Arrhythmias and left ventricular function after defibrillation during acute myocardial infarction in the intact dog

The purpose of this study was to assess the recovery of the left ventricular pressure (PLv), and the incidence and type of arrhythmias after effective low-dose defibrillation (I,,, = 18 - 70 A) in healthy hearts and in hearts with acute myocardial infarction (AMI) in the intact dog. In fifteen dogs 84 episodes of fibrillation-defibrillation were studied in the healthy heart and 53 episodes were studied in the acute phase of myocardial infarction % to 3 hours after occlusion of a part of the left anterior descending artery by a catheter technique. Time to recovery of PLV depended on duration of fibrillation (tF) and cumulative defibrillation current (I%), and became critical at t, > 45 seconds and I% > 45 A. Total duration of arrhythmias due to defibrillation increased with increasing tF and I%. Arrhythmias which have a relative greater chance of resulting in refibrillation or which may seriously decrease the cardiac output occurred more often with I% > 55 A (p < O-001), when 50% of episodes were followed by these arrhythmias. No differences were found in responses between the healthy heart and the heart with AMI. (AM HEART J 106:292, 1983.)

R. H. Geuze, Ph.D., and J. de Vente, Ph.D. Amsterdam, The Netherlands

Defibrillation with very high energies may result in necrosis of heart muscle cellsls* or even death of the animaL3 Necrosis of heart cells results in release of creatine kinase (C!K)I and may be detected in humans as the isoenzyme CK-MB.5 Defibrillation shocks usually cause arrhythmias, even at low ener- gies.4r6-8 These arrhythmias increase in duration with increasing energy and may result in refibrillation or a poor recovery of the circulation. The hemodynam- ic effects of a 400 joule shock are augmented by prolongation of the duration of fibrillation.g Very high energies result in decreased pump function.4

In human adults ventricular fibrillation (VF) is nearly always preceded by partial or total occlusion of coronary arteries, resulting in ischemic areas within the heart muscle and in arrhythmias.10-12 No experimental studies have been done on the effects of acute myocardial infarction on damage, arrhyth- mias, or hemodynamic changes caused by defibrilla- tion shocks. The present study directs special atten- tion to undesirable effects of defibrillation with delivered energies in the clinical energy range (30 joules to 300 joules) in the healthy and in the acute

From the Department of Medical Physics, Free University. Received for publication Oct. 2, 1981; revision received Feb. 3, 1982; accepted March 3,1982. Reprint requests: R. H. Geuze, Laboratory for Experimental Clinical Psychology, Turfsingel 46, 9712 KR Groningen, The Netherlands.

292

infarcted dog heart. The time from defibrillation to an acceptable level of systolic pressure in the left ventricle (LV) and the type and duration of arrhyth- mias due to defibrillation were studied as a function of defibrillation current and the duration of fibrilla- tion.

METHODS Preparation. Fifteen mongrel dogs weighing 22 to 35 kg

(mean, 28 + 5 kg) with heart weights between 180 and 300 gm (ventricles 203 2 40 gm) were used. After premedica- tion with droperidol and fentanyl (Thalamonal), 5 mg, with atropine, 0.25 mg, anesthesia was induced by thio- pental sodium (Pentothal), 12 mg/kg, and was maintained with inspiration of halothane and an occasional injection of pancuronium bromide (Pavulon), 0.07 mg/kg. Respira- tion was regulated with a Monoghan 300 D/M respiratory pump after insertion of an endotracheal tube. Arterial blood was sampled each hour to determine blood gas values, lactate, and free fatty acid levels. Acidity (pH) was kept within the normal range (7.30 to 7.45) by control of the respiratory rate and by venous bicarbonate infusion. Sedimentation rate of erythrocytes was lower than 30 mm/l hour in all dogs.

Catheters. A USC1 No. 7 French bipolar catheter was introduced through the femoral artery into the LV. This catheter was used for arterial blood sampling, measure- ment of LV pressure (PLv) and LV ECG, stimulation (50 Hz) of the LV to induce VF, and in case of ventricular arrest or severe bradycardia, to stimulate the ventricles. A USC1 No. 7 French monopolar catheter was introduced

Volume 106 Number 2, Cardiac effects of defibrillation in AM 293

through the jugular vein into the right atrium to measure right atria1 pressure and ECG and to sample venous blood.

Recordings. Right atrial ECG, LV ECG, and standard lead II ECG were continuously recorded. PLv and right atria1 pressure were measured through the catheters with Statham strain gauge transducers P23Db. Pressures were recorded before and during 5 minutes following defihrilla- tion. The long catheters (1.25 m) permitted slight oscilla- tions less than 20 % of maximum pressure va1ues.13 There- fore maximum P,v was calculated as mean pressure during the ejection phase of the LV.

Defibrillation. Defibrillation shocks were damped sine waves of 4 msec duration from an Electrodyne (Eld-2) defibrillator. Defibrillation wave form (current and volt- age) was recorded on analog tape from resistors in the output circuit of the defibrillator. Delivered energy, max- imum current, and resistance between the electrodes were calculated afterwards. Defibrillation electrodes 9 cm in diameter were applied to the shaven thorax after the skin had been rubbed with conductive paste.

Coronary occlusion. A No. 8 French Cook catheter with curled tip and a spring guide (0.9 mm) with a guttapercha ball fixed to its tip (Fig. 1) was introduced into the aorta through the femoral artery.14 A Philips x-ray monitoring system (BV22) was used to position the cath- eter tip into the sinus of the left coronary artery. Injection of a contrast agent (Telebrix 38) through the catheter allowed visualization of the left coronary artery system. When the catheter was well positioned, the spring guide was withdrawn and the guttapercha ball drifted down the left anterior descending coronary artery (LAD) some distance, resulting in total occlusion of the distal part (Fig. 2). An intravenous bolus injection of lidocaine (4 mg/kg) was given to prevent serious arrhythmias within the first 30 minutes after occlusion.

Definition of parameters. From studies on morphologi- cal damageI, 2 and arrhythmias,15 it is known that multiple shocks have a partial cumulative effect. This effect depends on the time interval between successive shocks. In this study successive shocks were generally 15 seconds apart and the accumulation factor (0.5) was estimated from these references.*, *K l5 So when multiple shocks were given in one fibrillation-defibrillation episode, cumulative delivered energy (E Yz ) and cumulative maximum current (1%) were calculated with EYz = E. + SE,., + ‘/4E,.2 + YEE,.~ andI% =I,+ %I,.,+ Y41n.a+ %I&, where n is the number of the shock in one episode, n 5 4. Of these two parameters, 1% showed the best correlation with the parameters measured.16

t, is the time from defibrillation to mean systolic PLv, becoming greater than 100 mm Hg (13.3 kPa) during more than 50 msec at least once a second (Fig. 3). At this level, a distinct arterial pulse can be felt in the femoral artery.

Measuring protocol. Fibrillation was induced by a 50 Hz, 15 mA current. Defibrillation was attempted after 15 seconds with 100 joules stored energy. In case of failure, a

14 ’

Fig. 1. No. 8 French Cook catheter with curled tip for occlusion of a part of the left anterior descending (LAD) coronary artery via the arteria femoralis. A spring guide (diameter 0.9 mm) with a guttapercha ball (diameter 2 mm) fixed to its tip is inserted.

200 joule shock was applied after 15 seconds, and this always produced defibrillation. After 30 minutes a second fibrillation-defibrillation episode was measured, with 50 joules energy if the first episode succeeded at first shock, otherwise with 150 joules energy. Second or third shocks were increased in stored energy by 50 and 100 joules if necessary. In the third episode after another 30 minutes, the energy of the first shock was selected near the estimated defibrillation threshold, being the mean value of the highest unsuccessful and the lowest successful energy.16 In three dogs the duration of fibrillation (tr) was varied from 15 to 60 seconds, while the stored energy was kept constant at a level two times threshold. In another three dogs the stored energy was varied from threshold to three times threshold values (5300 joules) and the dura- tion of fibrillation was kept constant at three values (15, 30, and 45 seconds). Each 30 minutes another episode was measured.

In nine dogs after the first three episodes the LAD artery was occluded. From l/2 to 3 hours after occlusion, six more episodes were measured with 30 minutes interval time. Energies ranged from (sub)threshold to three times threshold; duration of fibrillation ranged from 15 to 75 seconds. If t, was greater than 20 seconds, external manual heart massage was started. Five manual compressions were followed by a 5-second rest interval to see if PLv recovered. If not, heart massage was continued.

Three hours after occlusion or in nonocclusion experi- ments after 10 episodes, the heart was fibrillated, the thorax was opened, and the heart was excised. During 5 minutes blood was washed out of the heart by perfusion of the coronary arteries with perfusion fluid,4 The heart was cut into six to eight slices and noninfarcted tissue was colored in a 0.1 M phosphate buffer (pH = 7.4) with nitroblue tetrazoleum (NBT), 0.1 gm/L, for 15 minutes.17 Each slice was again cut into two slices and in three cases a rather sharp boundary was found between bloodless and blood-containing tissue due to nonperfusion of the occlud-

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Fig. 2. Contrast views of the left coronary arteries before (left) and after fright) occlusion of a part of the LAD artery. The occlusion catheter is at the left in the views. The left circumflex artery is superior. Eleven percent of total ventricular weight was infarcted after 3 hours of occlusion.

Fig. 3. Left, Recording of LV pressure before 30 seconds of VF and two shocks of 40 and 70 joules stored energy (II/z = 24 A). Right, Recovery of LV pressure from 1 second after the second shock. Arrow indicates mean systolic LV pressure returning to greater than 100 mm Hg. No arrhythmias followed defibrillation in this episode.

ed region. The infarcted tissue was separated from the noninfarcted tissue and blood-containing tissue was separated from the bloodless tissue. The heart, the ven- tricles, the infarcted tissue, and the blood-containing tissue were weighed. Infarct size was expressed as a percentage of total ventricular weight and in three cases as a percentage of the flow region of the occluded artery as well.

Statistical analysis. Values are given as mean rt stan- dard error of the mean (SEM). The x2 test was used in comparing the incidence of arrhythmias. Student’s two sample t test was used in all other cases. Probability (p) values >0.05 were considered nonsignificant (ns). Because t, and t,, showed a large variation, results are presented as averages +SEM of three or more episodes in one class of I!/2 and t+. Each average was composed of values of one or more episodes in at least two dogs. Difference between the averages was tested with Wilcoxon’s two sample test because t,, tA, and 11/2 showed no normal distri- bution.

RESULTS

A total of 84 episodes from multiple protocols in 15 dogs in nonoccluded hearts resulted in the same range of responses (ns), and are treated as one group. In the ischemic heart, 53 episodes were studied ‘/z to 3 hours after occlusion. The deflbrilla-

tion threshold ranged 20 to 200 joules delivered energy, or 25 to 47 A maximum current. Mean values were 58 + 7 joules, 29 r+_ 2 A in the healthy hearts, and 82 2 20 joules, 35 +- 4 A in the ischemic hearts (ns). In studies with open-chest defibrillation18 and in intracardiac defibrillation,‘g a comparable increase was reported. Transthoracic resistance was 25 to 76 !J (40 -+ 10 a).

Arterial lactate and free fatty acid (FFA) levels were 1.24 -I 0.15 mM (n = 9) and 0.46 +_ 0.06 mM (n = 4) before the first episode. After three episodes prior to occlusion, these levels were significantly elevated to 1.86 k 0.34 mM and 0.72 k 0.09 mM, without further rise. Mean systolic P,, increased from 25 mm Hg during VF to a potentiated level of 110% to 150% of control values 5 to 300 seconds after defibrillation (Fig. 3) and returned to normal values in 1 to 10 minutes. Mean right atrial pressure was augmented during VF, reaching values of 15 to 25 mm Hg and returned to normal values within 10 seconds after mean systolic P,, became greater than 100 mm Hg.

Occlusion. Infarct size 3 hours after occlusion of the LAD artery ranged from 0.6% to 24% of total ventricular weight. In three hearts the nonperfused

Volume 106 Number 2, Cardiac effects of defibrillation in AMI 295

7 HEALTHY HEART

Fig. 4. Duration of low mean systolic PLv (t,) vs cumulative defibrillation current (1%) in the healthy heart (left) and during the acute phase of myocardial infarction (right). Each point is the average value of one or more episodes in different dogs. Different symbols indicate different ranges of duration of fibrillation (t,). The number of values averaged is indicated. Horizontal and uertical bars represent standard error of mean value. Within one range of tF, values were not significantly different. Values combining long tF and high 1% differed significantly from values in the tr < 45 second range (*= p < 0.05, **= p < ciol).-

area was measured and infarct size was 60%) 67%) and 40% of the nonperfused area. Infarcts showed a coherent transmural area distal to the site of occlu- sion and were situated at the apex, the free left ventricular wall, and occasionally in a part of the septum.

Duration of low mean systolic PLv (t,). Tracings of Pi,” recordings immediately after defibrillation were analyzed (Fig. 3). t, was studied as a function of 1% for three ranges of duration of fibrillation: tr = 11 to 21 seconds, tr = 24 to 41 seconds, and tr = 45 to SO seconds (Fig. 4). Only with tr 145 seconds does the duration of low mean systolic PLv increase with increasing cumulative maximum current. For 1% > 45 A and tF L 45 seconds, the average values are significantly higher than in the episodes with tF < 45 seconds. Fig. 5 shows the effect of increasing tr on t,. Each point represents one episode, either in the healthy heart or during acute myocardial infarc- tion (AMI). When tp was greater than 20 seconds, manual external heart massage was started and mean systolic P,, usually recovered within 60 sec- onds. Thus values of tp greater than 20 seconds are influenced by the external heart massage. For tF 3 45 seconds, heart massage after defibrillation was necessary in 73% of episodes.

Duration of arrhythmias (t,). From the standard lead II ECG and from the right atria1 catheter ECG, tA was measured. In cases of diffuse arrhythmias, determination of tA is rather arbitrary. Late single premature beats were not included. Fig. 6 shows registrations of five episodes with increasing tr. The relation between 1% and tA was investigated in three ranges of tr: tF = 11 to 21 seconds, tr = 24 to 41 seconds, and tF = 45 to 75 seconds (Fig. 7). At short

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Fig. 5. Duration of low mean systolic pressure (tJ vs duration of ventricular fibrillation (tF) in 59 episodes in the healthy heart (0) and in 46 episodes in the acute phase of myocardial infarction (A), l/z to 3 hours after occlusion of the LAD artery. Heart massage was started if t, > 20 seconds (horizontal line). Vertical line shows that with tr > 45 seconds heart massage was often needed. The number of episodes in each quadrant is indicated.

duration of fibrillation tA is independent of the defibrillation current. For 1% > 70 A and tr > 45 seconds, the average values of tA were significantly greater than values with tr < 45 seconds, both in the healthy and in the ischemic heart. Durations of arrhythmias longer than 600 seconds were not included. Twice a persisting slow ventricular rhythm

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-

Fig. 6. ECG recordings of five fibrillation-defibrillation episodes in one dog. Respiration is superposed on a standard lead ECG. Top panel, 50 Hz stimulation induced ventricular fibrillation and spontaneous defibrillation. The next four panels show episodes with increasing ty and defibrillation with 300 joules stored energy (delivered energy = 150 joules, maximum defibrillation current = 48 A). Bottom panel shows 3 seconds of ventricular activity followed by 17 seconds with supraventricular premature excitations. In the middle three panels t, and t,, are relatively constant. t, considerably increased at tF = 60 seconds; there is no strict coupling between tn and t, . tF = duration of fibrillation; tA = duration of arrhythmias; t, = duration of mean systolic PLv < 100 mm Hg.

Volume 106 Number 2, Cardiac effects of defibrillation in AMI 297

Fig. 7. Duration of arrhythmias due to defibrillation (tA) vs cumulative defibrillation current (IM) in the healthy heart and during the acute phase of myocardial infarction. See legend to Fig. 4 for further details. Values combining 1% < 60 A and tF < 45 seconds differed significantly from values in the tF > 45 second range.

Table I. Incidence of arrhythmias due to defibrillation with delivered cumulative energies of 50 to 300 joules in the healthy and ischemic heart

Type of arrhythmias

Healthy heart, incidence 5’1 (N) Ischemic heart, incidence O; (N)

I53 <55 A I!$ >%A I ’ L < 55 A I!,! > 55 A

No arrhythmias Supraventricular premature excitations Short-lasting sinus bradycardia Atria1 fibrillation Supraventricular tachycardia* Ventricular premature excitations Slow ventricular rhythm Short-lasting VT (<lo set) Premature excitations (ci < 250 msec)* Ventricular runs* VT (paroxysmal) * VF’ Bradycardia/AV block* Number of episodes

12fu (8) 16 (11) 13 (9) 0 (0) 2 (1) 54 (36) 28 (19) 15 (10) 2 (1) 2 (1) 2 (1) 0 (0) 3 (2)

67

6 SC (1) 6 (1) 24 (4) 0 (0) 0 (0) 41 (7) 6 (1) 0 (0) 12 (2) 18 (3) 6 (1) 0 (0) 24 (4)

17

20°C (7) 9 (3) 0 (0) 0 (0) 0 (0) 54 (19) 20 (7) 3 (1) 6 (2) 6 (2) 3 (1) 0 (0) 0 (0)

34

llF<’ (2) 5 (1) 26 (5) 11 (2) 0 (0) 90 (17) 3” (‘5) 5 (1) 11 (2) 16 (3) 16 (3) 5 (1) 42 (8)

19

Absolute number (N) in brackets. The occurrence of multiple arrhythmias makes the total number in a column different from the number of episodes. Abbreviations: ci = coupling interval; VT = ventricular tachycardia; VF = ventricular fibrillation; AV = atrioventricular. *Indicates a type of arrhythmia that may result in refibrillation or that may seriously decrease cardiac output.

interfering with normal sinus rhythm occurred. In hearts with AM1 very high defibrillation current (1% = 100 A) and tF > 75 seconds resulted once in persisting atria1 fibrillation and once in VF.

Type of arrhythmias. Table I summarizes the inci- dence of arrhythmias due to defibrillation for low currents (11/z < 55 A) and high currents (1% > 55 A) in the healthy and the ischemic heart. In 13% of episodes no arrhythmias occurred at all. Supraven- tricular arrhythmias due to defibrillation were pre- mature excitations, short-lasting sinus bradycardia (<15 seconds), atrial fibrillation, and supraventricu- lar tachycardia. Ventricular arrhythmias were pre- mature excitations, slow ventricular tachycardia

(<lo seconds), premature excitations with a cou- pling interval <250 msec, ventricular runs (<5 sec- onds), (paroxysmal) ventricular tachycardia (VT), and VF from degenerating VT. Disturbance of AV conduction may have been present in all cases with ventricular excitations, but only in a case of bradycardia resulting from partial AV block was it counted in Table I. Short-lasting bradycardia occurred mainly at 1% > 55 A (p < 0.01). Arrhyth- mias which have relatively greater chance of result- ing in refibrillation or which may seriously decrease cardiac output by insufficient contractions occurred more often after use of high defibrillation current (p < O.OOl), when 50% of episodes were followed by

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these arrhythmias. No difference in tp, type, or formance. External heart massage combined with incidence of arrhythmias was found between the artificial ventilation reperfuses the heart22 and healthy and the ischemic heart. Arrhythmias due to may reestablish normal intracellular pH, supply- acute occlusion occurred mainly 5 to 30 minutes ing oxygen for ATP production necessary for con- after occlusion. traction.

DISCUSSION

Necrosis. At the therapeutic level of defibrillation current occasional necrosis3 or CK-MB release5 due to defibrillation may occur. In the present study it is unlikely that defibrillation caused necrosis of heart cells. The infarcted tissue was always located distal to the occlusion and in the flow area of the occluded branch of the LAD artery. Other parts of the heart never showed any macroscopic evidence of damage due to defibrillation. It is possible that defibrillation resulted in more necrotic cells in the border zone of the ischemic area. However, the estimated infarct sizes as a percentage of perfusion area are in close agreement with the data of Schaper et al.‘O

Heart massage. The critical period tF = 45 seconds may be prolonged by external heart massage during VF and by immediate start of heart massage after defibrillationz5 Gascho et al.26 found no difference in the success of defibrillation in patients with varying durations of fibrillation (I+ up to 30 minutes). Only patients with coronary disease and tF < 30 seconds defibrillated better than those with tF > 30 sec- onds.” However, usually heart massage is started while preparing the defibrillator and the patient for the shock, and no data are presented on recovery of circulation in these patients.

Recovery of P,,. The recovery of PLv after defibril- lation is determined mainly by the recovery of the contractility of the left ventricle and the afterload. After defibrillation the electrophysiologic perfor- mance of the heart may be perfectly normal, but still there may be little contraction of the ventricles (e.g., Fig. 6, bottom panel). In intracardiac defibrillation recovery of mean blood pressure was found to increase with tF (10 to 40 seconds).21 The study of Pansegrau and Abboudg suggests a correspondence between systolic P,, and cardiac output and LV strokework, all being potentiated at 1 minute after defibrillation (400 joules). We found that P,, tends to remain low with tF > 45 seconds, especially with high cumulative defibrillation currents 1% > 45 A. With external manual heart massage starting 20 seconds after defibrillation, PLv usually recovered within 60 seconds.

Arrhythmias after defibrillation. tA increased with increasing tF, and with cumulative defibrillation current (1%). The combination of high defibrillation currents I1/2 > 70 A and tF > 45 seconds especially results in long-lasting arrhythmias (Fig. 7). The positive correlation between tA and defibrillation parameters is known from studies during VF2’, 28 and during normal rhythm8 in the intact dog, in the perfused isolated rabbit heart,4 as well as in cultured heart cells.7 Arrhythmias with a relatively greater chance of resulting in refibrillation and those which may seriously decrease cardiac output occurred more often after defibrillation with high cumulative current (1%) (p < 0.001) (Table I). Because of the relative low defibrillation currents used in this study no complete ventricular arrest occurred.6.’ Other studies”. 4.7.8.2X found increasing severity of arrhyth- mias with increasing defibrillation current.

Critical tF. The critical boundary of tF = 45 seconds (Fig. 5) found in this study may well be species- dependent. This critical boundary can be explained by the hypothesis that during the first 45 seconds of VF and perfusion standstill a critical part of the adenosine triphosphate (ATP) available for contrac- tion has been consumed.‘2 The energy supply for contraction is mainly situated in the mitochondria and is dependent on oxygen suppl~.‘~*~~ Intracellular acidosis too may be responsible for the loss of contractility by displacement of Ca2+ from the con- tractile elementsz3 The electrophysiologic cycle of the heart consumes very little energy, so glycolysis could support normal electrical behavior.22 Defibril- lation can therefore result in conversion of VF without resulting in recovery of ventricular per-

Lactate and FFA. High arterial lactate and FFA levels (five times normal) and potassium loss from the ischemic cell may promote arrhythmias.12 Potas- sium loss 30 seconds after defibrillation was mea- sured in the isolated perfused rabbit heart.4 The twofold increase in lactate and FFA levels measured in the present study is too small to induce arrhyth- mias.12 However, the effect of a combination of several factors is not yet sufficiently analyzed. Although t, and tA both increase with increasing 1% and tF, no strict correspondence between these two parameters exists. High ventricular rate and prema- ture beats with a short coupling interval may delay the recovery of PLv, and insufficient perfusion of the heart muscle may lead to arrhythmias. However, fast recovery of PI,, may occur in spite of arrhyth- mias and the reverse may happen also (Fig. 6).

AMI. The dog heart shows a small decrease of maximum LV pressure but no decrease in cardiac

Volume 106 Number 2,

output in the first 3 hours after acute occlusion of the LAD artery.2g In AM1 arrhythmias are generated in the border zone of the occluded area.12 One might expect an increase in arrhythmias due to defibrilla- tion after occlusion of the LAD artery in the dog heart. On the other hand defibrillation, generating arrhythmias by itself, may terminate not only VF but also other kinds of arrhythmias, such as ectopic ventricular activity.6 The results in this study indi- cate that there is no increase in incidence of arrhyth- mias, tA, and tp, due to defibrillation after AMI.

Conclusion. The results of this study indicate that the time required for recovery of PLv and the duration of arrhythmias due to defibrillation are a function of the duration of VF and the cumulative current E/2, the latter being important only after prolonged periods of VF. The present study is limited since PLv was the only parameter used to characterize LV function. A more complete evalua- tion of hemodynamic responses after defibrillation was performed in a later study.30

The effect of excitation-contraction uncoupling after long duration of VF without perfusion of the heart muscle deserves more attention. Nearly all experimental studies use animal models with healthy hearts. Although in this study no effect was found from occluding the LAD artery, more effort should be made to study the effects of defibrillation in the pathologic settings in which patients often do fibrillate. REFERENCES

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10. Crampton K: Accepted, controversial, and speculative