Predictive power of increased heart rate versus depressed left ventricular ejection fraction and heart rate variability for risk stratification after myocardial infarction. Results of a two-year follow-up study.

OBJECTIVES: The aim of this study was to compare the predictive value of mean RR interval assessed from predischarge Holter recordings with that of heart rate variability and left ventricular ejection fraction for risk stratification after myocardial infarction. BACKGROUND: Heart rate variability is a powerful tool for risk stratification after myocardial infarction. Although heart rate variability is related to heart rate, little is known of the prognostic value of 24-h mean heart rate. METHODS: A total of 579 patients surviving the acute phase of myocardial infarction were followed up for at least 2 years. Predischarge heart rate variability, 24-h mean RR interval and left ventricular ejection fraction were analyzed. RESULTS: During the first 2 years of follow-up, there were 54 deaths, 42 of which were cardiac (26 sudden). Shorter mean RR interval was a better predictor of all-cause mortality as well as cardiac and sudden death than depressed left ventricular ejection fraction. Depressed heart rate variability predicted the risk of death better than mean RR interval for sensitivities < 40%. For sensitivities > or = 40%, mean RR interval was as powerful as heart rate variability. All three variables performed equally well in predicting nonsudden cardiac death. For cardiac death prediction, a left ventricular ejection fraction < 35% had a 40% sensitivity, 78% specificity and 14% positive predictive accuracy; a mean RR interval < 700 ms had a 45% sensitivity, 85% specificity and 20% positive predictive accuracy; and a heart rate variability < 17 U had a 40% sensitivity, 86% specificity and 20% positive predictive accuracy. CONCLUSIONS: Predischarge 24-h mean heart rate is a strong predictor of mortality after myocardial infarction that can compete with left ventricular ejection fraction and heart rate variability.

Comparative reactivity and mechanical properties of human isolated internal mammary and radial arteries.

OBJECTIVE: The aim of this study was to analyse the arterial wall mechanics and the vasoreactive properties of the radial artery in comparison with those of the internal mammary artery and to discuss their implications for coronary bypass grafts. METHODS: Measurements of pressure and diameter were obtained from cylindrical segments, whereas measurements of reactivity were obtained from ring segments from the same arteries. We used an echo-tracking technique of high resolution enabling to investigate, in vitro, the diameter and the wall thickness of arterial cylindrical segments. Furthermore, the compliance, distensibility and incremental elastic modulus of the radial and of the mammary arteries were determined for a wide range of transmural pressure (0-200 mmHg) in presence and absence of norepinephrine (NE). RESULTS: Our results show that NE caused vasoconstriction of the two arteries. Strain was found significantly higher for the radial artery than for the internal mammary artery at any given value of stress both in the presence and in the absence of NE. In presence of NE, compliance for radial artery, in the overall transmural pressure range, did not change, whereas, distensibility was significantly increased and the elastic modulus was significantly decreased. Under the same conditions, the distensibility of the mammary artery tended to decrease and its elastic modulus to increase. In parallel, the vasoreactive properties of the two arteries confirmed the previous results showing that radial artery developed a significant higher tension to vasoconstricting agents (KCl, NE and phenylephrine (PHE)) and higher relaxation to isradipine than internal mammary artery. Moreover, radial artery displayed a lesser sensitivity to sodium nitroprusside than internal mammary artery. Furthermore, sensitivity to NE was found to be 7-fold higher for radial artery than for internal mammary artery. CONCLUSION: Taken together, data on the mechanical and reactive properties of radial and internal mammary arteries show why the radial artery displayed a higher potential for spasm than the internal mammary artery and why the use of Ca2+ channel blocker can decrease the incidence of occlusion and spasm.

Short- and long-term assessment of heart rate variability for risk stratification after acute myocardial infarction.

Depressed heart rate variability (HRV) has been shown to be a powerful and independent risk factor in patients following acute myocardial infarction (AMI). A detailed comparison of the predictive values between short- and long-term HRV has not been made. The predictive value of short-term HRV for 1-year total cardiac mortality was studied in 700 consecutive patients after AMI. All patients underwent 24-hour Holter monitoring before discharge from the hospital (5 to 8 days after AMI) and were followed up for 1 year. Short-term HRV was computed as the standard deviation of all normal RR intervals (SDNN) from a 5-minute stationary period selected from 24-hour Holter electrocardiographic recordings. Long-term HRV was computed as an HRV index over the entire 24 hours. There was a significant but relatively poor correlation between SDNN and HRV index (r = 0.51, p <0.001). The positive predictive accuracy of SDNN for 1-year mortality (13% to 18%) was lower than the HRV index (17% to 43%) over a range of sensitivity of 25% to 75%. Assessment of HRV index in > or = 35% of the patients preselected by the lowest SDNN was able to achieve predictive power similar to that of HRV index assessed in all the patients. These data suggest that lower predischarge short-term HRV is associated with increased 1-year total cardiac mortality in patients after AMI. Analysis of long-term HRV for postinfarction risk stratification can safely be limited to patients preselected by depressed short-term HRV measures.

Effects of bisoprolol on heart rate variability in heart failure.

Analysis of heart rate variability (HRV) provides a non-invasive index of autonomic nervous system activity. HRV has been shown to be reduced in heart failure. Preliminary data indicate that beta blockers improve clinical status in patients with heart failure, but HRV improvement remains to be demonstrated. Fifty-four patients from the randomized double-blind, placebo-controlled Cardiac Insufficiency Bisoprolol Study were included in the HRV study. The bisoprolol daily dose was 5 mg once daily. We assessed HRV during 24-hour Holter recordings before randomization and after 2 months of treatment. HRV as measured in the time domain by root-mean-square successive differences (rMSSD), the percentage of adjacent RR differences >50 ms (pNN50), and the SD of RR intervals (SDNN), and in the frequency domain by high-frequency (0.16 to 0.40 Hz) and low-frequency (0.04 to 0.15 Hz) power. Most patients were in New York Heart Association functional class III. The mean left ventricular ejection fraction was 27 +/- 7%, and heart failure was idiopathic or ischemic. After 2 months, the patients receiving bisoprolol had a reduced mean heart rate compared with that in placebo patients (p=0.0004). Bisoprolol increased 24-hour rMSSD (p=0.04) and 24-hour pNN50 (p=0.04), daytime SDNN (p=0.05), and daytime high-frequency power (p=0.03) power. Bisoprolol induced a significant increase in HRV parameters related to parasympathetic activity in heart failure. Increased vagal tone may contribute to the protective effect of beta blockers and may have prognostic implications.

Noninvasive detection of an increased vascular mass in untreated hypertensive patients.

Structural changes of the arterial vasculature are of major pathophysiologic and prognostic significance in human hypertension. A high-resolution ultrasonic echotracking device was used to measure internal diameter and intima-media thickness of the radial artery, a medium-sized muscular conduit artery, in 60 hypertensive patients and in 40 age-matched control subjects. Of the 60 hypertensives, 33 were never treated and 27 were well-controlled by antihypertensive therapy. Radial artery mass and thickness/radius ratio were used to describe the radial artery structure. Radial artery mass was validated in vitro by comparing the weight of arterial segments to the ultrasonographic determination of their mass, calculated as: rho L(pi Re2-pi Ri2), where rho is the arterial wall density, L the length of the arterial segment, and Re and Ri the ultrasonic values of internal and external radii, respectively. Diastolic internal diameter did not differ among the three groups, but wall thickness, radial artery mass, and thickness/radius ratio were significantly higher in the untreated hypertensive group than in the control group. In treated well-controlled hypertensive subjects, radial artery mass and thickness/radius ratio were not different from that of control subjects. Among the population of untreated patients, significant univariate relations existed between radial artery mass and blood pressure and radial artery mass and age. In multivariate analysis, radial artery mass was independently predicted by mean blood pressure, age, and sex. Circumferential wall stress, calculated from diastolic internal diameter, wall thickness, and diastolic blood pressure, was not different in the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

[The choice of pacing sites: should we change our practice?]. / Choix des sites de stimulation cardiaque: doit-on changer notre pratique?

For the past 45 years the sites used for elective pacing have been the apex of the right ventricle and the right atrium. Although the initial objective of pacing was the "simple" correction of a conduction disorder, a more recent evolution has been to achieve a favourable haemodynamic effect, considering left ventricular filling and synchronisation of ventricular contraction as essential. Demonstration of the benefit in terms of survival brought about by pacing in atrioventricular block has not required large trials. However, it is possible that this improvement in morbidity and mortality is in part offset by the altered haemodynamics due to pacing at the right ventricular apex. At the atrial level, the prevention of AF is the holy grail of atrial pacing, but is far from being attained, perhaps because the physiopathological bases are not clear and have not really been demonstrated, casting doubt on the final objective. The choice of pacing site is essential in this context, as much in the atrium as in the ventricle. The current problem regarding this choice is the same as for all medical treatment, where the risk/benefit ratio is evaluated: if the usual sites are potentially deleterious, is it possible to continue using them or is it necessary to change implantation practices, and what level of proof is needed?

[Therapeutic strategies in acute myocardial infarction: antiarrhythmic therapy]. / Stratégies thérapeutiques lors de la phase aiguë de l'infarctus du myocarde: les antiarythmiques.

Antiarrhythmic therapy is a special case in the therapeutic strategy of acute myocardial infarction. There are very few controlled therapeutic trials and its use is mainly based on clinical experience rather than on scientific evidence. The most common arrhythmias requiring treatment in acute myocardial infarction are atrial fibrillation, ventricular tachycardia and ventricular fibrillation. There is no evidence to support the use Class I antiarrhythmics. Lidocain may be used in some cases. Similarly, contradictory results have been reported with the use of magnesium salts and the general tendency is not to use this ion in acute myocardial infarction. The most commonly used antiarrhythmic agents are the betablockers and amiodarone. The general principles of treatment should be respected: all antiarrhythmic drugs have negative inotropic effects, apart from digitalis. All antiarrhythmics may have a proarrhythmic effect including digitalis, especially in this clinical context. Whenever possible, continuous intravenous infusions are to be preferred to bolus injections. In addition, and when possible, electrotherapy is preferable to antiarrhythmic drug therapy. Finally, a number of cardiac arrhythmias observed in acute myocardial infarction should be "respected" or treated by electrotherapy but never by antiarrhythmic drugs.

[Predictive criteria of early recurrence of atrial arrhythmia after reduction by electrical cardioversion]. / Critères prédictifs de récidive précoce d'un trouble du rythme atrial après réduction par choc électrique externe.

The management of atrial arrhythmias aims not only to restore sinus rhythm but also to maintain it. Ten to thirty per cent of patients have early recurrence of atrial arrhythmias, the treatment of which remains empiric. The aim of this study was to define factors predictive of early recurrence of atrial arrhythmias and the consequences on the length of hospital stay. A series of 131 patients who underwent reduction of atrial arrhythmias by electrical cardioversion was studied retrospectively. A recurrence within 24 hours was observed in 12.2% of the patients. These recurrences significantly increased the length of hospital stay (6.8+/-6.3 versus 3.6+/-3.8 days, p=0.005). This study confirms two previously reported results with respect to more long-term recurrences. In the "early recurrence" group, the duration of the atrial arrhythmia was longer (p=0.003) and there were fewer treatments with amiodarone (p=0.03). In addition, original results were obtained. In the "early recurrence" group, the patients were more often treated with furosemide (p=0.02), class Ic antiarrhythmics (p=0.007) or anaesthetised with thiopental (p=0.002) than patients without early recurrences. Experimental data explain these results. However, they require confirmation by a prospective randomised trial.

[Electrophysiological remodeling induced by atrial fibrillation. An experimental curiosity or major factor in atrial fibrillation in man?]. / Remodelage électrophysiologique induit par la fibrillation atriale. Curiosité expérimentale ou déterminant majeur de la fibrillation atriale chez l'homme?

Atrial fibrillation usually progresses from a paroxysmal to a permanent arrhythmia, even in the absence of underlying cardiac disease. The treatment is more difficult when the arrhythmia is chronic. This progression may be explained by the aggravation of underlying cardiac disease with time. Another explanation is that the arrhythmia induces functional and structural changes of the atrial tissues (remodelling) which promote the perpetuation of the arrhythmia and which make treatment less effective. Although the electrophysiological changes predisposing to atrial fibrillation have been known for over 15 years, it was only in 1995 that experimental studies showed the presence of atrial electrophysiological remodelling induced by the arrhythmia. This process of long term adaptation of the atrial myocytes to the tachycardia comprises marked changes of the parameters which sustain the arrhythmia: changes in refractory period (decreased duration, inadaptation to the heart rate, increased dispersion), reduced conduction speed and sinus dysfunction. Atrial remodelling also affects the contractile function by the structural changes. The calcium currents play a major role in its development. This mechanism has not yet been completely defined in the clinical setting and its importance in sustaining the arrhythmia has not been clearly evaluated. Atrial fibrillation remains one of the most difficult arrhythmias to treat. A better understanding of cellular mechanisms of remodelling could open up new therapeutic approaches to limit the natural history of the arrhythmia with progression to chronicity and structural changes responsible for the degradation of atrial contractility.

[Risk of mortality after myocardial infarction: value of heart rate, its variability and left ventricular ejection fraction]. / Risque de mortalité après un infarctus du myocarde: apport de la fréquence cardiaque, de sa variabilité, et de la fraction d'éjection ventriculaire gauche.

Heart rate variability is a useful parameter for risk stratification after myocardial infarction. However, the relationship between heart rate itself and its variability has not been adequately studied. The authors compared the average RR interval of 24 hours recorded by Holter monitoring with the variability of heart rate and of left ventricular ejection fraction to assess the risk of death after myocardial infarction. A total of 579 patients was followed up for 2 years after acute myocardial infarction. During this period, there were 54 deaths, 42 of cardiac origin, 26 being classified as sudden death. The positive predictive value of left ventricular ejection fraction was lower than those of mean RR interval and the variability of heart rate for overall mortality, cardiac mortality and sudden death. The three indices were essentially equivalent for the prediction of non-sudden cardiac death. The positive predictive value of heart rate variability was better than the mean RR interval for sensitivities < 40%, for all cause mortality. However, for sensitivities > 40%, the two parameters were equivalent or slightly in favour of the mean heart rate over 24 hours. The authors conclude that the mean RR interval over 24 hours is an important prognostic index after myocardial infarction. This index is more powerful than left ventricular ejection fraction and comparable to heart rate variability.

[Radiofrequency ablation: physical bases and principles]. / Ablation par courants de radiofréquence; bases physiques et principes.

Radiofrequency currents are the reference physical agent for endocavitary ablation, especially of supraventricular tachycardias. They are delivered in a continuous mode or sinusoidal waves. Because of the high frequency between 200 and 3,000 kHz there is no stimulation of the neuromuscular cells. The mechanism of the resulting lesion is essentially related to heating of the biological surroundings of the active electrode. The temperature increase remains localised around the active electrode and its kinetics are progressive, which implies close and stable contact between the active electrode and the tissues. The lesional effect is obtained 60 to 90 degrees C in order to avoid the deleterious effects induced by temperatures of over 100 degrees C: boiling, coagulation, vaporization and carbonization of the tissues leading to an increase in impedence. The volume of lesions depends on many factors which are sometimes difficult to control in vivo. It is more closely correlated to the temperature of the active electrode than to the parameters of delivery (power, duration ...). The histological lesions correspond to scar tissue which respects the surrounding architecture. The major technological innovations of this method have resulted in an increase in the volume of the lesions produced, a reduction in the frequency of undesirable effects such as the formation of coagulum and in an immediate evaluation of the anatomic lesional effect. They have consisted in the introduction of specific electrodes and of systems of monitoring the electrical and thermal effects with the use of imaging techniques such as endovascular and transoesophageal echocardiography and angioscopy. New indications will require development of specific catheter-generator equipment to create lesions of size and shape adapted to the arrhythmogenic substrate.

[Reproducibility of signal-averaged electrocardiography]. / Reproductibilité immédiate de l'électrocardiogramme à haute amplification et moyennage.

The reproducibility of the parameters defining the presence of late potentials on the signal-averaged electrocardiogram is one of the limiting factors of the method. The authors studied the coefficients of correlation and reproducibility of these parameters in patients with coronary artery disease. In addition, they tried to determine which parameter was most often responsible for changing a diagnostic conclusion (i.e., presence or absence of late potentials). Two signal-averaged ECGs were recorded one after the other in 127 patients. The presence of late potentials was defined as the presence of a least two of the following criteria: total amplified and averaged QRS duration (tQRS) > 114 ms: duration of the last signal of under 40 microV (LAS) > 38 ms, and root mean square of the amplitude of the last 40 ms (RMS) < 20 microV. The correlation coefficients were 0.98, 0.96 and 0.94 for the duration of tQRS, LAS and RMS respectively (p < 0.0001). The coefficients of reproducibility were 7.0 ms. 7.0 ms and 16.1 microV respectively. Late potentials were present in 22% of patients. A change in diagnosis between the first and second recording was observed in 10 subjects (8% of the population). A combined change in LAS and RMS was responsible for 6 of these revised diagnoses, a change in LAS alone in 2 cases, of the RMS alone in 1 case and the tQRS alone in 1 case. In patients with coronary artery disease, the immediate reproducibility of the diagnosis of late potentials is affected by changes in LAS and RMS. The tQRS is only rarely responsible for a change in diagnosis. This study suggests that the result of the signal-averaged ECG should be interpreted with caution when the LAS or RMS are near their threshold values.

[Changes in heart rate variability after myocardial infarction. Value of Poincareé's diagram]. / Evolution de la variabilité de la fréquence cardiaque après infarctus du myocarde. Apport du diagramme de Poincaré.

The variability of the heart rate is reduced after myocardial infarction. It then progressively increases, to return to near normal values after several months. However, these changes in heart rate variability occur at the same time as slowing of the heart rate which makes interpretation difficult. Poincaré's diagram is constructed from a Holter recording plotting each RR interval against the preceding RR interval. The authors have developed a geometric approach to this diagram to evaluate parasympathetic tone for a given heart rate. By measuring the dispersion in height of the Poincaré's diagram, the authors evaluate the shor-term variability for a given RR interval. Two 24 hr Holter recordings were performed in 52 patients at one and two weeks after a myocardial infarction. The dispersion in the height of the Poincaré's diagrams was measured at the 10th, 25th, 50th, 75th and 90th percentiles of the total dispersion. The authors have shown an increase in the short-term variability of the shortest RR intervals (1th, 25th and 50th percentiles) which is not observed in the longer RR intervals (75th and 90th percentiles). In conclusion, theres is an increase in the heart rate variability at the shortest RR intervals. This suggests that the recovery of parasympathic tone after myocardial infarction occurs mainly at the fastest heart rates.

[Influence of the duration of recording in the reproducibility of the signal averaged electrocardiogram]. / Influence de la durée de l'enregistrement sur la reproductibilité de l'électrocardiogramme à haute amplification.

The authors studied the possibility of improving the reproducibility of the signal averaged ECG by increasing the number of averaged QRS complexes. One hundred patients were included in the study. In each cases, 400 QRS complexes were recorded on twice, consecutively, in strictly identical conditions. During each recording, the total duration of the amplified and averaged QRS complex (tQRS), the duration of the terminal signal below 40 microV (LAS) and the root mean square of the amplitude of the last 40 ms (RMS) were determined for 100, 200, 300 and 400 recorded QRS complexes. The presence of late potentials was defined as the positivity of two of the following criteria: tQRS > 114 ms, LAS > 38 ms, RMS < 20 microV. The number of contradictory diagnostic conclusions between two successive recordings of the same duration decreased progressively with the number of averaged QRS complexes: 10 for 100 QRS, 10 for 200 QRS, 9 for 300 QRS and 6 for 400 QRS complexes, but this improvement was not statistically significant. The absolute differences of tQRS and RMS between two successive recordings of the same duration were statistically different for the four durations of recording (p = 0.05) and there was a tendency towards statistical significance for LAS (p = 0.09). The best quantitative reproducibility of the 3 parameters was obtained with the recording of 300 QRS complexes. In conclusion, the reproducibility of the signal averaged ECG is improved when the number of average QRS complexes is increased. The authors' results suggests that reproducibility this is optimal with the amplification and averaging of 300 QRS complexes.

[Management of arrhythmias in patients with heart failure]. / Prise en charge des arythmies chez l'insuffisant cardiaque.

Cardiac failure is a common cause of arrhythmia. Many factors predispose to the genesis of arrhythmias in these patients. A number of non-invasive methods allow stratification of the risk of arrhythmia in cardiac failure. Approximately half the deaths of these patients are due to arrhythmia. Unfortunately, most of the investigations for risk evaluation have a high negative predictive value but a lower positive predictive value. The treatment of supraventricular arrhythmias, mainly atrial fibrillation, is complex in cardiac failure. Class I antiarrhythmics are contraindicated. The only remaining options are Class II, especially Sotalol, and Class III drugs, especially Amiodarone. In some cases, non-pharmacological methods such as ablation, pacing or an implantable atrial defibrillator must be considered. The treatment of ventricular arrhythmias is also difficult. In this indication, Class I antiarrhythmic agents must also be avoided. Non-sustained ventricular tachycardia may be treated by betablockers or amiodarone. The use of an implantable defibrillator is increasingly recommended after the results of several controlled large scale trials. The indication is obvious in patients resuscitated from sudden death and these devices are also beneficial in sustained ventricular tachycardia in patients with cardiac failure. Many studies are currently under way to determine the value of this therapeutic modality in indications now considered to be "prophylactic".

[Mechanisms of atrial fibrillation: recent advances]. / Mécanismes de la fibrillation auriculaire, acquisitions récentes.

Atrial fibrillation (AF) is due to the presence of multiple reentry pathways. Although this mechanism has been known for some time, new information has recently been acquired about the factors of atrial vulnerability and the conditions of myocardial alteration. There are two main factors of atrial vulnerability: intra-atrial conduction defects and abnormalities of the refractory periods. In addition, the concept of critical mass and the influence of the autonomic nervous system have to be taken into consideration. The abnormalities of the refractory periods liable to increase atrial vulnerability are their shortening, spatial dispersion and poor adaptation to the heart rate. All these changes may be demonstrated at cellular level. The product of the intra-atrial conduction velocity and the duration of the refractory period defines the wave length. The risk of developing reentry pathways increases as the wave length shortens. Moreover, the more the atrium fibrillates, the greater will be the decrease of the refractory periods, atrial fibrillation giving rise to atrial fibrillation. Histological lesions of the atrial tissue may be demonstrated, even in the absence of underlying cardiac disease. They mainly consist of fibrosis, fatty degeneration and myocytic hypertrophy. In the long-term, atrial fibrillation leads to a number of structural abnormalities of the atrial, and sometimes ventricular tissues, progressing to cardiomyopathy in some cases.

[Measurement of the vascular mass of the human radial artery by ultrasonics]. / Mesure de la masse vasculaire de l'artère radiale humaine par méthode ultrasonique.

OBJECTIVE: To determine the reproducibility of radial artery mass (RAM), in hypertensive patients. DESIGN AND METHODS: In 49 patients, RAM was measured using a high resolution echotracking device (Nius-02) which allows noninvasive measurement of diameter and wall thickness of the radial artery. RAM was validated in vitro by comparing weight of arterial segments to ultrasonographic measurement and determined as RAM = r (pi Re2-pi Ri2) where r is the arterial wall density (1.06 g/cm3), and Re and Ri are values of internal and external radii, respectively. Repeatability coefficient (RC2 = SDi2/n) was 1.3 mg. RESULTS: Blood pressure was (mean +/- SD) 146 +/- 19/85 +/- 15 mmHg, radial arterial diameter was 2,449 +/- 376 microns, radial wall thickness was 302 +/- 68 microns, RAM was 28 +/- 9 mg (range 13-43 mg). CONCLUSION: These results indicate that radial artery mass can be measured using a high resolution echotracking device.

[Dual chamber rate responsive pacing and chronotropic insufficiency. Comparison of double and respiratory sensors]. / Stimulation double chambre à fréquence asservie et incompétence chronotrope. Comparaison d'un capteur d'activité, de ventilation et d'un double capteur.

Late responsive DDD pacemakers are the most technically advanced devices presently available. These pacemakers are particularly useful in patients with chronotropic insufficiency when the sinus node is incapable of accelerating during exercise. The latest pacemakers have two sensors to reproduce optimal physiological sinus acceleration. The aim of this study was to analyse the performances of a new rate responsive pacemaker with a double activity and respiratory sensor, the interaction of which is automatically controlled by a sophisticated algorithm, in 12 patients (8 men and 4 women) with a mean age of 75 +/- 7 years. Analysis was based on the performance of the sensors used singly or in association: during three exercise stress tests with measurement of the VO2 max; during everyday activities using the data archived by the pacemaker and the answers to a simplified questionnaire on quality of life. The results showed that during exercise stress testing with measurement of VO2 max, the best performances were obtained with the double sensor or the respiratory sensor compared with the activity sensor alone, suggesting that these two sensors are more effective in intense exercise. This tendency was also observed in the analysis of the memory bank of the pacemaker which showed that the total duration of the faster heart rates was greater with the two sensors. On the other hand, the quality of life was not significantly different, whichever sensor was studied. Longer scale trials are necessary to appreciate the real value of these new double sensor pacing devices and to identify the best indications for their usage.

[Effect of dimethicone on pharmacokinetics and pharmacodynamics of ethyl biscoumacetate]. / Effet du diméticone sur la pharmacocinétique et la pharmacodynamie du biscoumacétate d'éthyle.

The influence of dimeticone (Gel de Polysilane Midy) on the pharmacokinetics and pharmacodynamics of oral ethyl biscoumacetate was studied in 6 healthy volunteers in a randomised single dose, two-way cross-over study. Each volunteer received at one week interval a single dose (300 mg) of ethyl biscoumacetate, either alone or with dimeticone. Ethyl biscoumacetate levels were measured in plasma for 24 hours. Pharmacodynamic parameters were measured for 96 hours. Ethyl biscoumacetate peak concentration was significantly higher when administered with dimeticone (40.3 +/- 25.3 mg/l vs 31.0 +/- 25.7 mg/l; p = 0.031), without significant change in the area under curve. Other pharmacokinetic and pharmacodynamic parameters did not differ significantly. The slight increase of the ethyl biscoumacetate bioavailability with dimeticone in repeated dosing might have pharmacodynamic consequence; a clinical trial should address this question.

[Chronotropic incompetence: when should a pacemaker be considered? Which pacing system and which settings?]. / Incompétence chronotrope: quand faut-il envisager l'implantation d'un stimulateur cardiaque? Quel stimulateur et quels réglages?

Chronotropic incompetence is defined as the inability to increase and maintain heart rate appropriately during exercise. Intolerance to exertion is manifested by a number of clinical symptoms, and is almost obligatory if heart rate cannot be increased. Several rate-modulating pacing systems have been developed. The most obvious and reliable way to increase heart rate during exercise is to detect the sinus node. Adding an atrial lead in a patient in complete AV block and VVI pacing is the most satisfactory way to correct chronotropic incompetence in some patients. Rate-adaptive sensors include motion sensors, respiration sensors, QT interval, and right ventricular contractility. Indications for rate-adaptive pacing should be based on clinical symptoms, demonstration of a lack of cardiac acceleration during exercise, and the presence of another indication for pacing.