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Biomedical subjects

D Beurrier

Publications and source records attributed to D Beurrier.

At least 55 records · Page 3Linked to original sources
PubMed1997

Hypertrophic cardiomyopathy: value of atrial programmed electrical stimulation in patients with or without syncope with special reference to the role of atrial arrhythmias.

Hypertrophic cardiomyopathy may be associated with both supraventricular and ventricular arrhythmias, which may play a role in the genesis of syncope. The aim of this study was to assess the findings of electrophysiological study and programmed atrial and ventricular stimulation and their possible role in syncope. Programmed atrial and ventricular stimulation using up to two extrastimuli in right atrium and three in right ventricle at three cycle lengths (600, 400 ms and spontaneous) was systematically performed in 56 patients with hypertrophic cardiomyopathy. Thirty seven had unexplained dizzinesses or syncopes (group I) and 19 did not present loss of consciousness (group II). Patients with syncopes had a higher prevalence of induced sustained supraventricular tachyarrhythmia (73%) than those of group II (16%) (P<0.05). Inducible supraventricular tachycardia was the only finding in 16 patients with syncopes. During the follow-up (3 years+/-6 months), empirical antiarrhythmic therapy suppressed the symptoms, except in two patients who developed atrial fibrillation despite therapy. The high incidence of inducible atrial tachycardia of these patients was not correlated with particular Holter findings or echocardiographic data. However, their mean age was rather high (58+/-12 years). In conclusion, atrial tachyarrhythmias may play a role in syncopes of middle-aged patients with hypertrophic cardiomyopathy. Moreover programmed atrial stimulation is an useful means to identify this syncope mechanism.

Adult↗
PubMed1997

Relationships between heart rate variability and antiarrhythmic effects of hydroquinidine.

Class I antiarrhythmic drugs may increase the incidence of cardiac death, and controlled treatment is required in patients with severe ventricular arrhythmias. Electrophysiologically guided antiarrhythmic therapy remains an important method to manage patients with sustained ventricular tachycardia (VT). The purpose of the study was to evaluate the correlations between baseline heart rate variability in ambulatory electrocardiographic recordings of patients with sustained ventricular tachycardia and the response to hydroquinidine on VT inducibility, and to look for the changes in heart rate variability during hydroquinidine treatment. Thirty-five patients with spontaneous and inducible sustained VT were studied. Programmed ventricular stimulation and time and frequency domain analysis of heart rate variability were studied in the control state and 9-12 days after treatment with 300-600 mg of hydroquinidine. In 11 patients (group I), hydroquinidine prevented VT induction. In 24 patients (group II), sustained VT remained inducible during treatment with hydroquinidine. In the control state, heart rate variability was similar in both groups. During treatment with hydroquinidine, heart rate variability tended to decrease in groups I and II, but the changes were significant only in group II: the coefficient of variance (CV) decreased from 13 +/- 4% to 10% +/- 3% (p < 0.01) and low frequency/high frequency amplitude ratio decreased from 4.6 +/- 3.3 to 2.87 +/- 2.42 (p < 0.05). In conclusion, baseline heart rate variability does not differentiate the responders and nonresponders to hydroquinidine. Hydroquinidine decreases heart rate variability in all patients, but principally in those with still inducible VT.

Adult↗
PubMed1997

Effects of radiofrequency catheter ablation on patients with permanent pacemakers.

The objective of this study was to assess the effects of radiofrequency energy application on implanted pacemaker functions. Radiofrequency (RF) catheter ablation may cause pacemaker dysfunction due to electromagnetic interferences. The effects of RF on pacemaker behavior were studied in a series of 38 pacemakers, implanted 18 +/- 26 months prior to a RF procedure using either a right ventricular approach (AV node ablation, n = 35) or a left ventricular approach (left concealed accessory pathway ablation, n = 1; VT ablation, n = 2). The 38 patients (mean age 65 +/- 9 years) included 20 men and 18 women. Before energy applications, the 23 different pacemaker models were programmed to the VVI mode at the lowest available rate. The continuous surface ECG was recorded throughout the procedure. Thorough testing of the devices was performed before and after each RF delivery. Unusual pacemaker responses occurred in 20 of the 38 cases studied (53%). The impact of RF delivery was unpredictable, and variable dysfunctions were observed at different times for a given patient or could vary for a given model. Unusual pacemaker responses included pacemaker inhibition (n = 8), untoggled backup mode (n = 3), electromagnetic interference noise mode (n = 3), temporary RF-induced pacemaker tachycardia (n = 2), erratic behavior (n = 1), oversensing of RF onset and offset (n = 8), and transient loss of ventricular capture, (n = 1). Postablation, most devices automatically toggled back to full functionality. The three devices in the untoggled backup mode had to be reprogrammed to obtain normal operations. At the end of the procedure, pacing thresholds remained unchanged in all but one patient, in whom the increase in ventricular threshold was due to a nicked lead. In conclusion, implanted pacemakers frequently exhibit transient, unpredictable responses to RF energy application. Although all pacemaker functions were restored postablation, some devices had to be reset manually. The anomalies observed during the RF application argue for the simultaneous use of an external pacemaker in pacing-dependent patients.

Adult↗
PubMed1997

Influence of late reopening of the infarct-related artery on left ventricular remodelling after myocardial infarction. IRIS Study Group.

AIMS: This trial was undertaken to assess the impact of late reopening of the infarct-related artery on left ventricular remodelling in post-myocardial infarction patients. METHODS: One hundred and fifty seven patients with recent myocardial infarction were routinely submitted to delayed (second week) catheterization. They also underwent systematic angioplasty of a significantly narrowed infarct-related artery with a suitable anatomy, or reopening of a totally occluded infarct-related artery, and repeat follow-up catheterization after 4 months. Changes in left ventricular ejection fraction, left ventricular volumes, and percent of regional hypokinesia were assessed over the study period. RESULTS: One hundred and thirty-two patients had two interpretable left ventriculograms and two interpretable coronary angiograms. At initial angiography, 56 out of 96 patients with a patent infarct-related artery were successfully submitted to percutaneous coronary angioplasty, of whom 25 had restenosis and eight had total reocclusion at follow-up angiography. Percutaneous transluminal coronary angioplasty was not attempted in the remaining 40 patients due to unsuitable anatomy in 18 or a nonsignificant lesion in 22. The infarct-related artery was totally occluded in 36 patients at initial angiography, and successfully reopened by means of angioplasty in 19, of whom seven showed a reocclusion at follow-up angiography. The independent predictors of left ventricular enlargement, identified by means of multivariate regression analysis, were initial stroke volume index < 40 ml.m-2 (odds ratio = 6.3, 95% confidence interval = [2.5; 16.6]), initial end-systolic volume index > 50 ml.m-2 (odds ratio = 7.1, 95% confidence interval = [1.5; 25.8]), anterior infarct location (odds ratio = 4.1, 95% confidence interval = [1.4; 11.5]) and reocclusion of the infarct-related artery (odds ratio = 7.3, 95% confidence interval = [1.3; 27.3]). Angioplasty of a patent but significantly narrowed infarct-related artery was not found predictive. CONCLUSIONS: This study demonstrates that reocclusion of a previously open infarct-related artery, as well as the initial low stroke volume index, enlarged end-systolic volume index and anterior infarct location are independent predictors of long-term left ventricular enlargement. These results emphasize the impact of long-term sustained patency of the infarct-related artery on the prevention of left ventricular dysfunction. The need for a larger randomized trial is recognised.

Adrenergic beta-Antagonists↗
PubMed1997

[Quinidine and high-amplification ECG].

High-amplification ECG (HA ECG) is now used routinely to evaluate ventricular tachycardia. The effects of 300 to 600 mg quinidine were determined in 26 heart disease patients with spontaneous and inducible ventricular tachycardia. Programmed ventricular stimulation was performed and an HA ECG recorded (40 Hz high-pass filter) before and under treatment. The stimulation became negative under treatment in nine patients (group I), whereas the 17 others had persistent inducible tachycardia (group II). HA ECG tracings were modified in groups I and II, with a QRS duration increase of 7% and 8%, respectively, and RMS 40 decrease of 37% and 29%, and an LAS increase of 16% and 17%. Furthermore, one of the three group I and four of the seven group II patients who had a normal HA ECG tracing before treatment developed HA ECG abnormalities under treatment. An arrhythmia-inducing effect of the treatment was noted in three group II patients; this effect was not detected by HA ECG. In conclusion, changes in HA ECG tracings were seen during quinidine therapy of patients with ventricular tachycardia, and this effect was independent from the effect of antiarrhythmic agents on induction of the ventricular tachycardia. In addition, abnormalities of high-amplification ECG tracings developed in some patients under quinidine therapy. These data suggest that class I antiarrhythmic agents modify high-amplification ECG tracings and that these modifications fail to predict whether the treatment will prove effective.

Adult↗
PubMed1997

[Possible mechanisms of false positive results of averaged ECG].

UNLABELLED: The objective of this retrospective study was to investigate the causes of high amplification (HA) ECG abnormalities detected in apparently healthy subjects. This study was based on 14 patients derived from a population of 167 admitted for assessment of malaise or supraventricular tachycardia and who had no apparent heart disease. The surface ECG showed fine QRS complexes (< 120 ms) with no left hemiblock on ECG. All of these subjects underwent a complete electrophysiological study and high amplification ECG using a 40 Hertz high-pass filter. For these 14 patients, the amplitude of the last 40 milliseconds (ms) of the mean QRS (RMS 40) was less than or equal to 20 microvolts (microV). Eight of them also had a duration of the terminal part of the QRS complex less than 40 microV (LAS) greater than 40 ms and 6 others had and LAS greater than 35 ms. The mean QRS interval was normal in all patients (< 120 ms). The usual causes for reduction of the RMS 40-were eliminated: programmed ventricular pacing using 3 extrastimuli under basal conditions and with isuprel remained negative. E chocardiography and the right ventricular angiography were normal. The surface ECG showed slight abnormalities: absence of Q wave in V6 without delay of the intrinsic-like deflection in 3 subjects, increased R wave in V1 in 2 subjects and especially deep S wave in V5-V6 with no left axis deviation in 10 patients. Programmed or increasing frequency atrial pacing induced RBB or LBB in 13 of these 14 subjects (RBB: 7, LBB : 3, RBB and LBB:3). Follow-up, ranging from 6 months to 3 years, did not reveal any cardiac events, but signs of RBB appeared in 3 patients and signs of LBB were observed in 1 patient. IN CONCLUSION: an abnormal high amplification ECG in apparently healthy subjects could be explained by minor conduction disorders essentially in the right branch. The presence of a deep S wave (> 2 mm) in V5-V6 is the commonest ECG sign in these subjects. This diagnosis can only be proposed after exclusion of right ventricular dysplasia in symptomatic patients.

Adult↗
PubMed1997

[Influence of anti-arrhythmia agents on heart rate variability].

UNLABELLED: Since analysis of heart rate variability (HRV) is able to identify subjects at risk of sudden death and as antiarrhythmics can interfere with this prognosis, the objective of this study was to determine whether antiarrhythmics (AA) modified the HRV measured on a 24-hour Holter recording and after rapid ventricular stimulation and whether the initial HRV and its possible modification during treatment with AA were correlated with the results of AA treatment in patients with ventricular tachycardia (sustained VT). The HRV was studied in 50 patients with heart disease and spontaneous sustained VT, reproduced by programmed ventricular stimulation. This analysis was performed at baseline with antiarrhythmic treatment consisting of low-dose beta-blocker and quinidines in 26 patients (group I) or amiodarone in 24 patients (group II). Treatment was effective (i.e. prevented induction of VT) in 9 patients in group I (group la) and 5 patients in group II (group IIa). Treatment was ineffective in the other 17 patients of group I (group Ib) and 19 patients of group II (group IIb). The initial HRV was similar in the patients of groups Ia and Ib or groups IIa and IIb. Temporal analysis did not reveal any significant variation of HRV during AA treatment. In contrast, spectral analysis of HRV and the HRV observed during ventricular stimulation demonstrated a significant reduction of this parameter (p < 0.05 for groups I and II combined). IN CONCLUSION: the initial HRV is not predictive of the results of treatment. Quinidines and amiodarone tend to decrease HRV regardless of the effect of the AA on the prevention of VT.

Adrenergic beta-Antagonists↗
PubMed1997

[Can 1/1 atrial flutter be foreseen by class I anti-arrhythmics?].

1/1 atrial tachycardia or "quinidine" flutter under class I antiarrhythmic drugs is a serious complication of these agents which, unfortunately, cannot be anticipated. The aim of this study was to review the cases of 11 patients who had suffered this complication of class I antiarrhythmic therapy to see if it could have been prevented. All drugs of this class were included. The 11 subjects were aged 57 to 78: 7 had no apparent underlying cardiac disease and the others had valvular (n = 1), hypertensive (n = 1) and ischaemic (n = 2) heart disease. They were treated for episodes of paroxysmal atrial fibrillation or tachycardia. In the absence of treatment, 7 patients had a short PR interval on the ECG (PR between 0.11 and 0.14 s). In the other 4, the PR interval was normal (0.16 to 0.20 s), but the P wave was widened with appearances of left atrial hypertrophy or an intra-atrial conduction defect. High amplification ECG performed in 3 patients showed continuity of atrial and ventricular depolarisation. Atrial stimulation showed excellent nodal conduction with a Wenckebach point of 200/min. The authors conclude that a short PR interval is predisposing factor to 1/1 atrial tachycardia with class I antiarrhythmics. High amplification ECG which allows identification of the end of the P wave with respect to the QRS complex could help identify subjects at risk when the P wave is widened and that, consequently, the PR interval appears to be normal.

Aged↗
PubMed1997

[Analysis of heart rate variability before and at the moment of cardiac death].

The study of heart rate variability is a new means of assessing autonomic nervous system function and the risks of cardiac and sudden death in patients with advandec cardiac disease. The aim of this study was to analyse changes in heart rate variability in the hours preceding cardiac death and just before its occurrence. Seventeen subjects aged 78.5 +/- 10 years, with advanced cardiac disease responsible for a reduction of left ventricular ejection fraction below 40%, died during Holter ECG recording. Ten died of ventricular fibrillation, 5 of bradycardia and 2 of non-rhythmic causes. General analysis of heart rate variability showed a decrease in all but 1 patient, the average standard deviation of normal RR intervals in subjects in sinus rhythm being 53 +/- 14 msec and the fractioned spectral power (low frequency/high frequency power) being 1 +/- .07. The change in heart rate variability did not allow prediction of the mechanism of death: the mean heart rate only increased before death in 3 of the patients with an ischaemic component in the hours before death, the indices of vagal tone were very low in the majority of patients and, just before death, a disequilibrium between the spectral powers with a sudden increase in LF/HF ratio of 10 of the 17 patients, irrespective of the cause of death, appeared. In conclusion, a decrease in heart rate variability was observed in all cases but did not predict the mechanism of death. Just before death occurred, some patients, especially those with acute ischaemia, showed a sudden change in the indices of heart rate variability indicating a terminal vaso-sympathetic disequilibrium.

Aged↗
PubMed1997

[Long-term reproducibility of programmed atrial stimulation].

Programmed atrial stimulation is a technique increasingly used to assess different pathologies but the reproducibility of the results is totally unknown. The aim of this study was to determine its reproducibility. Two electrophysiological studies were undertaken without antiarrhythmic therapy in an interval of one to three months (average 18 months) in 48 patients. The programmed atrial stimulation used 1 and 2 extrastimuli delivered in sinus rhythm and then three paced rhythms (sinus cycle -10%, 600 ms, 400 ms). Twenty-one patients had documented atrial arrhythmias (atrial fibrillation n = 13, flutter n = 3 or tachycardia n = 5) (group 1) and the 27 other patients had no spontaneous arrhythmias (group II). In group I, clinical tachycardial was reproduced in 18 patients during the initial stimulation procedure. During the second investigation, 17 remained inducible and in the 3 in whom stimulation was negative, it remained so in 2 of the cases. The reproducibility was therefore 90%. In group II, 12 patients had inducible sustained (for over 1 minute) tachycardia during the first procedure (44%) but this only remained inducible in 6 patients. In the other 15 subjects, stimulation was negative during the first procedure but 7 of them had inducible tachycardial during the second procedure. The reproducibility of the technique was therefore only of 52%. The authors conclude that the reproducibility of programmed atrial stimulation in patients with documented spontaneous paroxysmal arrhythmias is excellent. However, the reproducibility is mediocre in subjects without spontaneous arrhythmias and the induction of tachycardial in this group of patients should be interpreted with caution given the variability of the response to programmed atrial stimulation.

Adolescent↗
PubMed1997

[Prognostic value of serial electrophysiological tests in inducible sustained ventricular tachyarrhythmias].

The authors report the results of a study evaluating serial electrophysiological tests on a series of 166 patients with inducible sustained ventricular tachyarrhythmia. The initial electrophysiological investigation was indicated because of sustained ventricular arrhythmias documented in 95 patients or suspected in 71 symptomatic patients. Serial tests allowed identification of a protective antiarrhythmic treatment (non-inducible ventricular tachycardia) in 74 responding patients (44.6%) (group R) after 1.3 +/- 0.5 therapeutic trials versus 1.8 +/- 0.8 inconclusive trials in 92 non responding patients (group NR). Multivariate analysis demonstrated the absence of any underlying ischaemic heart disease (p < 0.01) and the presence of spontaneous ventricular fibrillation (p < 0.01) as independent predictive factors of success during serial testing. A follow-up of 43 +/- 29 months was available for 151 patients (91%). kaplan-Meier survival curves showed a better long-term prognosis for group R with survival rates of 97%, 87% and 70% at 1.3 and 6 years, respectively, versus 83%, 68% and 45% for group NR. Two variables were considered on multivariate analysis to be predictive factors of survival: left ventricular ejection fraction (p < 0.001) and response to serial electrophysiological tests (p < 0.02). Therapeutic ventricular pacing therefore remains a reliable method to select patients whose prognosis is improved with antiarrhythmic treatment after induction of sustained ventricular arrhythmia.

Electrophysiology↗
PubMed1996

[Myocardial infarction in patients over 75 years of age. Hospital characteristics and long-term follow-up].

OBJECTIVES: Analyze management of myocardial infarction in elderly subjects and assess long-term outcome. METHODS: We studied retrospectively a series of 151 consecutive cases of acute myocardial infarction in patients over 75 years of age and compared then with a group of young subjects under 65 years of age admitted for the same pathology during the same period (1989-1993). RESULTS: In the elderly population, female sex, past history of angina or infarction, atypical presentation and hemodynamic complications were more frequent in the elderly population (left ventricle failure 44 vs 13%, cardiogenic shock 17.2 vs 0.7% without any difference in localization. Mortality was higher in the elderly group (23.2 vs 2.6%) with 68.6% of the deaths due to primary cardiogenic shock. Beta-blockers were used less frequently in the elderly population (31.8 vs 83.0%) as was thrombolysis (26.5 vs 64.5%); coronography was performed less often (21.8 vs 92.7%) as was percutaneous revascularization (9.9 vs 36.4%) or surgery (1.3 vs 6.6%). Survival at 1, 2 and 5 years was 88, 76 and 57% in the elderly group (Kaplan-Meier plot). A past history of unstable angina and a critical episode of left ventricle failure were factors predicting overmortality. CONCLUSION: Acute myocardial infarction remains a severe condition in patients over 75 years of age with overmortality during hospitalization and poor long-term prognosis. Clinical signs of poor prognosis could help guide selection for more aggressive therapeutic management during the post-infarction period, notably in terms of coronary revascularization.

Aged↗
PubMed1996

Programmed ventricular stimulation after myocardial infarction does not help reduce the risk of ventricular events.

Programmed ventricular stimulation could be a useful technique to detect patients at high risk for ventricular arrhythmias and sudden death after acute myocardial infarction. However, prevention of arrhythmic events using this technique has never been demonstrated. To determine whether prophylactic antiarrhythmic therapy influences prognosis after acute myocardial infarction, 196 patients without spontaneous ventricular tachycardia (VT) but with inducible sustained monomorphic VT were followed for 3 +/- 1 years. Ninety-seven patients were not treated (control group). In 99 patients (study group), the antiarrhythmic therapy was guided by electrophysiologic study: One to four trials using class I, II, and III antiarrhythmic drugs were performed until the VT was not inducible or the induced VT was slower and was associated with hemodynamic stability. An effective antiarrhythmic drug prevented VT induction in 34 patients (34%; group I). Sixty-five patients (group II) still had inducible VT with the antiarrhythmic drug. Group II differed from group I in having a higher incidence of an inferior myocardial infarction location (57% vs. 47%; NS), a lower left ventricular ejection fraction (36.5% vs. 41%; NS), a slower rate of induced VT in the control state (227 vs. 255 beats/min; p < 0.05), and a higher number of drug trials (1.9 vs 1.3; p < 0.001). During the follow-up in the control group and in groups I and II, the incidence of total cardiac events was 25%, 15%, and 16% (NS), respectively, and the incidence of total arrhythmic events (VT, sudden death) was 18.5%, 9%, and 12% (NS). Only the risk of VT was reduced (14%, 0%, and 4%; p < 0.05). In conclusion, guided-antiarrhythmic therapy, including class III agents after acute myocardial infarction, was successful in only 34% of patients, and the incidence of arrhythmic events was not significantly decreased. Therefore, programmed ventricular stimulation does not help in managing patients at risk of ventricular arrhythmia after myocardial infarction but could help indicate the need for nonmedical treatment, such as device therapy.

Adult↗
PubMed1996

Significance and prevalence of inducible atrial tachyarrhythmias in patients undergoing electrophysiologic study for presyncope or syncope.

The purpose of the study was to report the prevalence of inducible supraventricular tachyarrhythmias (SVTA) in 827 consecutive patients aged 17 to 90 years who did not have spontaneous documented SVTA and who had unexplained presyncope and/or syncope. The electrophysiologic study (EPS) included programmed atrial and ventricular stimulation up to two extrastimuli at three cycle lengths, and the study of sino-atrial and AV conduction. The results were as follows. EPS was normal in 386 patients. Inducible junctional tachycardia or atrial flutter and fibrillation was the only finding in 187 patients (23%). In the remaining patients we found ventricular tachycardia in 103 (12%), heart block in 67 (8%), sick sinus syndrome in 56 (7%) and increased vagal tone in 28 (3%). The presence of an underlying heart disease (47%) and salvos of atrial premature beats on Holter monitoring (39%) were significantly correlated with the induction of SVTA. However, the comparison with similar groups without syncope indicates that only the induction of SVTA in patients with hypertrophic cardiomyopathy and mitral valve prolapse was significantly correlated with the history of syncope. In patients without heart disease or with prior myocardial infarction or decreased left ventricular function, the induction of SVTA, which is not associated with hypotension in the supine position, could require an induction after head-up tilting, because of the lack of specificity of programmed stimulation in these patients. Programmed atrial stimulation should be systematically performed in patients with unexplained syncope, in particular in those with hypertropic cardiomyopathy and mitral valve prolapse, who require a specific treatment, if a SVTA is induced. In other patients the results of programmed atrial stimulation should be interpreted cautiously.

Adolescent↗
PubMed1996

[Heart rate response to ventricular stimulation].

Analysis of heart rate variability (HRV) by Holter monitoring is the method of choice for assessing the cardiac autonomic regulation. Rapid ventricular stimulation also provokes changes in the autonomic nervous system tone. The aim of this study was to compare time and frequency domain analysis of HRV (Elatec version 3.02) with variations of HR observed after incremental ventricular stimulation to 200/min in 130 patients. In 80 patients, ventricular stimulation provoked an initial acceleration in HR followed by a slowing with a variation of over 10%. In the other 50 patients, these variations were not observed. Holter analysis of HRV showed concordance between the two methods. In time domain analysis, the standard deviation of normal R-R intervals, the coefficient of variability [(CV = SD/mean RR) and percentage of adjacent RR intervals with a difference of more than 50 msec (pNN 50) were significantly reduced in the abnormal group, the respective values in the normal and abnormal groups being: SD 122 vs 72 msec; CV 15 versus 9% and pNN50 9 versus 5%)]. In frequency domain analysis, there was a reduction of low and high frequency spectra and of the ratio of low/high frequencies in abnormal subjects. The authors conclude that the disappearance of HR changes after ventricular stimulation is correlated to the absence of HRV on Holter recording. This simple test may be performed systematically during electrophysiological investigations. The measurements are reproductible and the results are not affected by arrhythmias or technical problems of quality recording by the Holter method which may affect analysis of HRV.

Adult↗
PubMed1996

[Can signal-averaged electrocardiograms be interpreted in cases of complete bundle branch block?].

The aim of this study was to evaluate the results of signal-averaged (SA) ECG in cases of complete right (RBBB) or left bundle branch block (LBBB). One hundred and seven patients had RBBB; 42 without cardiac disease (0), 56 with chronic myocardial infarction (MI) and 9 with primary cardiomyopathy (CMP). Seventy-four patients had LBBB: 20 without cardiac disease, 26 with chronic myocardial infarction and 28 with primary cardiomyopathy. A SA ECG (Cardionics, Fidelity) was performed with a 40 Hz band pass and compared with the recordings of 72 healthy controls without bundle branch block. The duration of the averaged QRS (QRS dur), the voltage of the last 40 milliseconds (RMS40) and duration of terminal activity < 40 microV (LAS) were measured. The analysis of results showed that QRS dur was significantly longer in subjects with ventricular tachycardia (VT) (p < 0.05) and in those with advanced cardiac disease (p < 0.05), whatever the type of bundle branch block, and that only the RMS40 distinguished patients with VT from those without VT, irrespective of the underlying cardiac disease and the type of bundle branch block. However, the study of the diagnostic value of each parameter showed very mediocre results: RMS 40 < 20 microV in myocardial infarction and < 17 microV in cardiomyopathy had sensitivities and specificities in RBBB of 73% and 50% respectively, incalculable in CMP, in LBBB 70% and 33%, 77% and 60% respectively; the LAS was unusable. The authors conclude that it is hazardous to interprete SA ECG in bundle branch block, especially in advanced cardiac disease where the specificity of the criteria becomes very low (< 50%).

Bundle-Branch Block↗
PubMed1996

[Complete atrioventricular block, a possible complication of radiofrequency ablation of reciprocating nodal tachycardia].

Radiofrequency ablation of the slow pathway of the reentry circuit is the usual radical treatment of nodal tachycardia. It is, however, possible to create atrioventricular conduction defects, the significance of which is not known. The aim on this study was to report the history of these conduction defects created during ablation of the slow pathway of the intranodal reentry circuit. Four cases were observed in a series of 27 patients. In one female patient, complete atrioventricular block was observed for 5 minutes before conduction returned to normal followed by recurrence of the tachycardias. Three other women developed complete atrioventricular block one to four days after the ablation. The block regressed after a maximum delay of 7 days. Six months to one year after the procedure, these three patients remain free of tachycardia and have only first degree atrioventricular block on the surface ECG. These patients were not implanted with a pacemaker. The authors conclude that complete atrioventricular block after ablation of the slow pathway may be treated conservatively, providing it is well tolerated. It normally regresses within few days.

Adult↗