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Biomedical subjects

P Coumel

Publications and source records attributed to P Coumel.

At least 19 recordsLinked to original sources
PubMed1992

[Effect of atropine therapy on sudden infant death. A multicenter survey of 7851 children at risk].

The results of a multicentre inquiry started in 1988 in reference centres of sudden infant death are presented. This study concerns the sudden and unexplained mortality of infants under 1 year of age who were treated with atropinics for an alleged risk of sudden death. The 7,851 infants involved were divided into 2,605 siblings, 1,067 premature babies and 4,179 infants who experienced malaises. Only one of the 2,034 infants treated with atropinics (385 siblings, 435 prematures, 1,214 with malaise) died, as opposed to 27 deaths among the 5,817 infants who where not treated (10 deaths among 2,220 siblings, 6 among 632 premature and 11 among 2,965 infants with malaise); P = 0.005. These results are encouraging, but they suffer from the limitations and biases inherent in all large inquiries. They certainly do not allow us to conclude without reservation that vagal hyperreflectivity is the mechanism responsible for sudden infant death and that atropinics must be systematically given to all infants at risk. Wide and randomized prospective studies are highly desirable in this particular field.

Drug Evaluation↗
PubMed1992

Flecainide in quinidine-resistant atrial fibrillation.

Flecainide (100 mg twice daily) was used for prevention of paroxysmal atrial fibrillation (PAF) in 52 patients with frequent symptomatic attacks that were resistant or intolerant to quinidine (600-900 mg/day). Underlying heart disease was present in only 8 cases and left ventricular ejection fraction was always greater than 30%. No patient had had a myocardial infarction. Vagally induced PAF was clinically documented in 35 patients. Amiodarone, previously used and ineffective, was combined with flecainide in 33 patients. After 1-5.8 years of follow-up, complete disappearance of PAF was observed in 38 patients (73%). The success rate was slightly higher in patients with vagally induced PAF (p = 0.07). Extracardiac side effects necessitated withdrawal in only 3 cases. Permanent pacemaker was needed in 7 patients on amiodarone and flecainide because of excessive sinus bradycardia. Two patients, with previously documented atrial flutter, experienced presyncopal episodes of atrial flutter with 1:1 atrioventricular (AV) conduction and wide QRS complex. No death occurred during the follow-up. In this series, quinidine proved to be unsuccessful in 46 patients and it was withdrawn in 6. We concluded that flecainide is efficient and well tolerated for long-term prevention of PAF in patients resistant to quinidine. The possibility of 1:1 AV conduction during atrial flutter may suggest the use of verapamil or beta blockers in combination with flecainide in patients with previously documented atrial flutter.

Amiodarone↗
PubMed1992

Safety of bepridil: from review of the European data.

In France, bepridil has been available since 1981 for treatment of angina. Reports of arrhythmogenic effects (torsades de pointes) related to bepridil led to the assembly of a task force of physicians from France and the Netherlands. The task force found that the risk of torsades de pointes was indeed increased in elderly patients, especially women greater than 70 years old, as well as in those taking diuretics, which can precipitate hypokalemia. Postmarketing surveillance data developed from 1981 to 1989 have revealed 108 validated episodes of torsades de pointes in patients treated with bepridil. Improved patient selection has dramatically decreased the incidence of this complication. Several comparative clinical trials assessing the safety of bepridil have concluded that the drug may prolong the QT interval in certain patients; however, no occurrence of torsades de pointes was documented in these safety studies. The 9-year French experience suggests that bepridil is a safe and effective agent for treatment of angina pectoris in properly selected patients.

Aged↗
PubMed1992

Spontaneous arrhythmias in various models of cardiac hypertrophy and senescence of rats. A Holter monitoring study.

OBJECTIVE: The aim was to define experimental models of spontaneous arrhythmias in various models of cardiac hypertrophy in rats. METHODS: Cardiac hypertrophy was induced by several methods and 24 h Holter monitoring was recorded in conscious rats to quantify spontaneous arrhythmias in hypertrophied hearts. Male Wistar rats were studied. A group of young controls 1-2 months old (n = 16) was compared to four groups of animals with cardiac hypertrophy: (1) thyrotoxic rats which received a daily intraperitoneal injection of L-thyroxine for 7 d (n = 6); (2) rats subjected to abdominal suprarenal aortic stenosis (n = 11); (3) senescent rats 22-24 month old (n = 6); and (4) S-DOCA-salt (senescent animals rendered hypertensive by uninephrectomy and DOCA-salt treatment, n = 8). RESULTS: (1) Thyroxine resulted in 20% cardiac hypertrophy, with normal arterial tension, sinus tachycardia, a shorter P wave length and PR interval, and frequent (5/6) atrioventricular block. No premature beats were seen. (2) In aortic stenosis, atria and left ventricle were hypertrophied by 53% and systolic carotid pressure increased by 63%. The incidence of supraventricular premature beats was increased [frequency = 0.70 (SEM 0.3) per 24 h in control v 99(61) in aortic stenosis, p < 0.05]. Ventricular premature beats remained as rare as in control. (3) In senescent and S-DOCA-salt rats all types of spontaneous arrhythmias, but specially supraventricular arrhythmias and atrioventricular block, were frequent. Cardiac hypertrophy produced by DOCA-salt treatment in senescent rats had no effect on the incidence and nature of arrhythmias, but resulted in an increased QTc interval. CONCLUSIONS: Senescent rats and rats with aortic stenosis represent valid models of spontaneous arrhythmias occurring in the absence of ischaemia or toxic insult. Spontaneous arrhythmias in rats are mainly of supraventricular origin. Hyperthyroidism in rats is a model of atrioventricular block probably related to tachycardia. Holter monitoring in rats may have several potential pathophysiological and pharmacological applications.

Aging↗
PubMed1992

Efficacy of beta-blocking agents in reducing the number of shocks in patients implanted with first-generation automatic defibrillators.

The efficacy of beta-blockers was tested in 11 patients who avoided sudden death as a result of ventricular tachycardia or fibrillation due to coronary artery disease or non-ischaemic underlying heart disease, after implantation of an automatic defibrillator. Ten patients initially tolerated acebutolol despite prior class III or IV heart failure in six cases; nadolol replaced acebutolol in nine cases for long-term therapy. In these 10 patients, periods of treatment with and without beta-blocking agent were available, making possible a crossover comparison, during a follow-up lasting 31.6 +/- 17.8 months. One hundred and ten shocks were delivered: 14 were considered as probably inappropriate and ruled out, leaving the remaining 96 shocks to be analysed. The monthly rate of shocks was lower during beta-blocking treatment: 0.12 +/- 0.24 vs. 1.09 +/- 1.41 (P = 0.03). While taking beta-blockers, only four patients received shocks, compared to 10 (i.e. all cases) not administered beta-blockers (P less than 0.01). Despite the technical limitations of the study, since only a few spontaneous shocks could be documented on ECG recordings, the efficacy of beta-blockers in preventing occurrence of severe ventricular tachyarrhythmias seems likely, and deserves further investigations using new implanted devices with improved memory functions.

Acebutolol↗
PubMed1992

Efficacy of automatic multimodal device therapy for ventricular tachyarrhythmias as delivered by a new implantable pacing cardioverter-defibrillator. Results of a European multicenter study of 102 implants.

BACKGROUND: Third-generation implantable cardioverter-defibrillators are devices designed to treat ventricular tachycardia (VT) and ventricular fibrillation (VF) by means of overdrive pacing, cardioversion, or defibrillation. So far, the efficacy of tiered therapy has been documented only in small series. Therefore, a European multicenter clinical evaluation study of a new tachyarrhythmia control device, the Medtronic PCD pacer-cardioverter-defibrillator with epicardial patch-lead configuration, was undertaken. METHODS AND RESULTS: We report on 102 patients (mean age, 55 +/- 13 years) from 11 European centers. PCD devices implanted between May 1989 and February 1991 were included. The patients suffered from hemodynamically significant ventricular tachyarrhythmias not suppressed by antiarrhythmic drug therapy and unrelated to acute myocardial infarction; one patient had nonsustained VT and severely depressed left ventricular function. Seventy patients had coronary artery disease with old myocardial infarctions, 23 had cardiomyopathies of various etiologies, and nine patients had no detectable heart disease. Mean ejection fraction was 36 +/- 14% (range, 10-76%). Mean intraoperative defibrillation threshold (51 patients) was 10.6 +/- 5.1 J (range, 2-18 J). The documented follow-up ranged from 1 to 21 months (mean, 9.4 +/- 5.8 months), or 79.9 cumulative patient-years. Perioperative mortality was 3.9%. The actuarial survival rate at 12 months was 91%. One sudden arrhythmic death occurred. Sixty patients (58%) received device therapy. Seventeen patients had therapies only for "VF" episodes, 16 patients only for VT, and 28 patients for VT and "VF" episodes. Based on device memory data, 1,235 spontaneous VT episodes were detected and treated in 43 patients. Twelve hundred four of these VT episodes received painless initial antitachycardia pacing therapy, restoring sinus rhythm in 91%. The 108 ongoing episodes received 209 multiple therapeutic attempts. Eighty-five additional overdrive pacing therapies restored sinus rhythm in 30%. Initial ineffective antitachycardia pacing therapies received 51 cardioversion pulses. The success rate was 61%. Seventy-three additional cardioversion pulses were delivered to backup ineffective pacing therapy as well as ineffective secondary cardioversion pulses. Their success rate was only 40%. Two hundred eighty-six spontaneous episodes were detected in 44 patients as "VF." Overall defibrillation efficacy was 97.6%. CONCLUSIONS: The implanted device nearly eliminates sudden arrhythmic death in patients with documented, potentially fatal ventricular tachyarrhythmias. Automatic tiered therapy is highly effective to restore sinus rhythm, provided that an integrated two-zone tachycardia detection algorithm is used, assigning lower tachycardia rates to overdrive pacing and/or cardioversion and higher tachycardia rates to defibrillation. In general, spontaneous VTs can be terminated by automatic overdrive pacing, and painful or disturbing countershock therapies are not required to terminate the majority of spontaneous VT episodes.

Death, Sudden, Cardiac↗
PubMed1992

[Pro-arrhythmia effect of pyridostigmine. Apropos of a case].

A coronary patient with myasthenia gravis with a previous myocardial infarction presented with severe ventricular arrhythmias after the replacement of neostigmine by pyridostigmine for the treatment of the myasthenia. These arrhythmias were resistant to antiarrhythmic therapy associating betablockers and amiodarone throughout treatment with pyridostigmine but regressed when this drug was withdrawn. A test of reintroduction of pyridostigmine under medical surveillance led to the reappearance of the ventricular hyperexcitability, so confirming the responsibility of this drug. This would seem to be the first reported case of severe ventricular arrhythmias due to a proarrhythmic effect of pyridostigmine. The possible mechanisms of this effect are discussed.

Coronary Disease↗
PubMed1992

[Clinical aspects of polymorphic ventricular tachycardia].

Polymorphic ventricular tachycardia is defined as constant change of the QRS morphology. The diagnosis has important etiological, therapeutic and prognostic implications. This term covers several different entities which may be artificially distinguished by the electrocardiographic appearances during tachycardia, by changes of the resting electrocardiogramme, the mode of onset, the presence or absence of underlying cardiac disease and of intercurrent drug therapy. However, as the resting ECG may not be available in an emergency situation, or difficult to interpret, the clinical context is the key to diagnosis and treatment. Polymorphic ventricular tachycardia is classified according to the absence or presence of underlying cardiac disease respectively as torsades de pointe with long QT, torsades de pointe with a short coupling interval and catecholamine-induced ventricular tachycardia of childhood on the one hand, and, iatrogenic torsades de pointe, ventricular tachycardia in acute or chronic infarction and other cardiac diseases, on the other hand. Finally, the authors discuss the problem of polymorphic ventricular tachycardia induced by programmed ventricular stimulation.

Anti-Arrhythmia Agents↗
PubMed1992

[Value of signal-averaged electrocardiogram in ventricular arrhythmia without apparent heart disease].

Signal-averaged electrocardiography was performed in 132 subjects with various ventricular arrhythmias without clinically apparent heart disease and compared with the results obtained in a series of 45 normal subjects. The latter enabled definition of the following criteria of normality: QRS duration after averaging < 113 ms; Simson vector of the last 40 ms (RMS40) > or = 17 microV; low amplitude signal duration over 40 microV < 38 ms for a high pass bidirectional filter of 40-300 Hz. Complementary investigations (echo or angiography), performed in all cases, showed underlying abnormalities in 26 patients: 13 right ventricular dysplasias, 7 cardiomyopathies, 3 mitral valve prolapses and 3 minor congenital heart defects. These investigations were normal in the remaining 106 subjects. Of the 26 patients with cardiac disease, 15 had 3 criteria of positivity for late ventricular potentials, 6 had 2 criteria and the other 5 had no criteria of late ventricular potentials. Therefore, 81% of cases with cardiac disease had at least 2 diagnostic criteria of late ventricular potentials whereas only 4% of those without cardiac disease, and in the control group, had criteria of positivity (p < 0.001). Using these criteria, the predictive value of signal-averaged electrocardiography for the detection of underlying cardiac disease was good when 2 criteria are required for diagnosis of late ventricular potentials: sensitivity 81%, specificity 96%; predictive value of a positive test 78%, predictive value of a negative test 97%. Signal-averaged electrocardiography is therefore a good non-invasive method of diagnosing underlying cardiac disease in patients with ventricular arrhythmias without clinically apparent heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Heart rate variability and the onset of tachyarrhythmias.

The autonomic nervous system plays an important role in the genesis of cardiac arrhythmias but the precise definition of this role is quite complex. The fluctuations of the heart rate may provide useful information about the balance of the autonomic nervous system. However, one obvious limitation is represented by extrapolating to the ventricle events which occur at the sinus node level. It has been clearly documented that atrial fibrillation of vagal origin is preceded by a progressive decrease in heart rate. On the other hand, ventricular arrhythmias of adrenergic origin are preceded by progressive heart rate acceleration and by diminution of vagally mediated short term changes. The absolute value in heart rate is less important than the actual trend in allowing inferences on the relative sympathetic or vagal predominance. A better understanding of the changes in the autonomic balance will provide a key for the mechanisms underlying several clinical events.

Atrial Fibrillation↗
PubMed1991

Long-term follow-up after sustained monomorphic ventricular tachycardia: Causes, pump failure, and empiric antiarrhythmic therapy that modify survival.

We analyzed the actuarial cardiac mortality rate of 295 consecutive patients with sustained monomorphic ventricular tachycardia who were referred to us between 1978 and 1988. Patients were divided into four groups: group I of 156 patients with coronary disease, group II of 55 patients with nonischemic left ventricular disease, group III of 65 patients with right ventricular disease, and group IV of 19 patients without detectable heart disease. Patients were treated empirically according to a prospective schema: (1) class I antiarrhythmic drugs, (2) in case of recurrence of ventricular tachycardia: amiodarone or beta-blockers, (3) in case of recurrence of ventricular tachycardia: drug combinations or surgery. The mean follow-up duration was 61 +/- 40 months after the first occurrence of ventricular tachycardia, and the clinical outcome was known in 67.5% of patients at 5 years. The actuarial mortality rates were considerably higher in groups I and II compared with those in groups III and IV (p less than 0.01). The mortality rate was slightly higher in group I than in group II (p less than 0.05). In groups I and II, actuarial mortality rate were much higher when left ventricular ejection fraction was less than 0.30 (p less than 0.01). Comparisons between treatments showed no difference in actuarial mortality rates in patients with ventricular tachycardia and left ventricular ejection fraction greater than 0.30.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1991

Heart rate variability in left ventricular hypertrophy and heart failure, and the effects of beta-blockade. A non-spectral analysis of heart rate variability in the frequency domain and in the time domain.

An analysis of heart rate (HR) variability (HRV) was based on quantifying the number and amplitude of HR fluctuations over long (8-30 cycles) and short (2-4 cycles) sequences of acceleration and deceleration-forming oscillations. The 'product' (number times amplitude) is an equivalent of the power spectrum in the frequency domain. In the time domain, positive correlations with HR were found for the number of long (L) sympathetic-mediated oscillations, whereas they were negative for short (S) vagally-mediated oscillations. The L/S ratio, an index of the autonomic nervous system (ANS) balance, closely paralleled the circadian HR values. HRV was studied in the ambulatory ECG of three groups of 15 normal adults (group I), 13 patients with left ventricular hypertrophy (LVH, group II) and 13 patients with heart failure (HF, group III). In basic conditions the mean HR was 77.1 +/- 1.9 beats min-1 (mean +/- SEM) in group I, 76.8 +/- 3.3 in II, 79.5 +/- 3.5 in III (P = NS). The different types of oscillations had smaller 24-h average values of the product in groups II and III than in group I, but the trends did not reach significance. However, the pooled 24 hourly values of the L/S ratio in group I (1.17 +/- 0.09) were lower than in group II (1.33 +/- 0.06, P less than 0.05 at Ancova) and higher than in group III (1.06 +/- 0.09, P less than 0.001). A 3-day treatment with acebutolol non-uniformly slowed the mean HR:--9.5% in group I, --18.1% in II and -19.1% in III (P less than 0.001), and uniformly diminished the L/S ratio by 17% to 20% (P less than 0.01). In conclusion, the sympathetic predominance of the ANS balance in LVH and HF is reflected by the beta-blockade induced HR decrease that is twice as marked in patients as in controls. In basic conditions HRV tends to be depressed in LVH and even more in HF. The ANS imbalance, however, has different modalities depending on the presence of HF, probably because of the different status of beta-adrenergic receptors in this condition.

Acebutolol↗
PubMed1991

Future trends in antiarrhythmic therapy.

It is difficult to define what the trends will be in antiarrhythmic therapy in the coming years, particularly at a time when rhythmology has been somewhat destabilized by the unexpected results of large therapeutic trials on sudden death prevention. Schematically, drugs that do have established antiarrhythmic properties do not provide any benefit, and they can even make the patients' situation worse. On the other hand, beta-blockers, which do not satisfy the admitted rules of antiarrhythmic efficacy, are indeed capable of preventing death, and they are so doing in subgroups with heart failure, a classic contraindication. Finally, drugs such as calcium antagonists, which supposedly address the ischemic mechanism of death, do not seem to provide any benefit in this kind of trial, whereas drugs such as amiodarone have such a complex action that their probably favorable effect is not easy to explain. This uncomfortable situation probably relates to the fact that the various modes of reasoning concerning the mechanisms of arrhythmias and the effects of drugs have been too straightforward, not to say simplistic. Routinely observed arrhythmias may not have the same determinants as the arrhythmias finally responsible for death, particularly if the role of adrenergic stimulation is taken into account to explain the difference in severity. Routinely used antiarrhythmic drugs may well be effective on the former and innocuous for the patients, and at the same time ineffective on the latter and detrimental to the more severely diseased patients. Our modes of evaluation of the real effects of the drugs certainly have to be revisited, as well as the important parameters to be taken into account in the evaluation of arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1991

Sudden cardiac death, implanted defibrillation, and clinical electrophysiology.

A mere 25 years ago, the technique of external defibrillation became the starting point for the development of clinical electrophysiology by permitting routine use of endocavitary programmed electrical stimulation of the heart without undue risk. Major advances in knowledge of clinical arrhythmias and the understanding of their mechanisms were, thus, permitted. Mirowski's implanted defibrillator also constituted a major breakthrough therapeutically; unfortunately, however, some 10 years later, it has not yet induced similarly hoped for consequences in terms of progressing knowledge concerning lethal arrhythmias, largely due to the absence of Holter functions in the implanted devices. As a result of this, in our opinion, better established therapeutic indications are still needed. The reasons for the present situation, we believe, may be partly technical but are conceptual as well. The key point is that even the clear demonstration of the great practical efficacy of a therapeutic tool does not exempt us from the obligation of determining the mechanisms of this effect.

Arrhythmias, Cardiac↗