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Ann Thorac Surg 1996;61:629-634
© 1996 The Society of Thoracic Surgeons

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Original Article: Cardiovascular

Myocardial Salvage by the Use of Reperfusion and Intraaortic Balloon Pump: Experimental Study

Department of Clinical Therapeutics, University of Athens School of Medicine, Athens, Greece

Accepted for publication October 3, 1995.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Background. Thrombolytic therapy improves left ventricular ejection fraction and survival. The study was undertaken to evaluate the effects of intraaortic balloon pump used in conjunction with reperfusion in reducing infarct size.

Methods. Twenty-two dogs were subjected to proximal left anterior descending coronary artery occlusion. In group 1 (n = 7) occlusion lasted for 6 hours. In group 2 (n = 6) 2 hours of occlusion was followed by reperfusion. In group 3 (n = 9) after 2 hours of occlusion the dogs were assisted with the intraaortic balloon pump throughout the 4 hours of reperfusion. At the end of 6 hours the infarcted myocardium of the left ventricle was determined and expressed as percentage of the myocardium at risk.

Results. In group 1, the infarcted myocardium was 79.3 ± 9.9% of the myocardium at risk, in group 2, 59.0 ± 19.9% (p < 0.05 versus group 1), and in group 3, 37.1 ± 16.7% (p < 0.001 versus group 1 and p < 0.05 versus group 2). Endocardial viability ratio was increased by the intraaortic balloon pump; in group 1 it was 1.02 ± 0.14, in group 2, 1.25 ± 0.24, and in group 3, 1.47 ± 0.31 (p < 0.001 versus group 1 and p < 0.02 versus group 2).

Conclusions. Reperfusion and intraaortic balloon pump increased salvage of the ischemic myocardium over that achieved by reperfusion alone in a canine occlusion–reperfusion model.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Thrombolytic therapy has been widely accepted as the treatment of choice during the early phase of acute myocardial infarction. Various thrombolytic agents have been shown to restore coronary blood flow in 31% to 89% of the patients. Large-scale studies have shown that thrombolytic therapy decreases mortality rate by 11.3% to 4.7% after acute myocardial infarction. The decrease in mortality rate is believed to be the result of preserved left ventricular (LV) function. Some randomized studies [1] have shown that LV ejection fraction was significantly improved in patients treated with thrombolytic therapy compared to those who received conventional therapy.

Experimental studies [2, 3] have also shown that unloading of the left ventricle in conjunction with reperfusion salvages more myocardium than the reperfusion alone. Other studies have suggested that the intraaortic balloon pump (IABP) without reperfusion reduces infarct size [4].

In the present study, the effect of reperfusion in conjunction with IABP assistance, on the size of acute myocardial infarction was assessed in experimental animals.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
General Experimental Procedure
Fifty-one mongrel dogs weighing 18 to 35 kg were anesthetized with intravenous sodium pentobarbital (30 mg/kg body weight) and placed on a lidocaine drip. After intubation, respiration was controlled with a volume ventilator supplying a mixture of room air and oxygen. The chest was opened through a left lateral incision at the fifth intercostal space and the heart was suspended in a pericardial cradle. A catheter was placed into the aortic arch through the left carotid artery and heart rate and blood pressure were monitored throughout the experiment. Arterial blood gases were obtained every 30 minutes and pH was maintained between 7.35 and 7.45 by appropriate adjustment of respirator settings and sodium bicarbonate administration. The temperature was kept within 0.5°C of the baseline level. No pharmacologic agents other than lidocaine, sodium bicarbonate, streptokinase, and normal saline infusion were used. A tube was placed in the left atrium through the left atrial appendage for left atrial pressure recording and gentian violet administration. A few minutes were left for stabilization of the preparation and aortic pressures and mean left atrial pressure were recorded. Then the proximal left anterior descending coronary artery was occluded and hemodynamics were recorded at the end of every hour thereafter.

In group 1 occlusion lasted for 6 hours. In group 2, 2 hours of occlusion was followed by reperfusion, using release of occlusion for 4 hours and streptokinase injection 750,000 IU over 30 minutes. In group 3, after 2 hours of occlusion, the dogs were assisted with the IABP throughout the 4 hours of reperfusion, using release of occlusion for 4 hours and streptokinase injection 750,000 IU over 30 minutes. In each experiment the hemodynamic parameters before the ligation of the left anterior descending coronary artery were used as the baseline control (time, 0), the mean value of the first and second hours for each parameter (time, 1 to 2 hours) was used as the value of the nonperfused period for groups 2 and 3 and the corresponding period for group 1 and the mean value of the third to sixth hours (time, 3 to 6 hours) was used as the value of the reperfusion period for groups 2 and 3 and the corresponding period for group 1. Six hours after the initial occlusion, the left anterior descending coronary artery was resnared, providing the snare had been released at the second hour and gentian violet (1%, 3 mL/kg) was injected into the left atrium over a 30-second period. Within the next 5 seconds the heart was electrically fibrillated and subsequently excised. All animals have received human care in compliance with the ``Guide for the Care and the Use of Laboratory Animals'' published by the National Institutes of Health (NIH publication 85-23, revised 1985).

Morphometric Measurements
The left ventricle and septum were separated from the remainder of the heart and cut into several sections, each 1 cm thick, perpendicular to the apex–base axis. The area of the left ventricle at risk of infarction was identified by the absence of gentian violet dye, which was delivered to those regions supplied by the right coronary artery, the left circumflex coronary artery, and the left anterior descending coronary artery segments before the ligated point. The borders of the area at risk were traced with sinice dye on the heart slices. All sections were placed into a 1% of triphenyltetrazolium chloride solution at 37°C for 20 minutes [5]. With this method the infarcted area of the heart failed to stain red due to lack of nicotinamide–adenine dinucleotide or substrate stores. Tracings of both sides of each ventricular section, as indicated by the gentian violet and triphenyltetrazolium chloride reaction, were drawn on clean plastic sheets. The area of each of the demarcated regions of each ventricular section was quantitated by planimetry.

All slices were weighed. Based on (1) the weight of each slice (W_v), (2) the entire area of both sides of each slice (A_v), (3) the area at risk of both sides of each slice (AR_v),and (4) the infarcted area of both sides of each slice (IA_v), the weight of the myocardium at risk (MR_v), and the infarcted one (IM_v) in grams were estimated as follows: MR_v = (AR_v x W_v)/A_v and IM_v= (IA_v x W_v)/A_v.

For each experiment the MR as a percentage of the whole left ventricle was given by the equation: Comp: equationMR/LV% = Sum of all slices MR_v / Weight of all LV slices x 100 and the infarcted myocardium as a percentage of the myocardium at risk was given by the equation: Comp: equationIM/MR % = Sum of all slices IM / Sum of all slices MR x 100.

Study Groups
Twenty-nine of the 51 animals of the study were not evaluated for a variety of reasons. Twelve of the 29 died because of refractory ventricular fibrillation that occurred within the first 2 hours of the left anterior descending coronary artery occlusion (before the randomization into the three study groups). Four of the 29 died because of refractory ventricular fibrillation during the following 4 hours (2 in group 2 and 2 in group 3). Six of the 29 died because of electromechanical dissociation (3 in group 1, 2 in group 2, and 1 in group 3). One of the 29 died because of balloon rupture (group 3) and 3 of the 29 died because of technical problems during the preparation (before the initiation of the protocol). Finally, 3 of the 29 (1 in each group) were not evaluated because the myocardium at risk was less than 20% of the LV mass. The remaining 22 dogs were distributed into three different groups and completed the entire protocol.

In group 1 (n = 7), representing the controls, the period of myocardial ischemia was six hours without any intervention. The right femoral artery was ligated 1.5 hours after the occlusion of the left anterior descending coronary artery to mimic the animals that underwent mechanical assistance with the IABP.

In group 2 (n = 6), representing reperfusion that might have been achieved by thrombolysis but without any remaining stenosis, the left anterior descending coronary artery snare was released after a 2-hour occlusion period, and at the same time, 750,000 units of streptokinase was administered intravenously over 30 minutes. These animals underwent 4 hours of reperfusion without any adjunct support or therapy. The right femoral artery was also ligated 1.5 hours after occlusion of the left anterior descending coronary artery.

In group 3 (n = 9), the IABP was placed into the descending aorta through the right femoral artery 1.5 hours after occlusion of the left anterior descending coronary artery. The IABP console (Datascope 82Au: location of manufacturer) was synchronized to the R wave of the electrocardiogram to provide aortic diastolic augmentation. In this group, 2 hours of occlusion of the left anterior descending coronary artery was followed by reperfusion using the release of occlusion for 4 hours and a streptokinase injection of 750,000 IU over 30 minutes. During the 4 hours of reperfusion the dogs were assisted by the IABP.

Statistics
The myocardium at risk of infarction was expressed as a percentage of the whole LV myocardium. The infarcted myocardium was expressed as a percentage of the myocardium at risk. Data for each group were expressed as mean ± standard deviation. One-way analysis of variance and unpaired Student's t test were used to identify differences among the three studied groups regarding the hemodynamic parameters, the infarcted myocardium, and the myocardium at risk. Paired Student's t test was used to evaluate changes in the hemodynamic parameters over time in each studied group.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Hemodynamics
In these experiments the following hemodynamic parameters were measured or estimated: (1) aortic end-diastolic pressure; (2) systolic aortic pressure; (3) tension–time index [6]; (4) the double product (heart rate x systolic aortic pressure); (5) left atrial pressure; and (6) endocardial viability ratio, which represents the ratio of diastolic pressure–time index to tension–time index and is considered to be analogous to the ratio of oxygen availability/oxygen consumption of the myocardium [7].

The baseline hemodynamics were similar in the three groups before the left anterior descending coronary artery occlusion and in the first 2 hours after the occlusion (Table 1; one-way analysis of variance). However, the hemodynamics were significantly different among the groups in the last 4 hours of the experiment (Table 1; one-way analysis of variance and unpaired t test). The aortic end-diastolic pressure was 111.1 ± 21.4 mm Hg without reperfusion or IABP assistance (group 1), 99.7 ± 21.7 mm Hg with reperfusion alone (group 2) and 91.8 ± 18.6 mm Hg with reperfusion and mechanical assistance (group 3, p < 0.001, versus group 1). The mean aortic systolic pressure was 139.7 ± 21.2 mm Hg in group 1, 135.4 ± 22.9 mm Hg in group 2, and 115.9 ± 13.3 mm Hg in group 3, (p < 0.001, versus groups 1 and 2). The mean tension–time index was 3,013 ± 950 mm Hg • s • min^-1 in group 1, 2,859 ± 718 mm Hg • s • min^-1 in group 2, and 2,402 ± 371 mm Hg • s • min^-1 in group 3 (p < 0.01, versus groups 1 and 2). The product (systolic aortic pressure multiplied by heart rate) was 26,878 ± 6,414 mm Hg/min in group 1, 26,156 ± 6,714 mm Hg/min in group 2, and 19,932 ± 3,123 mm Hg/min in group 3 (p < 0.001 versus groups 1 and 2). Regarding left atrial pressure there were no significant differences among the three groups during the entire experimental period. However, the left atrial pressure was significantly increased after the first 2 hours of left anterior descending coronary artery occlusion in groups 1 and 2 and remained unchanged from baseline in the assisted animals, group 3. In group 1, the left atrial pressure was 9.7 ± 4.7 mm Hg during the first 2 hours of occlusion and increased to 15.6 ± 6.0 mm Hg during the last 4 hours (paired t test, p < 0.01). In group 2, the left atrial pressure increased from 8.6 ± 3.2 mm Hg to 12.9 ± 4.8 mm Hg during the 4 hours of reperfusion (p < 0.02), whereas it remained almost unchanged in group 3 (from 13.1 ± 5.6 mm Hg during the first 2 hours of ligation to 15.5 ± 5.8 mm Hg during the reperfusion and assistance period, p = not significant). The endocardial viability ratio, during the third to sixth hour after initial occlusion of the artery, was significantly higher in the assisted animals: 1.02 ± 0.14 in group 1, 1.25 ± 0.24 in group 2, and 1.47 ± 0.31 in group 3 (p < 0.001 versus group 1 and p < 0.02 versus group 2; Fig 1).

View larger version (25K): [in this window] [in a new window]   Fig 1. . Endocardial viability ratio (EVR) during the third to sixth hour of left anterior descending coronary artery ligation in the control group (Group 1), during the 4 hours of reperfusion in the reperfusion group (Group 2), and during the 4 hours of reperfusion and mechanical assistance with the intraaortic balloon pump group (Group 3).

View larger version (16K): [in this window] [in a new window]   Fig 2. . Myocardium at risk (MR) as a percentage of the whole left ventricular myocardium weight (LVM).

View larger version (15K): [in this window] [in a new window]   Fig 3. . Infarcted myocardium (IM) expressed as a percentage of the weight of the myocardium at risk (MR) in the control group (Group 1, 6 hours after ligation of the left anterior descending coronary artery), in the reperfusion group (Group 2, 2 hours of left anterior descending coronary artery occlusion plus 4 hours of reperfusion), and in the intraaortic balloon pump group (Group 3, 2 hours of left anterior descending coronary artery occlusion plus 4 hours of reperfusion in conjunction with intraaortic balloon pump assistance).

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment References

It has been postulated that beneficial effects of thrombolysis on the heart might occur independently of the thrombolytic agent's ability to lyse proximal epicardial arterial thrombi, by mechanisms like the direct vasodilating effect of streptokinase [8] or its cardioprotective effects in isolated heart preparations. In addition, thrombolytic agents may dissolve microthrombi that might have been formed throughout the occlusion period and reduce the nonreflow phenomenon that occurs during reperfusion [9, 10]. Thus, the experimental procedure used resembles the usual clinical setting of early myocardial infarction with reperfusion and although it cannot be used for the evaluation of thrombolysis, it is considered appropriate for the evaluation of the IABP in the early reperfusion phase of acute myocardial infarction.

The fact that a large number of animals died of fibrillation or arrest during the experiment may indicate that lethal injury conditions were excluded from all groups.

Intraaortic Balloon Pump Effects
In our study, the infarcted myocardium was 79.3% of the myocardium at risk when neither reperfusion nor thrombolysis was used, and reduced to 59.0% when reperfusion plus thrombolysis was used, and to 37.1% when the IABP assistance was added to reperfusion plus thrombolysis. The reduction of the infarcted myocardium obtained by the additional use of the IABP in our experiments, might have been achieved with a variety of different effects of the IABP such as on the coronary blood flow [11], the coronary collateral flow [4, 12] or the hemodynamics.

Previous experimental studies have shown that the rate of infarct progression and its size were markedly influenced by the level of myocardial oxygen consumption [13] and the LV systolic pressure [14]. In addition, it was found that the augmentation of the diastolic arterial pressure by the IABP enhances thrombolysis, leading to faster reperfusion [15].

It must be emphasized that restoration of perfusion is the most effective way of salvaging ischemic myocardium. In experimental animals, the extent of salvage depends on the duration of occlusion, whereas necrosis begins from the subendocardium and moves progressively to the subepicardium [16], probably because of the higher myocardial oxygen consumption state of the subendocardium [13].

In our study during the reperfusion period part of the myocardium at risk seemed to be in a very critical condition for necrosis and its salvage probably depended not only on the oxygen availability but also on the oxygen demand. Indirect indexes of oxygen demand and balance of oxygen demand and oxygen availability such as the aortic systolic pressure, tension–time index, the double product, and the endocardial viability ratio suggested that the animals assisted with the IABP had lower myocardial oxygen demand, a better subendocardial perfusion, and a better balance of oxygen availability to oxygen demand. It is possible that the reduction of oxygen demand obtained by the IABP slowed the rate of infarct progression [13] and thus gave time to the myocardium at risk to recover from the injury by the restoration of perfusion.

In a recent experimental study [17] either the IABP or the hemopump was used in conjunction with reperfusion to eliminate infarct size. The reduction in the infarct size obtained by the IABP or the hemopump was similar to that obtained by the IABP in our study. Regarding LV systolic pressure there was a trend toward modest reduction by the IABP that was also shown in our study and an apparent decrease by the hemopump.

In that same study, the animals were assisted for the entire 3-hour period of the experiment (2 hours of ischemia and 1 hour of reperfusion), whereas in our study the animals were assisted only during the reperfusion period of the experiment (2 hours of ischemia and 4 hours of reperfusion). Despite the difference in the experimental design, comparison regarding the hemodynamics and infarct sizes may suggest that a short period of mechanical assistance and a modest reduction of the LV systolic pressure induced by the IABP during the early reperfusion period in acute myocardial infarction are probably adequate to salvage almost the maximum of the myocardium at risk. However, it should be mentioned that another study performed in vitro showed no limitation of myocardial infarction by unloading the left ventricle during reperfusion [18].

Clinical Implications
The concomitant use of the IABP and reperfusion in acute myocardial infarction complicated by cardiogenic shock improved survival rate [19]. Recently, a clinical randomized study [20] showed that the use of the IABP after patency restoration in acute myocardial infarction reduced reocclusion rate and improved the overall clinical outcome. On the basis of this clinical experience, together with the wide availability of the IABP and the results of the present study, a randomized clinical study using intravenous thrombolysis versus mechanical assistance with the IABP in conjunction with thrombolysis early in extensive anterior wall myocardial infarction seems reasonable to be considered.

Potential difficulties are the risk of leg ischemia and severe bleeding complication.

In conclusion, the results of the present experimental study suggest that mechanical assistance with the IABP during the initial reperfusion period of acute myocardial infarction further limits infarct size, more than that observed with reperfusion and thrombolysis and it might be considered for clinical use.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Address reprint requests to Dr Nanas, Department of Clinical Therapeutics, ``Alexandra'' Hospital, University of Athens School of Medicine, Vas. Sofias and 2 K. Lourou Str, GR: 115 28, Athens, Greece.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Nanas, J. N. Articles by Moulopoulos, S. D. Search for Related Content PubMed PubMed Citation Articles by Nanas, J. N. Articles by Moulopoulos, S. D.