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Biomedical subjects

L Jacquemin

Publications and source records attributed to L Jacquemin.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Evaluation of high amplification ECG and the study of sinus variability in the detection of patients at risk of sudden death].

In order to define the best strategy of prognostic evaluation in relation to patients in heart failure, 415 patients with impaired left ventricular function (ejection fraction < 40%) were prospectively included, between June 1993 and 1996, in a study comparing the respective value of high amplification ECG and Holter analysis of sinus variability, 308 patients in sinus rhythm and narrow QRS complexes were included. The patients were distributed into 4 groups according to the presence or absence of late potentials and altered sinus variability (group I with 2 normal examinations, group II with late potentials and normal variability, group III without late potentials, but with altered variability and group IV with 2 abnormal examinations). The sudden and overall mortality was significantly greater in groups III (28 and 11%) and IV (28 and 9%) than in group I (7 and 3%) and II (11 and 2%). The presence of potential was unable to identify patients at risk of ventricular tachycardia and sudden death. In another 60 patients with complete branch block, the prognosis was also correlated with the alteration of sinus variability. In conclusion, high amplification ECG correctly evaluated the prognosis of subjects in heart failure. However, analysis of sinus variability should be systematically proposed to detect subjects at high risk of mortality, whether the subject has large or narrow QRS complexes.

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

Incomplete bundle-branch block and ST-segment elevation: syndrome associated with sustained monomorphic ventricular tachycardia in patients with apparently normal heart.

This paper reports on three cases of patients with an apparently normal heart admitted for sustained monomorphic ventricular tachycardia. The only abnormal finding showed in the electrocardiogram (ECG) in sinus rhythm that exhibited an entity associated with incomplete right bundle-branch block and persistent ST-segment elevation. The ECG entity was variable and disappeared transiently. Spontaneous ventricular tachycardia in one patient was inducible by programmed stimulation. There was no underlying heart disease. The origin of the ventricular tachycardia in one patient was located by pace mapping in the left ventricle at the left ventricular basal septum. The follow-up (from 6 months up to 6 years) demonstrated a good prognosis. This particular ECG entity associated with monomorphic ventricular tachycardia could have been missed because of the variations in the ECG in sinus rhythm and was associated with a favorable prognosis.

Adult↗
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

Bradycardia-induced polymorphic ventricular tachycardia after radiofrequency catheter modification of atrioventricular junction.

We report the case of a 59-year-old man with a dilated nonischemic cardiomyopathy who had chronic rapid atrial fibrillation despite several therapies. Radiofrequency modification of the atrioventricular (AV) junction slowed the mean ventricular rate from 120 beats per minute (bpm) to 60 bpm. Five hours after the procedure and during the following 1 week, despite ventricular pacing at 90 bpm, the patient developed nonsustained or sustained polymorphic ventricular tachycardias. Finally, pacing at 90 bpm was successfully used in this patient. In conclusion, patients who have undergone modification of AV conduction may be at high risk of life-threatening ventricular arrhythmias in the first week following the procedure.

Atrioventricular Node↗
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

[Coronary angiography: 1st or 2nd-line test?].

Coronary angiography, although now performed extremely frequently, remains an invasive and expensive examination, whose place, as first-line diagnostic method, must be discussed; Its main advantage is to provide a definitive diagnosis of coronary atherosclerosis as well as simple prognostic indicators (single vessel, two-vessel or three-vessel disease; concomitant evaluation of left ventricular function by associated radiological ventriculography). However, it is unable to precisely assess the degree of coronary wall disease and, more importantly, cannot evaluate the functional repercussions of stenosis. Under these conditions, only cases in which myocardial revascularization is expected to provide a definite clinical benefit (presence of frank angina symptoms) probably justify first-line coronary angiography. In all other cases, coronary angiography is a useful examination to provide reference "mapping" of the coronary lesions, but an obvious clinical benefit for the patient cannot be expected from systematic use of this technique. In particular, in such situations, coronary angiography should not be the only element on which the decision to perform myocardial revascularization should be based: the "oculostenotic reflex" must always be avoided.

Angina Pectoris↗
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↗