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Electrical cardioversion is a critical treatment for the survival of patients with cardiac arrest due to ventricular tachycardia or fibrillation. Consequently, it is necessary to determine if they are due to myocardial infarction or to damage produced by electrical cardioversion and other resuscitation maneuvers.
In this study we proposed to determine a if electrical cardioversion procedures produce myocardial damage and to quantify it in two clinical electrical cardioversion situations: external, or conventional, cardioversion and internal either through a specific defibrillation system or through the electrodes of an automatic defibrillator ; b the extension of the possible myocardial damage and its correlation with cardioversion variables energy applied , and c the concentrations and kinetics of cTnI and the different markers of myocardial injury after electrical cardioversion.
This study included patients referred to the Arrhythmia Unit of our hospital for electrical cardioversion. All patients gave their written consent. All patients who in the preceding month presented myocardial infarction, unstable angina, muscular trauma including treatment with intramuscular injections , or infectious disease were excluded. We prospectively and consecutively analyzed the data of 30 patients who underwent electrical cardioversion.
The group of external cardioversion was formed by a total of 15 patients 11 men and 4 women. Thirteen of them 11 men and 2 women underwent scheduled cardioversion for supraventricular arrhythmias atrial fibrillation in 8 and atrial flutter in 5 and 3 patients 1 man and 2 women underwent electrophysiological study with programmed pacing who required defibrillation by external electrical cardioversion ECv all 3 for atrial fibrillation.
On the other hand, in the group of internal cardioversion a total of 15 patients 10 men and 5 women were analyzed. In 7 of them 3 men and 3 women conversion of atrial fibrillation was carried out by means of internal electrical cardioversion ICv.
In these patients ICv was performed because they had been previously refractory to ECv. Finally, in the remaining 8 patients 6 men and 2 women cardioversion was performed for ventricular defibrillation that occurred during implantation of an automatic defibrillator.
ECv was carried out using two different systems: a in 5 patients with two rectangular self-adhesive plates of 8. The procedure was carried out under mild sedation with propofol mg. Discharges of monophasic, exponential and truncated direct current were administered, synchronized with the QRS wave, between two plates or paddles. The initial energy ranged from to J and discharges were repeated until sinus node rhythm was achieved or two maximum energy discharges were delivered J.
All shocks were monophasic. The electrodes were connected to an external defibrillator capable of delivering biphasic, low-energy discharges. The shocks were administered with progressively greater energies from 2 to 15 J.
The shocks were always monophasic. The defibrillator was implanted in the electrophysiology laboratory. Percutaneous puncture of the subclavian vein was performed, leaving a 0. An incision was made in the left pectoral region, below the clavicle. Later a pocket was prepared under the fascia of the greater pectoral muscle.
The sensing and defibrillation electrode was introduced into the apex of the right ventricle through a The electrodes were mostly passive fixation electrodes Medtronic or CPI , except for those used with the Medtronic Transvene system active fixation.
Anesthesia with intravenous propofol was administered mg dose, based on weight and age. A first low-energy 0. Then ventricular fibrillation was induced, either by a shock on T or with alternating current. In the first shock energies between 15 J and 20 J were used and reduced progressively until reaching the threshold or achieving an acceptable minimum defibrillation energy safety margin of more than 10 J.
These shocks were always biphasic. In all patients, after each procedure any change in the clinical state, modifications of the ST segment, and the appearance of new arrhythmias were recorded.
For serum determinations of markers, 5-ml samples of peripheral blood were collected in tubes without anticoagulant in accordance with the following scheme: pre-cardioversion extraction baseline and extractions 2 h, 8 h, and 24 h after the procedure.
All samples were centrifuged within 60 min of collection. From a fresh aliquot of the baseline sample, a biochemical study was made that included the determination of glucose, creatinine, urea, sodium, potassium, and aspartate aminotransferase activity.
Routine Hitachi analyzer techniques were used Roche Diagnostics. CK activity was determined with an Integra analyzer Roche Diagnostics.
The Wilcoxon test was used in variables without a normal distribution, and their results were expressed as the median and interquartile intervals. To determine statistical differences between continuous variables, the Student t test was used. Patient weight ranged from 62 to 95 kg The 30 patients analyzed underwent 73 electrical discharges with direct current. No complications were observed during or after cardioversion in any patient, nor were changes in the ST segment detected.
In all patients, conversion of the arrhythmia was achieved and 24 of the 25 patients remained in sinus rhythm after 24 h. With respect to the number of cardioversions, cumulative energy and maximum energy applied, we found significant differences between external cardioversion with a smaller number and higher energy and internal cardioversion larger number and lower energy. It should be emphasized that in the internal cardioversion group, although there were no significant differences in the maximum energy applied, we observed a larger number of cardioversions and greater cumulative energy in patients with automatic defibrillator 4 cardioversions and 76 J versus 3 cardioversions and 25 J for internal defibrillators and internal cardioversion, respectively.
In this respect, there were no differences between types of external cardioversion plates and paddles. Markers of myocardial lesion after external cardioversion. The different parameters evaluated in the routine biochemical study of the baseline sample presented values within normal reference limits in 14 patients. Only some of these parameters were altered in a female patient diagnosed as kidney failure CK, 3. In the same patients abnormal myoglobin concentrations were found, and in two of them, abnormal CK-MB mass concentration.
These 5 patients had received at least one defibrillation shock at an energy over J; in addition, they required cumulative energies of more than J, which was statistically significant P. In contrast with the rest of the markers, cTnI concentrations remained within normal limits, and no pathological elevations were detected in any patients.
Not only were no abnormal values detected, but in the 15 patients in our study cTnI concentration constantly remained below the limit of detection of the technique 0. As far as the kinetics of the markers Figure 1 , it must be emphasized that the peak values of the earliest markers were reached in 8 h myoglobin and 24 h CK-MB mass in most patients 13 of In this figure, the markers of myocardial lesion markers in patients in the external electrical cardioversion group ECv that surpassed the cutoff point of the marker in any extraction are shown.
The concentration of the marker in each extraction, peak value reached, and cutoff point are shown in relation to time hours after the procedure.
In the case of cardiac troponin I cTnI , no patient had values above the limit of detection of the technique 0. Two patients presented slight elevations in CK-MB mass at 24 h, whereas a third patient had a clear elevation from 2 h on, although this patient also reached the peak value at 24 h. This same patient patient 11 , who had extremely pathological myoglobin and creatinine CK values, is shown on a secondary Y axis in the graphs of these markers for purposes of illustration.
Correlations in external cardioversion. The coefficients of correlation between the peak values of the same markers and the total energy applied were also higher than 0. Markers of myocardial lesion after internal cardioversion. These percentages of patients with pathological results were similar to those obtained after ECv for the same markers Table 2. These two patients were the two men who underwent defibrillator implantation and received the largest number of electrical discharges: 14 and 7, versus a median number range of 4 cardioversions in the other 10 patients.
We found pathological elevations of CK activity in 3 more patients in this group, all of whom had an implanted defibrillator. The myoglobin concentrations and observed CK activity after ICv were significantly lower P The 7 patients in the ICv group who underwent ICv for atrial fibrillation were the patients with the lowest number of cardioversions 1.
It is notable that in these 7 patients none of the markers studied reached abnormal values. With regard to kinetics, in the ICv group the peak values of the earliest markers myoglobin and CK-MB mass were reached in an earlier extraction 2 and 8 h post-cardioversion, respectively than in the ECv patients in most cases.
The peak cTnI value occurred 8 h post-cardioversion in the only 3 patients in which cTnI concentration changed. It should be emphasized that the 2 patients in which myoglobin rose without an elevation in cTnI and CK-MB mass presented peak values at 8 h instead of 2 h as in the patients in which cardiospecific markers did rise.
Correlations in internal cardioversion. The best correlations between peak marker values, the number of cardioversions, and cumulative energy were obtained with the most cardiospecific markers cTnI and CK-MB mass; 0. We found no correlation between any of the markers and the maximum energy reached all less than 0. Since Beck established in the basis for the emergency treatment of cardiac arrest and ventricular fibrillation by external application of continuous electrical current, this has been introduced in clinical practice for the conversion of tachyarrhythmias.
The application of discharges of direct current can cause reversible damage of subcellular structures involved in oxidative phosphorylation 12 and originate a variable release nonspecific proteins of striate cardiac muscle, including CK, CK-MB, and myoglobin, which makes the diagnosis of a previous acute myocardial lesion difficult.
External electrical cardioversion. In our study, cTnI concentrations always remained undetectable after cardioversion. In contrast, we observed pathological elevations in CK activity, CK-MB mass, and myoglobin, respectively, as in previous studies. Since the studies of Resnekov and McDonald in the late s, 21 it is known that the peripheral skeletal muscular damage is the most common adverse effect of ECv. Injury of the chest wall skeletal muscle, which produces release of noncardiospecific markers after cardioversion, has been clearly demonstrated by histopathological studies 22 and imaging techniques with radionuclide uptake.
In our series of patients, an excellent correlation was demonstrated between the elevation of noncardiospecific markers CK activity and myoglobin , the number of cardioversions, and the total amount of applied energy, with coefficients of correlation of more than 0.
As for the correlation between markers after ECv, there was a magnificent correlation between peak CK and myoglobin values, scant correlation between these markers and CK-MB mass r Some studies have reported slight elevations in troponins, cTnI in a small percentage of patients 3 of 38 and with low values 0. We did not observe such elevations in our study, probably because the converted arrhythmias were supraventricular and no patients with ventricular tachycardia were included.
Internal electrical cardioversion. In the ICv group, we observed elevation of the cTnI concentration and other markers to pathological values in two patients who underwent defibrillator implantation. In addition, in a third patient cTnI elevation to detectable values 0. These elevations took place in the patients who received more total energy and greater number of cardioversions. After repeated ICv during defibrillator implantation, we observed abnormal CK and myoglobin concentrations without elevation of the most cardiospecific markers in other patients.
These elevations must be induced by the same circumstance as those detected in electrical cardioversion. In the case of ICv, these elevations are smaller, because less energy is used and this energy is transmitted to skeletal muscle in a more indirect way. In the 4 patients who underwent ICv in our study, we did not detect any variation in marker values.
In these patients we used fewer cardioversions and applied less total energy, since it is a very effective technique for achieving conversion to sinus node rhythm of patients with atrial fibrillation in which the ECv technique has failed for different reasons.
It should be remembered that the cTnI titers reached around 1. This type of damage is very similar, as much in the concentrations reached as in their kinetics, to that observed in electrophysiological studies by catheterization. On the other hand, the CK and myoglobin values reached after ICv in our study are clearly lower than those reached after ECv.
Consequently, it seems that ICv is capable of converting arrhythmias, with minimal myocardial damage in a low percentage of patients, and produces less skeletal muscle damage than ECv. Usefulness of cardiac troponin I in emergent cardioversion.
The combined effects of prolonged cardiopulmonary resuscitation and multiple cardioversions have not yet been properly established, which is why caution is necessary when extrapolating these results to this type of patients.
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I Docente. Os dados foram analisados por meio do teste t pareado. Esses dados da literatura internacional corroboram esta pesquisa. Arq Bras Cardiol ;69 6 Sampaio LABN. Automatic external defibrillators in the hospital as well?