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Results of Translation by Babelfish from French to English  click here for the Original

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Although the forecast of many cardiovascular affections improved considerably these last years, the problem of mortality and in particular of sudden mortality remains whole among certain patients who have an advanced cardiopathy. Indeed, when the fraction of ejection of the left ventricle is lower than 30 %, the total and sudden mortality of these subjects reaches 20 more to 40 % at the end of one year [ 1 ]. the evaluation of the factors of risk of sudden death thus remains significant. The analysis of sinusal variability proved to be a useful examination to evaluate the risks of sudden and rhythmic total mortality after a myocardial infarction or cardiac insufficiency [ 2-5 ]. The identification of the exact mechanism of the mortality of these patients, having a loss of their sinusal variability, appears desirable if a prevention must be considered. The goal of this work was to seek the mechanism of the mortality of the patients who have an advanced cardiopathy and his possible relationships to modifications of the autonomous nervous system, reflected by the various indices studied in sinusal variability. 

METHODS Patients  For 12 years, we have observed 17 apparently sudden deaths during a Holter recording 24 hours. These deaths all occurred in a hospital medium, service of rehabilitation for one of them, service of general medicine for 4 others and cardiology for 12 patients. Three patients could be reanimated. The 17 patients were old 53 to 88 years (average: 78,5 ± 10 years); they were 8 women and 9 men. Five patients were hospitalized for faintnesses, 5 for a recent myocardial infarction (J4 with J6), a patient for episodes of paroxystic auricular fibrillation and the others were treated for a cardiac insufficiency. All the patients had a cardiopathy subjacent evolved/moved with with the echocardiography a fraction of ejection evaluated below 40 %. It acted of an ischaemic cardiopathy of origin in 9 cases, of a primitive cardiomyopathy in 3 cases, of a valvular cardiomyopathy of origin in 2 cases, of a cardiopathy of hypertensive origin in 2 cases and of a cardiopathy of unknown cause at a 82 year old woman. Four subjects were in chronic auricular fibrillation. The patients had a whole a cardiovascular processing: digitalic at 2 of them, antiarythmiques of class 1 among 2 other patients (hydroquini-dine for one, disopyramide for the other), beat-blockings among 3 patients, amiodarone among 3 patients, small amounts of dopamine at a patient. The death generally occurred the afternoon (8 cases), the night among 5 other patients, in the evening among 3 patients and the morning only in 1 case.

Method of study

The Holter recordings were read on an apparatus Elatec (Ela Médical). The variability of the sinusal rate/rhythm was studied in analysis of time and spectral analysis, thanks to the software Elatec version 3.02. The temporal analysis of sinusal variability made it possible to determine the following indices: 
    - Fr C: average heart rate; 
    - SDNN: standard deviation of all normal intervals RR over the 24 hours; 
    - pNN50: percentage of the difference between average intervals RR normal and those which have more than 50 ms compared to this average RR. 

Sinusal variability is evaluated all the 5 min but also on 24 H or during the day and the night. In transformed spectral analysis of Fourier the analysis is carried out and calculated on 256 S with a over-lapping of 128 S. the measurement of the low frequency spectra (BF) and high frequency (HF) is indicated for 24 h. for the day and the night and hour per hour. Two curves corresponding to a low frequency and high frequency spectral tape are obtained on the nycthémère, as well as a curve indicating the report/ratio low/high frequency.

 RESULTS

Analyze electrocardiographic recording of the 24 H front and during the death of the patient

 Lenregistrement Holter showed the presence of an arrhythmia ventricuiaire of rank IV among 11 patients in the hours preceding the death. 

The death does not seem due to a disorder of the rate/rhythm in 2 cases: it appears simply a progressive deceleration {slowing?} of the heart rate among these 2 patients. 

The death is ascribable with a complete bradycardia per block auriculoventriculaire or asystole among 5 patients. 

The death is due to a disorder of the rate/rhythm ventricuiaire among 10 patients, tachycardia mono-morphe ventricuiaire degenerating into fibrillation ventricuiaire in 3 cases, primary fibrillation ventricuiaire in 3 cases, tachycardia ventricuiaire polymorphic likely to resemble a twist of points and degenerating into fibrillation ventricuiaire in 3 cases and flutter ventricuiaire in a case.

Analyze clinical characteristics associated with these causes with death 

The deaths in connection with a disorder of the ventricular rate/rhythm are found among 5 patients who had been allowed for faintnesses or losses of consciousness. 

       fig. 1 - Heart rate variability in a 79 year old woman who died of bradycardia (bottom) (patient 15). The heart rate variability is reduced (SO : 26 ms LF/HF ratio : 0.98) ; LF and HF increase suddenly before death, with an increase in LF/HF ratio.

Five patients died a few days after the acute phase of their myocardial infarction (J4 with J6). Only one of these deaths is due to a ventricular tachycardia. The Holter recording of the 24 H showed at this patient of many salvos of ventricular tachycardias before occurred of the event final-In 6 cases, the deaths probably are supported by a cardiovascular processing with a contemporary bradycardia of the introduction of a beat-blocking processing the same day and a block auriculoventriculaire under digoxine; 2 of the 3 patients who presented a final ventricular tachycardia were treated by a drug with tonicardiaque aiming with low dose of dopamine at one of them and an overdose digitalic at the other; in the case of polymorphic ventricular tachycardias, two of them could correspond to " twists of points ". caused by disopyramide for one, deThydroquinidine for the other, but this diagnosis is impossible to affirm on a Holter recording 2 tracks. The 3rd patient had been treated by amiodarone for 8 days because the assessment of its losses of consciousness had made it possible to show that in programmed ventricular stimulation one induced a constant ventricular tachycardia monomorphe. 

Table I
It is thus difficult to accuse the amiodarone; if a arythmogene effect of the amiodarone is drawn aside. this product was shown in all ineffective cases. Ischaemia is frequently found in our series. It explains in 3 cases of the episodes of bradycardia per block auriculoventriculaire, because they were preceded by a know-shift by ST Net before the final event; it explains one of ventricular fibrillations which was preceded by a Net know-shift of ST (table I). Analyze sinusal variability in the hours which preceded the death All the patients, except one, have a severe deterioration of their sinusal variability (fîg.1). If we exclude the 4 patients with auricular fibrillation from the temporal analysis of sinusal variability (fig. 1). the analysis of the standard deviation being impossible since the rate/rhythm is not sinusal any more. it appears that the standard deviation among other patients is always lower than 60 ms safe at a patient, varying from 26 to 86 ms with a total average of 53 ± 14 ms. 

In the whole of the population, the report/ratio of the spectral capacities is also ploughed up, variable from 0,16 to 3,44. with an average report/ratio with 1 ±0.7. This deterioration of sinusal variability is found whatever the final mechanism of the death, bradycardia, fibrillation or causes nonrhythmic (table 1). Analyze sinusal variability occurring right before the death The heart rate remains stable in 7 cases, accelerates in 5 cases in particular in the cases of ischaemia and slows down in 5 cases. Among 13 patients, it appears an abrupt variation of the spectral powers with a brutal rise with the profit in the low frequency spectrum and the report/ratio low fréquence/haute frequency thus increases in 10 cases (fig. 1 and 2). Only in 3 cases, the rise in the power of the high frequency spectrum is more significant than that of the low frequency spectrum, with a final reduction in the report/ratio low fréquence/haute frequency (fig. 3, new page), element in favour of an increase in tonicity sympathetic nerve at the time of the death. 

These modifications are again independent of the mechanism of the death, bradycardia or tachycardia. They are however constant in the cases associated with an ischaemia. In 4 cases, there is no modification of sinusal variability before the death. Two of the 4 deaths are not rhythmic. Lastly, the modifications of the parameters of the temporal analysis are not always concordant with those of the parameters of the spectral analysis, although they are likely to reflect the same variations of the autonomous nervous system. Thus pNN5O and high frequency which reflect tonicity vagal do not vary constantly in the same direction (table II).

DISCUSSION

This work confirms certain data gathered which are the presence of an advanced subjacent cardiopathy among these patients and the frequency of the disorders of ventricular exitability final, like already showed it J.-F. Leclercq and coll in a French co-operative study on the sudden death documented during a recording Holter [ 6]. This study also confirms that the loss of sinusal variability is an element bad forecast [ 2-5 ]. 

fig- 2 - Study of heart rate variability in an 88 year old woman who died of ventricular tachycardia (bottom). Heart rate variability is reduced (SO : 43 ms, LF/HF ratio : 0-16). The LF increased suddenly before death explaining the increase in LF/HF ratio.

The relations between the modifications of the autonomous nervous system and sudden death were already underlined by several authors [ 7, 8 ], these studies preceding having shown that the loss of tonicity vagal and the adrenergic increase in tonicity could facilitate the disorder of the final rate/rhythm. However, Coumel [ 7 ] recently showed that it was difficult to authenticate these variations of the autonomous nervous system at the time of the death, by showing that there was generally no obvious variation of the heart rate immediately before the death; that did not want to say that the autonomous nervous system was not causes some and simple-vagal was besides ineffective to decrease the risks of ventricular fibrillation postinfarctus [ 15 ]. In our study the rise in the low frequency spectrum is more in favour of an increase of tonicity sympathetic nerve at the time of the death, than of the modifications of vagueness. 

The study of sinusal variability such as it is currently proposed, is thus enough frustrating to predict the mortality of the patients and especially its mechanism. That tends to confirm that sudden cardiac deaths have extremely multiple origins [ 16-18 ] and that the only really proven element is the gravity of the subjacent cardiopathy [ 19 ]. Sudden death is plurifactorielie. from where the difficulty of prevention. In addition, the multiplicity of the mechanisms of mortality of our patients confirms the difficulty in classifying cardiac deaths in spite of, moreover, of many recent proposals [20-22].

     fig. 3 - Study of heart rate variability in a 86 year old woman who died of ventricular fibrillation (bottom). The heart rate variability was modified (SD : 50 ms, LF/HF ratio :0.66). Death was preceded by a sudden increase of LF and HF so that LF/HF did not change.

Conclusion

This study confirms that the sudden mortality of cardiac subjects occurs at those which have a very advanced cardiopathy and which have for the majority a loss of their sinusal variability. However, the mechanism of the death is extremely divergent from one patient to another and if it appears an abrupt imbalance vagosympathic at the time of the death it is not at all certain that this imbalance is responsible for the disorder of the final rate/rhythm which is of nature variabie. bradycardic or tachycardic.