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Ann Thorac Surg 1995;59:373-378
© 1995 The Society of Thoracic Surgeons

Combining Percutaneous Bypass With Coronary Retroperfusion Limits Myocardial Necrosis

Department of Cardiothoracic Surgery, Boston University Medical Center and The University Hospital, Boston, Massachusetts

Accepted for publication September 19, 1994.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
After an acute coronary occlusion that results in hemodynamic instability, the institution of percutaneous bypass (PB) can effectively support the failing myocardium. However, PB cannot augment coronary blood flow, and substantial regional myocardial necrosis can still occur. This experimental study was undertaken to determine whether combining PB with coronary venous retroperfusion using pressure-controlled intermittent coronary sinus occlusion (PICSO) would limit myocardial necrosis after an acute coronary occlusion. In 30 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 30 minutes of cardioplegic arrest and 180 minutes of reperfusion with the snares released. During the period of coronary occlusion, 10 pigs were placed on PB, 10 pigs received PB + PICSO, and 10 pigs received no support (unmodified). Hearts treated with the combination of PB + PICSO had the highest wall motion scores (unmodified, 1.4 ± 0.3; PB, 1.4 ± 0.3; PB + PICSO, 2.8 ± 0.3 [p < 0.05 versus unmodified and PB]) and the lowest area of necrosis in the area at risk (unmodified, 73% ± 3%; PB, 43% ± 2%; PB + PICSO, 14% ± 2% [p < 0.05, PB and PB + PICSO versus unmodified; p < 0.05, PB + PICSO versus PB]). We conclude that combining PB with coronary venous retroperfusion significantly limits myocardial necrosis.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Percutaneous bypass (PB) has been successfully used to support patients with hemodynamic instability after unsuccessful percutaneous transluminal coronary angioplasty (PTCA) and to assist patients with critical coronary anatomy undergoing high-risk PTCA [1–4]. Although PB has been shown to stabilize patients with circulatory collapse after failed PTCA, it has not been shown to be effective in reversing ongoing regional ischemia [4, 5]. Data from patients undergoing supported angioplasty have shown that 20% of patients will have chest pain, electrocardiographic changes, or echocardiographic evidence of segmental myocardial dysfunction during balloon inflation [4]. Our own experimental studies [5] using a model of acute coronary occlusion in the pig have shown that although PB results in a smaller infarct size than that occurring when no mechanical support is provided, it is not as optimal as the reduction in infarct size seen in hearts treated with an intraaortic balloon pump (IABP). These findings might be explained by the fact that although PB effectively reduces myocardial demands and prevents ventricular distention in the acutely ischemic myocardium, it does not directly augment coronary perfusion.

In a recent experimental study involving pigs with an acute coronary occlusion, we [6] demonstrated that the addition of IABP support to PB resulted in the highest wall motion scores, the least tissue acidosis, and the lowest area of necrosis. However, we have found that in clinical practice, it is not always possible both to insert the IABP and to establish PB simultaneously. The other femoral artery may be too diseased to allow the passage of a guidewire. A bailout catheter may have already been inserted in an attempt to prevent the injured vessel from being completely occluded. If this catheter is removed, there is the fear that ``control'' of the vessel will be lost, resulting in further ischemic damage. We have also encountered the clinical situation in which the other groin is inaccessible for puncture because of a hematoma resulting from a recent catheterization. Because of these limitations, we looked for other methods that might enhance the PB technique.

In addition to the IABP, myocardial oxygen supply after an acute coronary occlusion may be improved by coronary venous retroperfusion. Pressure-controlled intermittent coronary sinus occlusion (PICSO) is a form of coronary venous retroperfusion that redistributes coronary venous blood flow to the ischemic myocardium by changes in pressure gradients throughout the coronary venous system [7]. In the PICSO technique, a balloon-tipped catheter is positioned in the orifice of the coronary sinus and connected to a pneumatic pump that automatically increases and decreases pressure in the coronary venous system according to a preset cycle. Our previous work and the work of others have shown that after periods of regional ischemia, PICSO reduces reperfusion injury [8], enhances the distribution of antegrade cardioplegia [9], improves the washout of ischemic metabolic end-products [7, 8], improves regional myocardial function [7, 10], and decreases infarct size [10, 11]. This experimental study was undertaken to determine whether combining coronary venous retroperfusion using PICSO with PB would optimize the recovery of acutely ischemic myocardium after the revascularization of an acute coronary occlusion.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Experimental Preparation
The study comprised 30 adult pigs weighing 30 to 35 kg. All animals received humane care in compliance with the ``Guide for the Care and Use of Laboratory Animals'' published by the National Institutes of Health (NIH publication 85-23, revised 1985).

After the induction of general anesthesia with 75 mg/kg of -chloralose, the heart and great vessels were exposed using a median sternotomy incision, and the azygos vein was ligated. The animals were heparinized (3 mg/kg), and the second and third diagonal vessels were occluded with snares just distal to the takeoff of the left anterior descending coronary artery for 90 minutes. Intravenous lidocaine hydrochloride was administered to treat ventricular arrhythmias.

After the 90-minute period of coronary occlusion, all animals were placed on total cardiopulmonary bypass (Sarns membrane oxygenator; Sarns, Inc, Ann Arbor, MI) using a 17F cannula in the right femoral artery and a 36F venous return catheter in the right atrium. A 24F catheter was inserted into the left atrium so that volume could be infused to alter left ventricular end-diastolic pressure during echocardiographic measurements. During bypass, mean arterial pressure ranged from 70 to 75 mm Hg, pump flow was kept at 80 mL • kg^-1 • min^-1, hematocrit averaged 27% ± 3%, and systemic pH was maintained at 7.40 ± 0.03.

After bypass was established, hearts were arrested for 30 minutes with multidose antegrade hypothermic crystalloid potassium cardioplegia (K⁺ = 25 mEq/L; pH = 7.6; temperature = 4°C) supplemented with topical hypothermia. After the period of cardioplegic arrest, the aorta was unclamped, the coronary snares were released, and all hearts were reperfused on cardiopulmonary bypass at 37°C for 3 hours.

Treatment Groups
During the 90-minute period of coronary occlusion, the animals were divided into three treatment groups (Fig 1).

View larger version (35K): [in this window] [in a new window]   Fig 1. . Experimental protocols. (PB = percutaneous bypass; PICSO = pressure-controlled intermittent coronary sinus occlusion.)

PERCUTANEOUS BYPASS GROUP.
In 10 pigs, PB was instituted for 90 minutes by placing a Sarns 17F cannula in the right femoral artery and a 21F cannula, inserted through a cutdown in the right femoral vein, in the inferior vena cava. The cardiac index was maintained by keeping oxygen venous saturation between 65% and 70%. Activated clotting times were greater than 400 seconds.

PERCUTANEOUS BYPASS AND PRESSURE-CONTROLLED INTERMITTENT CORONARY SINUS GROUP.
Ten pigs were treated with a combination of PB + PICSO support during the 90-minute period of coronary occlusion. Simultaneously, as the PB catheters were inserted, a 9F triple-lumen balloon-tipped catheter (DLP, Inc, Grand Rapids, MI) was inserted into the proximal coronary sinus through a pursestring suture in the right atrium. The catheter was then connected to a coronary sinus pressure feedback control box (Meditech Labs, Watertown, MA) that automatically inflated and deflated the balloon according to a preset cycle of eight cycles of inflation and four cycles of deflation as previously described [8, 9].

Measurements
Myocardial tissue pH was measured with a pH probe (Khuri tissue ischemia monitor; Vascular Technology Inc, North Chelmsford, MA) and standardized according to myocardial temperature as described previously [6]. Tissue pH was measured in the center of the area at risk between the second and third diagonal vessels and recorded on-line. To account for initial differences in pH during preischemia, analysis focused on changes in pH from baseline values between the three groups after coronary occlusion and at 60 and 180 minutes during the period of reperfusion.

Two-dimensional echocardiograms were obtained with a hand-held 3.5-MHz ultrasound transducer (ATL, Tempe, AZ) [6, 12]. The ventricle was arbitrarily divided into eight anatomic areas, and wall motion was qualitatively analyzed by a numerical score: 4 = normal, 3 = mild hypokinesis, 2 = moderate hypokinesis, 1 = severe hypokinesis, 0 = akinesis, and -1 = dyskinesis. Echocardiographic sections for wall motion analysis were obtained as left ventricular end-diastolic pressure was varied using the right heart bypass technique at a constant afterload (mean aortic pressure = 65 mm Hg). Only sections with the same left ventricular end-diastolic volume during the preischemic, coronary occlusion, and reperfusion periods were used for analysis so that preload conditions were similar. Measurements were made in a blinded fashion by an experienced echocardiographer (S.B.) and were averaged for the periods of preischemia, coronary occlusion, and reperfusion for each experiment and, in turn, for each of the three treatment groups.

The areas of risk and necrosis were determined by histochemical staining techniques using triphenyltetrazolium chloride [13, 14] in a method previously described [6]. The areas of risk and necrosis were planimetered to obtain (1) the area of risk compared with the total left ventricular mass and (2) the percent area of infarct in that area of risk.

Statistical Analysis
Statistical evaluation between the three experimental groups was performed using analysis of variance techniques. Differences between variables measured on a continuous scale within each group were assessed by paired Student's t test. All data were presented as the mean ± the standard error. A p value of less than 0.05 was considered significant.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Four of the ten hearts in the unmodified group had development of ventricular fibrillation during the 90 minutes of coronary occlusion, and cardioversion to normal sinus rhythm was successfully performed. Their mean arterial pressure ranged from 65 to 75 mm Hg with a left ventricular end-diastolic pressure of 5 to 7 mm Hg. In the hearts treated with PB, the cardiac index ranged from 1.8 to 2.2 L • min^-1 • m^-2 with a mean arterial pressure of 65 to 70 mm Hg and venous saturations of 65% to 70%. The left ventricular end-diastolic pressure ranged from 1 to 2 mm Hg, and none of these animals had ventricular fibrillation. There was one episode of ventricular fibrillation, which was successfully treated by cardioversion, in the hearts treated with PB + PICSO. Peak coronary sinus pressure in these animals increased to 49 ± 3 mm Hg during balloon inflation and returned to 4 ± 2 mm Hg during deflation. The mean arterial pressure ranged from 68 to 75 mm Hg with a left ventricular end-diastolic pressure of 1 to 3 mm Hg.

Changes in Myocardial pH
The changes in myocardial pH are shown in Figure 2. There was no difference in myocardial tissue pH in the area at risk prior to coronary occlusion between the three groups (unmodified, 7.38 ± 0.10; PB, 7.36 ± 0.06; PB + PICSO, 7.32 ± 0.07). After 90 minutes of coronary occlusion, all groups showed evidence of significant tissue acidosis in the area at risk (changes in myocardial pH: unmodified, -0.93 ± 0.12; PB, -1.07 ± 0.06; PB + PICSO, -0.93 ± 0.10 [all, p < 0.001 versus preischemic values]). During the period of reperfusion, all hearts showed significantly less tissue acidosis (p < 0.01) compared with coronary occlusion values. After 3 hours of reperfusion, hearts treated with PB + PICSO showed the least amount of tissue acidosis, and this was significantly lower than that in PB hearts by analysis of variance techniques (changes in myocardial pH: unmodified, -0.41 ± 0.13; PB, -0.60 ± 0.10; PB + PICSO, -0.30 ± 0.08; [p < 0.05, PB versus PB + PICSO]).

View larger version (23K): [in this window] [in a new window]   Fig 2. . Changes in myocardial pH (pH). All hearts have significant tissue acidosis after 90 minutes of coronary occlusion. After reperfusion, hearts treated with percutaneous bypass (PB) + pressure-controlled intermittent coronary sinus occlusion (PICSO) have less tissue acidosis than the PB group.

View larger version (23K): [in this window] [in a new window]   Fig 3. . Wall motion scores. Grading was on a scale of 4 (normal) to -1 (dyskinesis). All hearts have decreased wall motion scores after 90 minutes of coronary occlusion. The scores do not deteriorate during reperfusion in the percutaneous bypass (PB) + pressure-controlled intermittent coronary sinus occlusion (PICSO) hearts and remain significantly higher than scores in the other two groups.

View larger version (16K): [in this window] [in a new window]   Fig 4. . Area of necrosis in area at risk. Hearts treated with percutaneous bypass (PB) and PB + pressure-controlled intermittent coronary sinus occlusion (PICSO) have significantly less necrosis than the unmodified group. Hearts treated with PB + PICSO had significantly less necrosis than those treated with PB alone.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

Our clinical studies and those of others suggest that patients who show electrocardiographic changes immediately after failed PTCA have a higher incidence of perioperative myocardial infarctions [16–18]. Furthermore, despite prompt and complete surgical revascularization, emergent coronary artery bypass grafting after failed PTCA results in operative mortality rates as high as 12% and infarction rates approaching 60% [16, 18, 19]. This suggests that if operative mortality and infarction rates are to be lowered, interventions aimed at reducing myocardial necrosis must begin immediately after an acute coronary occlusion in the catheterization laboratory.

Our previous animal studies [5] using a model of 90 minutes of coronary occlusion involving the second and third diagonal vessels, 30 minutes of cardioplegic arrest, and 180 minutes of reperfusion suggested that PB resulted in incomplete recovery of ischemic myocardium. When animals were placed on PB during the 90-minute period of coronary occlusion, the area of necrosis was significantly reduced from 73% to 43% compared with that in animals without mechanical support (p < 0.05). However, PB failed to reverse tissue acidosis and did not improve wall motion scores.

This incomplete recovery from ischemic injury prompted us to perform additional animal studies using the same model to attempt to improve myocardial oxygen supply with the percutaneous technique. When the IABP was added to PB, there was a significant decrease in the area of necrosis to 25% (p < 0.05) [6]. There was also significant improvement in the recovery of wall motion and significantly less tissue acidosis. Our experimental findings correlated with the recent clinical results of Phillips and co-workers [20], who combined PB with IABP support in 16 patients in cardiogenic shock. Ten patients were successfully weaned from all mechanical support, and 7 were long-term survivors.

Our clinical experience indicates, however, that it is not always possible to establish IABP and PB simultaneously. The other femoral artery may be too diseased, it may be inaccessible because of recent hematomas, or it may contain a bailout catheter or a stent in the injured coronary vessel. Consequently, we turned to coronary retroperfusion as an alternative means to augment coronary blood flow. Although coronary retroperfusion techniques cannot support the myocardium when hemodynamic instability occurs, our earlier work [8–10] with PICSO suggested that this form of coronary venous retroperfusion was effective in reducing ischemic injury. In a similar animal model [10], the use of PICSO alone significantly reduced the area of necrosis to 27% compared with 73% for hearts without retroperfusion (p < 0.02). When PICSO was combined with IABP support, the area of necrosis was decreased to only 15% (p < 0.02) [21]. In our present study, PICSO lowered the area of necrosis to 14% and significantly lowered tissue acidosis and improved wall motion scores compared with the unmodified group and the group treated with only PB (see Figs 2, 3). In fact, when we compared the PICSO + PB group with the IABP + PB group of our earlier study, there was a significant reduction in the area of necrosis in the PICSO–treated group (14% ± 2% versus 25% ± 5%; p < 0.05).

The results of this experimental study support the premise that PB is enhanced by techniques that augment myocardial oxygen supply. In those clinical situations where PB + IABP cannot be performed simultaneously, coronary retroperfusion with PICSO appears to be another method to limit myocardial necrosis. The PICSO catheter can be inserted percutaneously through either the internal jugular vein or the femoral vein and guided into the coronary sinus. The same catheter could be used to administer retrograde cardioplegia, which has been shown to provide superior myocardial protection than antegrade cardioplegia during revascularization of an acute coronary occlusion [22]. Further, antiarrhythmic agents [23], oxygen free radical scavengers [24], and essential substrates [10] may be more effectively delivered to the jeopardized myocardium using the retrograde catheter. The intermittent occlusion of the coronary sinus used with the PICSO technique avoids trauma to the coronary sinus and myocardial edema that can occur when coronary sinus pressures constantly exceed 50 mm Hg [25]. Clinical studies by Mohl and colleagues [26] using PICSO in patients during coronary artery bypass grafting have shown that this technique can be performed safely.

Although PICSO was used for this study, other forms of coronary venous retroperfusion, such as synchronized retroperfusion, may also result in improved recovery of ischemic damage when PB is necessary [27–29]. Furthermore, whereas our studies simulated a failed PTCA requiring emergent surgical revascularization, coronary venous retroperfusion may also enhance PB when used in patients during assisted angioplasty [28, 29].

No experimental study can totally mimic the events of an acute coronary occlusion that might occur after unsuccessful PTCA. The ischemic injury that follows the acute occlusion of a normal vessel may differ from that of a vessel that has had a chronic subtotal occlusion. Nevertheless, the coronary anatomy of the pig is similar to that in humans. Techniques that result in a significant reduction in myocardial necrosis in this model will have an important role in clinical practice.

We conclude from this study that the addition of coronary venous retroperfusion techniques to PB optimizes the recovery of ischemic myocardium after surgical revascularization of an acute coronary occlusion. These interventions should be initiated in the catheterization laboratory as soon as ischemic changes develop. Clinical studies will be necessary to determine whether the institution of these combinations of techniques that act at different spectrums of the supply-demand equation will ultimately decrease the increased mortality and infarction rates associated with emergent coronary artery bypass grafting after failed PTCA.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
We appreciate the secretarial assistance of Ms Ellie LaBombard in the preparation of the manuscript.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Presented in part at the Forty-third Annual Meeting of the American College of Cardiology, Atlanta, GA, Mar 13–17, 1994.

Address reprint requests to Dr Lazar, Department of Cardiothoracic Surgery, The University Hospital, Suite B404, 88 E Newton St, Boston, MA 02118.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments 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 Author home page(s): Harold L. Lazar Richard J. Shemin Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lazar, H. L. Articles by Shemin, R. J. Search for Related Content PubMed PubMed Citation Articles by Lazar, H. L. Articles by Shemin, R. J.