Biomedical subjects

A Terrier de la Chaise

Publications and source records attributed to A Terrier de la Chaise.

At least 19 recordsLinked to original sources

PubMed2006

Supraventricular tachyarrhythmia as a cause of sudden cardiac arrest.

INTRODUCTION: Supraventricular tachyarrhythmias (SVTA) are an accepted cause of cardiac arrest in patients with Wolff-Parkinson-White syndrome (WPW) and hypertrophic cardiomyopathy but their participation in other conditions is less well understood. The purpose of the study was to examine the role of SVTA in sudden cardiac arrest (SCA) by comprehensive evaluation of patients successfully resuscitated from SCA. METHODS: A total of 169 survivors of SCA in the absence of acute myocardial infarction underwent systematic evaluation that included echocardiography, Holter monitoring, coronary angiography and electrophysiological study (EPS) with additional testing in selected cases using provocative drug testing with isoproterenol, ajmaline or ergonovine. RESULTS: SVTA was found as the only possible cause or as the cause facilitating SCA in 29 patients: (1) 3 had a WPW syndrome related to accessory pathway with short refractory period; (2) for 12 patients, SVTA was the cause of cardiovascular collapse; heart disease (HD) was present in 11 cases, but disappeared in two of four with dilated cardiomyopathy after the restoration of sinus rhythm; (3) in 14 patients, SVTA degenerated either in a VF or ventricular tachycardia (VT); HD was present in 12 cases, but disappeared in one; two had no HD and recurrent similar arrhythmia was documented by cardiac defibrillator in one of them. SVTA induced coronary ischemia was the main cause of SCA. CONCLUSION: Rapid SVTA was a cause of SCA, either by cardiovascular collapse or by the degeneration in VT or VF. The complication generally occurred in patients with advanced HD or with rapid SVTA-induced cardiomyopathy and rarely in patients without HD. The incidence of SVTA as the only cause or the facilitating cause of SCAs is probably underestimated, because it is difficult to prove.

Adolescent↗

PubMed2006

[Prevalence of supraventricular tachycardia and tachyarrhythmias in resuscitated cardiac arrest].

Supraventricular arrhythmias are considered to be benign when the ventricular rate is slowed and treated by anticoagulants. The aim of this study was to determine the possible influence of these arrhythmias in resuscitated cardiac arrest. Between 1980 and 2002, 151 patients were admitted after a cardiac arrest. Supraventricular arrhythrmias were identified as a possible cause of the cardiac arrest in 21 patients. They underwent echocardiography, exercise stress test, Holter ECG monitoring , coronary angiography and electrophysiological investigation. After these investigations, three patients had a malignant form of the Wolff-Parkinson-White syndrome, two were asymptomatic and, in the third patient, ventricular fibrillation was induced by treatment with diltiazem. In 8 patients, a rapid supraventricular arrhythmia was considered to be the cause of cardiac arrest by cardiogenic shock; 2 patients had hypertrophic cardiomyopathy, 5 had severe dilated cardiomyopathy which regressed in one patient. In ten patients, cardiac arrest due to ventricular tachycardia or fibrillation was provoked by a rapid (> 220 beats/min) supraventricular arrhythmia; two patients had no apparent underlying cardiac pathology. In the others, myocardial ischaemia or acute cardiac failure were considered to be the cause of the cardiac arrest. The authors conclude that rapid supraventricular arrhythmias may cause cardiac arrest either by cardiogenic shock or degenerescence to ventricular tachycardia or fibrillation. Usually, this event occurs in patients with severe cardiac disease but it may occur in subjects without cardiac disease or by an arrhythmia-induced cardiomyopathy.

Adolescent↗

PubMed2006

[Significance of isuprel infusion in unexplained syncope after myocardial infarction].

UNLABELLED: The prognosis for patients with complications and syncope following myocardial infarction depends on the left ventricular ejection fraction (LVEF) and the mechanism of the syncope. The aim of this study was to evaluate the results of an electrophysiological study (EPS) following isoproterenol infusion in patients with a negative EPS under basal conditions. The population included 60 patients, aged 60 +/- 12 years, 5 of whom had syncope on effort or with stress. The EPS included measurement of AV conduction, with programmed atrial and ventricular stimulation. It was repeated following infusion of 2 to 4 microg/kg of isoproterenol. RESULTS: An arrhythmia was identified as preceding the syncope in 27 patients (45%): ventricular tachycardia (VT) n = 16, supraventricular tachycardia (n = 5), 2nd or 3rd degree AV block (n = 3), vaso-vagal reaction (n = 3): 3 subjects developed coronary ischaemia. The subjects with VT on Isuprel differed from those without VT, with a lower LVEF (34 +/- 8 vs 45 +/- 14%) (p < 0.05), a higher incidence of effort related syncope (4 vs 1) and a higher risk of cardiac death (6/16 vs 2/44) (p < 0.01). In conclusion, we recommend repeating the electrophysiogical test under Isuprel in patients with complications after MI and a negative EPS in the basal state whether or not they have exercise related syncope, which will reveal an arrhythmia in 45% of cases. Subjects with inducible VT are at high risk of cardiac death.

Adult↗

PubMed2004

[Does syncope change the results of programmed ventricular stimulation in patients with previous myocardial infarction?].

UNLABELLED: The induction of a ventricular tachycardia (VT) after myocardial infarction (MI) is associated with a high risk of VT and sudden death (SD) in asymptomatic patients; the purpose of the study was to know if syncope modifies the results of programmed ventricular stimulation (PVS) and the clinical consequences. METHODS: PVS using two and three extra stimuli delivered in two sites of right ventricle was performed in 1057 patients without spontaneous VT or resuscitated SD at least 1 month after an acute MI; 836 patients (group I) were asymptomatic and were studied for a low ejection fraction or nonsustained VT on Holter monitoring or late potentials; 228 patients (group II) were studied for unexplained syncope. The patients were followed up to 5 years of heart transplantation. RESULTS: Sustained monomorphic VT (< 280 b/min) was induced in 238 group I patients (28%) and 62 group II patients (29%); ventricular flutter (VT > 270 b/min) or ventricular fibrillation (VF) was induced in 245 group I patients (29%) and 42 group II patients (18%) (P < 0.05); PVS was negative in 353 group I patients (42%) and 124 (55%) group II patients (NS). The patients differ by their prognosis; cardiac mortality was 13% in group I patients and 34% in group II patients with inducible VT < 280 b/min (P < 0.01), 4% in group I patients and 13% in group II patients with inducible VF (P < 0.05), 5% in group I patients and 7% in group II patients with negative study (NS). In conclusion, syncope did not change the results of programmed ventricular stimulation after myocardial infarction. However, syncope increased significantly cardiac mortality of patients with inducible ventricular tachycardia, flutter or fibrillation.

Adult↗

PubMed2004

[Causes and prognosis of syncope in patients with primary dilated cardiomyopathy].

The causes of adverse prognosis of patients with primary dilated cardiomyopathy remain controversial. Classically, it is thought that syncope is associated with an increased risk of mortality. The aim of this study was to try and identify the causes and prognostic significance of syncope in patients with primary dilated cardiomyopathy. Sixty-five patients aged 31 to 80 with primary dilated cardiomyopathy were admitted for investigation of syncope. The average ejection fraction was 27 +/- 10%. Invasive and non-invasive investigations including complete electrophysiological investigations, were performed. Sustained monomorphic ventricular tachycardia was induced in 14 patients (21.5%), ventricular flutter or fibrillation was induced in 9 patients (14%), a supraventricular arrhythmia in 17 patients (26%), and a conduction defect alone or associated with another arrhythmia in 7 patients (11%). A pathological result of tilt testing was observed in 5 patients (8%). No cause of syncope could be demonstrated in 15 patients (23%). During follow-up (4 +/- 2 years) there was a mortality of 15% which was only correlated with the reduction in left ventricular ejection fraction. The authors conclude that there are many causes of syncope in primary dilated cardiomyopathy: ventricular arrhythmias represent only 35% of cases and do not impact on the prognosis; above all, left ventricular ejection fraction is the most important prognostic factor.

Adult↗

PubMed2003

[Risk factors for cardiac mortality in cases of syncope with previous history of myocardial infarction].

Syncope is considered to be a clinical sign predictive of sudden death in patients with a previous history of myocardial infarction. The aim of this study was to determine the prognostic factors in this population. The study population included 228 patients with myocardial infarction over one month old and who had no documented ventricular tachycardia. The patients were referred for investigation of syncope. The left ventricular ejection fraction (LVEF) was measured by echocardiography or radionucleide technique. Complete electrophysiological study including programmed atrial and ventricular stimulation was performed in all cases. The patients were followed up for 6 months to 5 years or until cardiac transplantation (average 3+/-1 years). One hundred and nineteen patients had a LVEF <40% (Group I) and 109 patients had a LVEF >40% (Group II). Sustained monomorphic ventricular tachycardia (VT) with a rate inferior to 280/min was induced in 44 patients in Group I (37%) and in 18 patients in Group II (16.5%), p<0.05. Ventricular flutter or fibrillation was induced in 24 patients in Group I (19%) and in 19 patients in Group II (17%) (NS). Different causes of syncope (conduction disturbances, supraventricular tachycardia, increased vagal tone, severe coronary ischaemia) were found in 23 patients in Group I (19%) and 32 patients in Group II (29%) (NS). Syncope was unexplained in 43 patients in Group I (36%) and 40 patients in Group II (37%) (NS). The prognosis was very different. In Group I, the cardiac mortality was 49% in patients with inducible monomorphic VT <280/min, 35% in those with inducible ventricular flutter or fibrillation but only 9% in patients without inducible ventricular arrhythmias. In Group II, the prognosis was independent of the results of programmed stimulation and much better: cardiac mortality was 5.5% in patients with inducible VT, 5% in those with inducible ventricular flutter or fibrillation and 4% in patients without inducible ventricular arrhyhtmias. The authors conclude that LVEF is the most powerful predictor of cardiac mortality and sudden death in cases of syncope with a past history of myocardial infarction. The prognosis also depends on the results of programmed ventricular stimulation when the LVEF is inferior to 40%. Sustained monomorphic VT is the most frequently induced arrhythmia in this case and the prognosis of these patients is particularly poor. On the other hand, syncope does not appear to be a poor prognostic factor in the group with normal LVEF, even when it is possible to induce VT.

Adult↗

PubMed2001

Predictors of atrial flutter with 1:1 conduction in patients treated with class I antiarrhythmic drugs for atrial tachyarrhythmias.

OBJECTIVES: The purpose of the study was to look for the predictor factors of atrial proarrhythmic effects of class I antiarrhythmic drugs. BACKGROUND: Class I antiarrhythmic drugs may induce or exacerbate cardiac arrhythmias. The predictors of ventricular proarrhythmia are known. The predictors of atrial flutter with 1:1 conduction are unknown. METHODS: Clinical history, EGG, signal-averaged EGG (SAECG) and electrophysiologic study were analysed in 24 cases of 1:1 atrial flutter with class I AA drugs and in 100 control patients without history of 1:1 atrial flutter with class I AA drugs. RESULTS: The ages of patients varied from 46 to 78 years. Underlying heart disease was present in nine patients. The surface EGG revealed the presence of a short PR interval (PR<0.13 ms), visible in leads V5, V6 in eight (35%) patients with normal P wave duration; in other patients with prolonged P wave duration, PR seemed normaL On SAECG recording, there was a pseudofusion between P wave and QRS complex. The electrophysiologic study revealed some signs indicating a rapid AV nodal conduction (short AH interval or rate of 2nd degree AV block at atrial pacing >200 beats/mm) in 19 of the 23 studied patients. All patients, except one, had at least one sign indicating a rapid AV nodal conduction (short PR and/or P wave-QRS complex continuity on SAECG). In the control group, seven patients (7%) had a short PR interval (P<0.01) and 11 (11%) had a pseudofusion between P wave and QRS complex on SAECG (P<0.001). The P wave-QRS complex pseudofusion on SAECG had a sensitivity of 100% and a specificity of 89% for the prediction of an atrial proarrhythmic effect with class I antiarrhythmic drug. CONCLUSION: We recommend avoiding class I AA drugs in patients with a short PR interval on surface EGG and to record SAECG in those with apparently normal PR interval to detect a continuity between P wave and QRS complex, which could indicate a rapid AV nodal conduction, predisposing to 1:1 atrial flutter with the drug.

Adult↗

PubMed2000

Long-term reproducibility of ventricular tachycardia induction with electrophysiological testing in patients with coronary heart disease and depressed left ventricular ejection fraction.

The Multicenter Automatic Defibrillator Implantation Trial (MADIT) has recently confirmed the role of programmed ventricular stimulation (PVS) to identify the high risk patients of sudden death after myocardial infarction and to prevent this risk. The purpose of this study was to evaluate the long-term reproducibility of PVS in these patients. Thirty patients with coronary heart disease without spontaneous documented sustained ventricular tachycardia (VT) underwent two programmed stimulations in the absence of antiarrhythmic drug treatment between 2 and 6 years (mean 4 years). No patient had a myocardial infarction or intervening cardiac surgery during this period. The protocol of study was similar using up to three extrastimuli in two sites of the right ventricle, delivered in sinus rhythm and driven rhythm (600 ms, 400 ms, respectively). On the first PVS, 17 patients had inducible sustained VT (group I). Thirteen patients did not have inducible VT (group II). On the second PVS all group I patients but one had inducible VT, but the cycle length was significantly modified in 11. In group II, five patients had inducible VT and in the other patients the PVS remained negative. In conclusion, in patients with coronary heart disease, but without documented VT, the long-term reproducibility of PVS was excellent in those with inducible VT (94%); the patients remain at risk of VT and a prophylactic implantable cardioverter defibrillator could be considered. In patients with initially negative study, reproducibility of PVS was lower (61.5%), probably because of the progressive remodeling after myocardial infarction. Therefore, the occurrence of new symptoms in patients with previously negative study requires a second programmed ventricular stimulation.

Adult↗

PubMed2000

[Action of sotalol on high-amplification electrocardiogram].

D,l sotalol is an antiarrhythmic widely used for treating ventricular excitability, especially ventricular tachycardia (VT). The means of assessing its efficacy is 24 hour Holter monitoring and programmed ventricular stimulation. High amplification ECG has also been proposed for predicting the effects of the drug on the induction of VT. The aim of this study was to assess the results of high amplification ECG before and after taking sotalol and to compare them with those of programmed ventricular stimulation. This study was performed in 24 patients with spontaneous and inductible ventricular tachycardia due to ischaemic heart disease. The two investigations were performed under basal conditions and after treatment with 160 to 320 mg/day of d,l-sotalol for 8 days. Nine patients had VT which could not be induced after treatment. In the other 15 cases, the VT remained inducible and was not significantly slowed. Analysis of different parameters of high amplification ECG, the QRS duration, RMS 40 and LAS did not show any difference after treatment in cases with inducible VT or VT suppressed by treatment. In conclusion, d,l sotalol, even at antiarrhythmic doses, does not seem to change the parameters of high amplification ECG, and it is therefore not necessary to stop treatment to carry out this investigation. Moreover, it was impossible to predict the effect of d,l sotalol on VT by high amplification ECG.

Adult↗

PubMed2000

[Prolongation of the averaged QRS complex. A simple prognostic factor in patients with post-infarction bundle branch block and a history of syncope].

Patients with a history of myocardial infarction and complete bundle branch block with syncopal episodes have a high risk of sudden death: the identification of the cause of the syncope is therefore essential. The aim of the study was to assess the diagnostic value of non-invasive techniques used in the investigations of syncope: 24 hour Holter recording, high amplification ECG and measurement of left ventricular ejection fraction. The results of these investigations were compared with those of complete electrophysiological investigation evaluating atrioventricular conduction and the inducibility of tachycardia. The patient population was 134 patients, 83 with right bundle branch block and 51 with left bundle branch block. Ninety one patients had inducible sustained ventricular tachycardia and 24 had atrioventricular conduction defects: of these, 14 also had ventricular tachycardia. During follow-up, there were 12 sudden deaths and 13 deaths from cardiac failure. Uni- and multivariate analysis showed induction of ventricular tachycardia to be a significant risk factor for global mortality and sudden death but prolongation of the averaged QRS complex (> 165 msec) was also an independent risk factor of global cardiac mortality. The authors conclude that simple prolongation of the averaged QRS duration > 160 ms in patients with right bundle branch block and > 170 ms in patients with left bundle branch block after myocardial infarction and syncope is a significant poor prognostic factor. However, this sign is not predictive of sudden death.

Adult↗

PubMed2000

[Predictive value of induction of atrial flutter or fibrillation in paroxysmal junctional tachycardia].

The association of different types of tachycardia in a given patient is a well-known phenomenon and the development of ablative methods rises hopes that treatment of one of them may suppress the others. The aim of this study was to determine the significance of induction of atrial flutter or fibrillation (AF) during electrophysiological investigation of patients investigated for paroxysmal junctional tachycardia. The initial population of 500 patients was limited to 485 patients, aged 12 to 86, with a normal intercritical ECG and without a Wolff-Parkinson-White syndrome, who underwent electrophysiological investigation for junctional tachycardias since 1978 and in whom the tachycardia could be reproduced. The study was performed by the endocavitary approach in 262 cases and by the transoesophageal approach in 213 cases with a similar protocol, programmed atrial stimulation with 1 and 2 extrastimuli under basal conditions, eventually completed by the repetition of the protocol with low doses of isoproterenol. The electrophysiological study showed that the tachycardia involved a latent bundle of Kent in 103 cases, a double nodal pathway in 343 cases or another circuit in 39 cases. During this study, sustained AF was induced in 66 cases (13.5%) with a similar incidence in Kent bundles (14.5%), intranodal reentry (11%) and other forms of reentry (11%). During follow-up, ranging from 6 months to 10 years, 7 patients with induced AF and 9 without inducible tachycardia, developed permanent AF. The occurrence of the arrhythmia was significantly correlated with the mechanism of reentry (latent Kent 8/103 cases, intranodal reentry 8/343 cases, p < 0.05), and with the induction of the same arrhythmia by oesophageal investigation alone (p < 0.001). The initiation of the arrhythmia by endocavitary stimulation did not seem to have any positive predictive value. In conclusion, the induction of atrial flutter or fibrillation during investigation of a subject with paroxysmal junctional tachycardia without a patent Wolff-Parkinson-White syndrome, does not seem to be predictive of future development of atrial flutter or fibrillation, unless the investigation was undertaken by the oesophageal approach.

Adolescent↗

PubMed2000

[Paroxysmal junctional tachycardia and normal ECG in sinus rhythm. Is their mechanism influenced by the age of the patient at the time of the study?].

At the time of the curative treatment of paroxysmal junctional tachycardias, to determine the mechanism of the tachycardia is important. Five-hundred forty intracardiac or esophageal electrophysiological studies were performed in patients aged from 9 to 86 years and then revieved. There was no preexcitation syndrome on surface ECG. Programmed atrial stimulation was performed in basal state and if necessary repeated after infusion of isoproterenol. Atrioventricular nodal reentrant tachycardia was the most frequent cause of junctional tachycardia (72%) since childhood and in all stages of life. Concealed accessory pathway reentrant tachycardias were identified in 22% of tachycardias with a stable incidence during the course of life. Various mechanisms of tachycardia were identified in the remaining patients. In conclusion, the mechanism of paroxysmal junctional tachycardia is not correlated with the age of the patient.

Adolescent↗

PubMed1998

Increased atrial vulnerability in arrhythmogenic right ventricular disease.

Supraventricular tachyarrhythmias (SVTA) may occur in patients with the arrhythmogenic right ventricular dysplasia (ARVD). The purpose of the study was to evaluate the incidence of SVTA in 47 patients with ARVD proved by right ventricular angiography. Thirty-three men and 14 women, aged 21 to 72 years (mean 44 +/- 18) were admitted for nonsustained or sustained ventricular tachycardia. Eight patients had a history of spontaneous SVTA several years before ventricular tachycardia occurrence. Protocol of the study consisted of programmed atrial stimulation with one and two extrastimuli delivered during sinus rhythm and two driven rhythms (600 and 400 msec), programmed ventricular stimulation with up to three extrastimuli and was performed in the control state and after infusion of isoproterenol. The results of programmed atrial stimulation were compared with those obtained in 36 asymptomatic subjects without heart disease and with a mean age of 50 +/- 18 years (control group). Sustained SVTA (> 1 minute) was induced in seven of eight patients with spontaneous SVTA, in 27 (69%) of those with ARVD, who did not have spontaneous SVTA, and in two control subjects (5.5%) (p < 0.001). SVTA was inducible in the control state, but ventricular tachycardia induction required isoproterenol in 11 of 27 patients. Two patients without SVTA history but with inducible SVTA developed later spontaneous SVTA. ARVD was associated with a significantly higher incidence of inducible SVTA than in a control population. Supraventricular tachycardias may precede ventricular tachycardias. This association argues for a diffuse myocardial disorder in ARVD.

Adolescent↗

PubMed1998

[Influence of time (4 years) on the results of programmed ventricular stimulation].

The reproducibility of programmed ventricular stimulation has been previously demonstrated for periods of a few hours to several months. It has not been studied over longer intervals. The aim of this study was to assess the reproducibility of the method at long-term (> 2 years). Forty-six patients with underlying cardiac disease underwent two programmed ventricular stimulations in the absence of antiarrhythmic treatment at intervals of 2 to 6 years (mean 4 years). None of the patients had myocardial infarction or cardiac surgery during this period. The protocol was identical: up to 3 extra-stimuli were delivered in the two right ventricular sites over 3 cycles. Twenty-eight patients had inducible sustained monomorphic ventricular tachycardia during the first investigation (Group I): the investigation was negative in the remaining 18 patients (Group II). During the second investigation, 26 of the 28 patients in Group I had inducible ventricular tachycardia, the rate of which decreased from 206 +/- 50 bpm to 196 +/- 54 bpm. The induced ventricular tachycardia was slower in 15 patients and faster in 5 patients. The mode of induction was different in 12 cases. In Group II, 4 patients (22%) had inducible sustained ventricular tachycardia at the second investigation. The authors conclude that the reproducibility of programmed ventricular stimulation remains good in the long-term in subjects within inducible tachycardia, demonstrating the stability of the arrhythmogenic substrate; the frequency of this tachycardia is generally slower. In subjects with an abnormal initial investigation who became symptomatic, it may be useful to repeat programmed ventricular stimulation.

Adult↗

PubMed1997

The signal-averaged electrocardiogram is of limited value in patients with bundle branch block and dilated cardiomyopathy in predicting inducible ventricular tachycardia or death.

An abnormal signal-averaged electrocardiogram (SAECG) has predictive value for arrhythmic events in patients with idiopathic dilated cardiomyopathy and a normal conduction. The purpose of this study was to investigate whether the presence of a complete bundle branch block (BBB) affects prognostic information of the SAECG. We prospectively obtained SAECGs in 128 patients with idiopathic dilated cardiomyopathy. Forty-three of them had BBB and 85 had a normal QRS duration. According to their clinical history and results of ventricular programmed stimulation, patients were divided into 4 groups: (1) group IA with BBB and ventricular tachycardia (VT) (n = 18); (2) group IB with BBB but without VT (n = 25); (3) group IIA without BBB but with VT (n = 40); (4) group IIB without BBB and without VT (n = 45). Patients were compared with 129 patients without heart disease and without VT. Fifty-seven of them had BBB (group III) and 72 had normal conduction (group IV). The filtered QRS duration was longer in group IB than in group III (175 +/- 21 vs 149 +/- 16 ms, p <0.001), and in group IIB than in group IV (111 +/- 19 vs 96 +/- 12 ms, p <0.05). QRS duration was similar in groups IA and IB (176 +/- 24 vs 175 +/- 21 ms) but longer in group IIA than in group IIB (131 +/- 24 vs 111 +/- 19 ms, p <0.001). The low-amplitude signal duration (LAS) and the root-mean-square voltage (RMS) of the last 40 ms of the filtered QRS did not differ between groups IB and III and IA and IB. LAS and RMS were, respectively, longer (44 +/- 20 vs 31 +/- 13 ms, p <0.01) and lower (21 +/- 20 vs 43 +/- 33 microV, p <0.001) in groups IIA and IIB. In groups IA and IB the combination of 2 of the 3 available criteria: QRS duration >170 ms, RMS <20 microV, LAS >45 ms lead up to the best overall statistical result, with a sensitivity and specificity of 78% and 56%, respectively. In groups IIA and IIB, using conventional late potential criteria, the sensitivity and specificity of the SAECG for VT detection were 65% and 73%, respectively. The risk of sudden death was not predicted by the SAECG, and total cardiac mortality was only dependent on left ventricular ejection fraction. In conclusion, QRS duration was prolonged in all of the patients with a dilated cardiomyopathy compared with those without heart disease. BBB did not change the sensitivity but decreased the specificity of the SAECG to predict any VT risk in dilated cardiomyopathy. The risk of sudden death and total cardiac mortality could not be predicted by the SAECG.

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

[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

[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↗