes of sustained VT and two of them suddenly died. All patients had complete right bundle branch block. Patients with VT were characterized by a significantly longer fQRS duration at all filter settings. On the contrary, there was no difference in standard QRS duration in patients with or without VT. At a multivariate analysis, left ventricular ejection fraction and fQRS were independent predictors for VT. CONCLUSIONS: A longer fQRS duration is associated with an increased risk in developing malignant ventricular arrhythmias in asymptomatic patients after total correction of tetralogy of Fallot.     

Use-dependent electrophysiologic effects of amiodarone in coronary artery disease and inducible ventricular tachycardia.

Amiodarone produces use-dependent block of cardiac sodium channels in vitro. This study assessed whether similar use-dependent block occurred in 19 patients with coronary artery disease and inducible, sustained, monomorphic ventricular tachycardia treated with amiodarone. Beat-to-beat measurements of ventricular paced QRS durations during 12-beat trains at cycle lengths of 700, 600, 400 and 300 ms were analyzed at a baseline antiarrhythmic drug-free study and after 2 and 10 weeks of amiodarone therapy. At the drug-free study, there were no significant changes in paced QRS durations within the 12-beat trains at any pacing cycle lengths. After 2 and 10 weeks of amiodarone therapy, progressive prolongation of paced QRS durations occurred over the 12-beat trains at pacing cycle lengths of 600, 400 and 300 ms (p less than 0.05). Significant changes in QRS duration were not observed at a pacing cycle length of 700 ms. This progressive prolongation in QRS duration can be fitted as a function of beat number to a monoexponential equation and occurred with an onset time constant of 1.02 +/- 0.41 beats (306 +/- 122 ms) at a pacing cycle length of 300 ms. The magnitude of QRS prolongation increased as the pacing cycle length was shortened. The magnitudes of QRS prolongation were similar after 2 and 10 weeks of amiodarone therapy. In conclusion, use-dependent prolongation in QRS duration occurs at rapid pacing cycle lengths in humans receiving amiodarone.     

Ventricular Late Potentials Are Associated with the Presence of Viable Myocardium After Anterior Myocardial Infarction

Background: The aim of the study was to evaluate the relationship between myocardial viability (MV) detected by Tl‐201 rest/redistribution protocol (RR‐SPECT) and the presence of ventricular late potentials (VLPs) in acute myocardial infarction (AMI). We analyzed signal‐averaged ECGs (SAECGs) in 28 patients (age 57 ± 10 years) with a first anterior AMI within 48 hours of symptoms (SAECG1) and prior to discharge (SAECG2). VLPs were defined according to the presence of filtered QRS (QRS‐D) > 114 ms and duration of low amplitude signals (LAS) a 30 ms or root mean square voltage (RMS40) < 25 μ;V, using a 25‐Hz filter, or a duration of LAS > 39 ms or RMS40 < 20 μ;V, using a 40‐Hz filter. RR‐SPECT was performed 17 ± 6 days after AMI. Segments were considered viable when counts were > 60% in early images or when a fill‐in > 10% was detectable on delayed images of those segments with a first count between 31% and 59%. Methods: Patients were divided into two groups: with MV (group 1 = 16 patients) if almost one third of segments appeared to be viable; without MV (group 2 = 12 patients). No difference was found between the two groups in SAECG1, whereas, using a 25‐Hz filter, a greater QRS‐D (106.6 ± 13.5 vs 93.5 ± 6 ms) and LAS (31.2 ± 8.7 vs 18.1 ± 6.4 ms) as well as a smaller RMS40 (43 ± 33.5 vs 71.3 ± 30.4 μ;V) characterized the SAECG2 of group 1. Sensitivity and specificity of VLPs in detecting MV were 31% and 100%. When using cut‐off values derived from median distribution of the population (QRS‐D & 99 ms, LAS a 24 ms and RMS40 > 51 μ;V), sensitivity raised to 75% and specificity was 92% with a positive and negative predictive value of 92% and 73%. Conclusions: The presence of MV is associated with a greater incidence of VLPs. SAECG performed at the time of discharge may facilitate the identification of patients with μ;V after anterior AMI.     

Comparison of individual and combined effects of procainamide and amiodarone in patients with sustained ventricular tachyarrhythmias

To compare the individual and combined electrophysiological effects of amiodarone and procainamide, 35 patients with sustained ventricular arrhythmias underwent programmed stimulation in the control state, after procainamide (mean concentration, 8.7 +/- 2.8 micrograms/ml), after 13 +/- 2 days of amiodarone (1,400 mg/day x 7 days, then 400 mg/day), and after amiodarone with procainamide (mean procainamide concentration, 7.8 +/- 2.2 micrograms/ml). Sustained ventricular tachycardia (VT) was inducible in all 35 patients during treatment with procainamide alone and with amiodarone alone. Procainamide and amiodarone similarly increased the VT cycle length (+68 vs. +61 msec), the corrected QT interval (+63 vs. +49 msec), and the ventricular effective refractory period measured at paced cycle lengths of 600-550 msec (+23 vs. +21 msec) and 400 msec (+25 vs. +23 msec). Procainamide had a more pronounced effect on QRS duration than amiodarone during sinus rhythm (+18 vs. +8 msec, p less than 0.01) and during paced cycle lengths of 600-550 msec (+32 vs. +23 msec, p less than 0.01) and 400 msec (+37 vs. +28 msec, p less than 0.1) but a similar effect on the QRS duration during VT (+32 vs. +29 msec). During combination therapy, VT initiation was prevented in only two (6%) patients. The combination therapy produced a greater increase (p less than 0.001) than individual therapy in all the electrophysiological intervals assessed, with the exception of the sinus cycle length. On each drug regimen, a cycle length-dependent increase (p less than 0.05) in paced QRS duration was noted (400 more than 600-550 msec).(ABSTRACT TRUNCATED AT 250 WORDS)     

A comparison of standard and high-dose regimens for the initiation of amiodarone therapy.

The effects of two regimens for the initiation of amiodarone therapy were compared in 92 patients with inducible sustained ventricular tachycardia (VT) at baseline electrophysiologic testing. Two groups of 46 patients each received a total of 16.8 gm of oral amiodarone before follow-up electrophysiologic testing. Group A (standard dose) received 1200 mg/day for 14 days, and group B (high dose) received 2400 mg/day for 7 days. Amiodarone suppressed the induction of sustained VT in six subjects (13%) in group A versus 10 (22%) in group B (p = NS). In subjects who continued to have inducible VT after amiodarone loading, the mean increase in cycle length of induced VT was similar in group A (delta = 85 +/- 73 msec) and group B (delta = 78 +/- 59 msec). The mean increase in sinus cycle length, AH and HV intervals, paced QRS duration, and ventricular refractory periods was also not significantly different between the two groups. Side effects developed in 10 (22%) patients in group B but were serious only in one, and one patient required a reduction in dosage. Thus compared to the 14-day standard-dose regimen, the 7-day high-dose regimen was well tolerated and had similar effects on VT inducibility and electrophysiologic variables. Its use may significantly shorten the duration of hospitalization in patients with life-threatening inducible VT who are undergoing loading with amiodarone on an inpatient basis.     

Value of electrophysiologic studies in hypertrophic cardiomyopathy treated with amiodarone

The relation of electrophysiologic effects of amiodarone to long-term outcome was studied in 35 patients with hypertrophic cardiomyopathy (HC). Indications for electrophysiologic studies were: cardiac arrest (n = 3), syncope/presyncope (n = 27) and asymptomatic ventricular tachycardia (VT) (n = 5). Twenty-eight patients (80%) had VT, 3 (9%) atrial tachycardia and 3 (9%) paroxysmal atrial fibrillation during 24-hour Holter monitoring. The studies were repeated after a total amiodarone dose of 58 +/- 122 g and during a maintenance median daily dose of 400 mg. Amiodarone abolished paroxysmal atrial arrhythmias in all 6 patients. However, it caused marked atrioventricular nodal conduction abnormality in 3 patients and heart block or marked HV interval prolongation (to greater than or equal to 100 ms) in 4 patients. Sustained VT was induced in 26 patients (74%) at baseline study and in 23 patients (66%) taking amiodarone therapy. With amiodarone, VT was no longer inducible or was more difficult to induce in 11 patients (31%), and the drug abolished VT during Holter monitoring in all patients. However, VT was easier to induce with amiodarone or was induced only with amiodarone in 18 (51%) patients. Amiodarone significantly slowed the rate of induced VT (from 248 +/- 29 to 214 +/- 37 beats/min, p less than 0.001). This was associated with a change in its morphology from polymorphic to monomorphic VT in 7 patients. During a follow up of 18 +/- 14 months (range 2 to 56), amiodarone was discontinued because of adverse effects in 8 patients (23%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of pre-infarction angina on ventricular late potentials in patients with acute myocardial infarction and successful thrombolysis

OBJECTIVE: Pre-infarction angina is considered as a good clinical model of ischaemic preconditioning which facilitates myocardial protection. Late potentials (LP) have prognostic significance following acute myocardial infarction (AMI). It is also well established that thrombolytic therapy reduces the incidence of LP. Our aim was to evaluate the relationship between pre-infarction angina and LP in patients receiving successful thrombolytic therapy. METHODS AND RESULTS: We prospectively studied 55 patients presenting with AMI (<6 hours). All patients received thrombolytic therapy and were evaluated with coronary angiography at predischarge. Signal-averaged recordings (SAECG) were obtained serially prior to thrombolysis, 48 hours after and 10 days later. Pre-infarction angina was present in 14 (25%) patients. There were no significant differences between the clinical characteristics and angiographic findings of the groups. Baseline SAECG parameters of the groups were also similar. After thrombolysis, the 48th hour values of LAS (the duration of the terminal low amplitude signals), and both the 10th day values of LAS and RMS (root mean square voltage of the last 40 ms of the QRS) were significantly better in the pre-infarction angina group. The mean filtered QRS duration and RMS 40 values changed significantly at the 10th day recordings of patients with pre-infarction angina [QRS duration, 110+/-34 ms before to 91+/-11 ms after (p = 0.039); RMS 40, 40+/-17 microV before to 50+/-14 microV after (p = 0.02)]. The incidence of LP significantly decreased after thrombolytic therapy in the pre-infarction angina group, however, this change was not observed in patients without angina. CONCLUSION: Presence of pre-infarction angina reduces the incidence of LP following thrombolysis in AMI. This might be explained by the possible beneficial effect of ischaemic preconditioning on the arrhythmogenic substrate.     

Recording of abnormal late ventricular activity by high-resolution magnetocardiography

High-resolution magnetocardiography (HR-MCG) is a new noninvasive technique for detection of very low-amplitude magnetic fields generated by the electric activity of the heart. We studied 11 patients with documented sustained ventricular tachycardia after myocardial infarction (VT group), 11 patients with old myocardial infarction without ventricular tachycardia (MI group) and 11 normal controls (N group) with HR-MCG and high-resolution electrocardiography (HR-ECG). After averaging and high-pass filtering (25 Hz, 40 Hz, 60 Hz and 80 Hz) the XYZ leads of HR-ECG were combined to vector magnitude and the magnetic recordings from 3 × 3 grid locations were enveloped with Hilbert transformation. Then the QRS duration and the root-mean-square (RMS) amplitude of the last 40 ms, 50 ms and 60 ms of the QRS were calculated. The QRS duration was significantly longer in the VT group compared to the MI and the N group both in HR-MCG and HR-ECG. Also the RMS values were clearly smaller in the VT group with both methods. There were no significant differencies in the diagnostic power of these two methods. The 25 Hz high-pass filtering separated best the VT group from the MI group and the N group. In conclusion HR-MCG is a new non-invasive method for identification of patients at risk of malignant ventricular arrhythmias after myocardial infarction.Abbreviations HR-ECG high-resolution electrocardiography - HR-MCG high-resolution magnetocardiography - LAS low amplitude signal - LF late fields - LP late potentials - MI myocardial infarction - RMS root-mean-square - VT ventricular tachycardia     

Clinical efficacy and electropharmacology of continuous intravenous amiodarone infusion and chronic oral amiodarone in refractory ventricular tachycardia

The clinical efficacy and electropharmacologic effects of continuous intravenous (i.v.) amiodarone infusion (10 to 20 mg/kg/day for 4 to 7 days) followed by chronic oral amiodarone therapy (400 to 800 mg/day for 24 to 53 days) were evaluated in 17 patients with refractory sustained ventricular tachycardia (VT) or ventricular fibrillation. Intravenous amiodarone infusion prolonged the RR interval (from 754 +/- 85 to 860 +/- 157 ms, p less than 0.05), PR interval (from 192 +/- 53 to 212 +/- 54 ms, p less than 0.01) QRS duration (from 103 +/- 21 to 117 +/- 25 ms, p less than 0.001) and QTc interval (from 423 +/- 22 to 466 +/- 31 ms, p less than 0.001). Chronic oral amiodarone treatment had similar but more pronounced effects on electrocardiographic intervals. The ventricular effective refractory period tended to prolong after i.v. amiodarone infusion (p less than 0.1 to greater than 0.05) but prolonged significantly after chronic oral amiodarone (p = 0.025). Mean serum amiodarone concentration was 1.7 +/- 1.0 mg/liter with infusion and 1.5 +/- 0.6 mg/liter with oral therapy. Intravenous amiodarone infusion suppressed spontaneous VT in 5 of 9 patients with frequent VT recurrences, but had no effect on cycle length of spontaneous VT. Chronic amiodarone therapy either suppressed spontaneous VT recurrences or prolonged cycle length during VT recurrences. VT induction after i.v. amiodarone was not predictive of VT induction or spontaneous VT recurrences after chronic oral amiodarone treatment. Thus, i.v. amiodarone has limited value in acute control of VT and clinical or electrophysiologic response to it is not predictive of long term therapeutic results with amiodarone.     

Results of signal-averaged electrocardiography and electrophysiologic study in patients with nonsustained ventricular tachycardia after healing of acute myocardial infarction

Programmed stimulation and signal-averaged electrocardiography were performed in 43 consecutive patients with nonsustained ventricular tachycardia (VT) after healing of inferior (29 patients) or anterior wall (14 patients) acute myocardial infarction. Twenty-two patients had inducible sustained VT. Patients with inferior infarction and inducible sustained VT had significantly longer filtered QRS durations (125 +/- 19 vs 112 +/- 15 ms, p less than 0.01) and significantly lower voltage in the last 40 ms of the filtered QRS complex (19 +/- 5 vs 30 +/- 14 microV, p less than 0.05) than those without inducible sustained VT. In contrast, the signal-averaged electrocardiographic measurements in patients with anterior infarction and inducible sustained VT did not differ significantly from those without inducible sustained VT. The results of these studies were compared with those of 2 control groups: 45 patients without ventricular arrhythmias after myocardial infarction and 95 patients with spontaneous and inducible sustained VT after myocardial infarction. The signal-averaged electrocardiographic measurements in patients with spontaneous nonsustained VT after inferior infarction were intermediate between the control group without arrhythmias and the control group with sustained VT. The signal-averaged electrocardiograms in patients with nonsustained VT after anterior infarction were not significantly different from those in patients without ventricular arrhythmias. The study shows that the site of infarction influences the signal-averaged electrocardiogram in patients with VT after myocardial infarction. The signal-averaged electrocardiogram may be useful in identifying patients with nonsustained VT after a remote inferior myocardial infarction who have inducible sustained VT.