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Ann Thorac Surg 1995;60:47-54
© 1995 The Society of Thoracic Surgeons
Department of General and Cardiothoracic Surgery, Duke University Medical Center, Durham, North Carolina
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. Seventy-eight dogs underwent 34 orthotopic complete atrioventricular transplantations using a validated brain-dead organ donor model, hypothermic cardiac preservation, and right and left ventricular function analysis (preload-independent recruitable stroke work). Four groups were studied: controls, transplantation from brain-dead organ donors, graft preservation without brain death, and donor brain death and graft preservation before transplantation.
Results. Without brain death, cardiac arrest alone as well as the combination of cardiac arrest and preservation did not significantly decrease cardiac function after transplantation. After brain death alone, right ventricular and left ventricular function decreased significantly by 30% and 25%, respectively, but subsequent transplantation did not cause further cardiac dysfunction. Preservation after brain death led to a further significant decrease in right ventricular function after subsequent transplantation, and dopamine hydrochloride was required to wean 4 animals from cardiopulmonary bypass.
Conclusions. Brain death causes a significant loss of right and left ventricular function. These injuries are greater in the right ventricle and may contribute to early right ventricular failure after transplantation. Brain death and cardiac preservation interact significantly to impair right ventricular function further. Future studies of graft preservation should use brain-dead organ donors.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Prevailing problems associated with cardiac transplantation include the shortage of donor organs, coronary artery disease of the graft, and acute cardiac failure after transplantation. Data from the Registry of the International Society for Heart and Lung Transplantation demonstrate an unchanged early mortality rate of between 9% and 10% for adult patients undergoing cardiac transplantation, and the majority of those deaths were due to cardiac failure not related to infection or rejection [1–3]. This cardiac failure may be related to the myocardial changes occurring during brain death in the organ donor. Previous studies [4–6] in potential clinical donors and in experimental brain-dead animals have shown that brain death leads to major histopathologic and functional changes in the myocardium. An objective analysis of cardiac function [7] after brain death showed that brain death leads to a loss of myocardial performance of 22% and 37% for the left ventricle and the right ventricle, respectively. A gradual increase in the amount of inotropic support required to stabilize hemodynamics in the brain-dead heart-beating donor is frequently observed.
In the clinical setting, the majority of early deaths after cardiac transplantation are due to right ventricular failure, which is the result of elevation of pulmonary vascular resistance in the recipient or loss of contractility of the donor heart [8]. Brain death-induced cardiac injury may be further worsened by cold ischemic arrest and preservation occurring at the time of initial organ harvest. Therefore, this experiment was designed to study the effects of brain death in combination with extended myocardial preservation on right ventricular and left ventricular myocardial performance and contractility after cardiac transplantation using a validated, reliable, reproducible model of canine brain death and load-independent measurements.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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All animals were intubated with a 9F endotracheal tube and mechanically ventilated with a Bear 1 ventilator (Inter Med; Bear Medical Systems, Inc, Riverside, CA). The tidal volume was set at 15 mL/kg, fraction of inspired oxygen at 100%, and positive end-expiratory pressure at 3 cm H2O, and the rate-controlled ventilation mode was adjusted to maintain partial pressure of arterial carbon dioxide between 30 and 40 mm Hg. The arterial pH, partial pressures of oxygen and carbon dioxide oxygen saturation, hematocrit, and potassium levels were measured (Gem-Stat; Mallinckrodt Sensor Systems, Ann Arbor, MI) at 30-minute intervals as well as 15 minutes after any ventilator setting changes were made or medications administered. Blood samples were drawn from a right external iliac artery pressure catheter (Gould Inc, Cardiovascular Products Division, Oxnard, CA). Metabolic acidosis was corrected with IV 8.4% sodium bicarbonate (Abbott Laboratories, North Chicago, IL), and the potassium level was balanced between 4.0 and 5.0 mmol/L by means of IV potassium chloride (Lyphomed Inc, Deerfield, IL), which was given through an 18-gauge peripheral venous catheter.
An esophageal temperature probe was placed, and the body temperature of the cardiac donor was maintained between 36° and 37°C throughout the experiments by application of heating pads, blankets, and heated, humidified inspiration gas. The urinary bladder was catheterized transurethrally to record the urine output. Electrocardiographic monitoring was performed from three limb electrodes.
Experimental Groups and Study Design
The effects of brain death and myocardial preservation on cardiac function after cardiac transplantation were studied in four experimental groups. Group I (n = 20; mean weight, 25.6 ± 0.5 kg) consisted of the control animals in which cardiac graft ischemic time and hypothermic preservation time were kept as brief as possible. In group 2 (n = 16; mean weight, 26.8 ± 0.5 kg), cardiac transplant function was assessed after 4 hours of brain death in the organ donor and after subsequent transplantation. In the third group (group 3; n = 16; mean weight 26.9 ± 0.4 kg), cardiac transplant function was analyzed in the recipient after 4 hours of hypothermic cardiac graft preservation in a hyperosmolar solution. In group 4 (n = 16; mean weight, 26.8 ± 0.4 kg), cardiac graft function in the recipient was analyzed after 4 hours of donor brain death and 4 hours of cardiac graft hypothermic preservation.
Assessment of Donor and Recipient Cardiac Function
A standard median sternotomy and an anterior pericardiotomy were performed to expose the heart. A flowmeter (model T208X, Transonic Systems Inc, Ithaca, NY) was applied around the pulmonary trunk to measure right ventricular output. Hemispheric ultrasonic dimension transducers (outer diameter, 1.5 mm) (No. 1-1015-5A; Vernitron, Bedford, OH) were positioned across the base-apex major axis, the anteroposterior minor-axis diameters of the left ventricle, and the septal–free wall minor-axis diameters of both the right and left ventricles to measure the ventricular cavitary volumes. Millar pressure catheters (model MPC-500; Millar Instruments Inc, Houston, TX) were placed into the right and left ventricles, left atrium, and pulmonary artery for continuous pressure recording of right and left ventricular pressures, end-diastolic right and left ventricular pressures, left atrial pressure, and pulmonary artery pressure.
Dynamic right ventricular volume was measured according to the ellipsoidal shell subtraction method [9]. Right ventricular and left ventricular end-systolic pressure/volume and stroke work to end-diastolic volume relations as well as end-diastolic segment length or chamber volume were then evaluated. The relationship between stroke work and either end-diastolic segment length or chamber volume was quantified by the highly linear relationship of slope and x-intercept during vena cava occlusion [10]. The slope (preload-recruitable stroke work [PRSW]) and x-intercept (volume) of these linear regressions represent load-independent indices of right ventricular and left ventricular systolic function and myocardial contractility. Direct measurements of right ventricular and left ventricular filling pressures were taken at the end of diastole after the A wave and were termed right ventricular and left ventricular end-diastolic pressure, respectively. Systemic and pulmonary vascular resistances were calculated by standard formulas applying mean pulmonary artery and aortic pressures, cardiac output, and left ventricular and right ventricular end-diastolic pressures.
Induction, Diagnosis, and Validation of Brain Death
Brain death was induced by a rise in intracranial pressure through inflation of a subdurally placed balloon, which caused global brain and brain stem ischemia and herniation. Analgesic and anesthetic agents were discontinued after brain death was induced. A previously introduced validated model of canine brain death was used and is described elsewhere [11]. In brief, brain death was determined to occur when corneal and pupillary reflexes became absent. Electroencephalographic changes were recorded, and the cessation of neuronal-electric brain activity by electroencephalographic monitoring was defined as a recorded unchanged oscillating noisy-spiked curve without high-amplitude waves or spikes. Brain death was confirmed neuropathologically at the end of all experiments.
Donor Management
The micromanometers and flow probes were removed after data collection, and the ultrasonic dimension transducers remained attached to the epicardium but disconnected from the sonomicrometer and protected from immersion. The animals were fully anticoagulated with systemic injection of 350 IU/kg of heparin sodium (Elkins-Sinn Inc).
The inferior vena cava was ligated distally at its emergence from the diaphragm followed promptly by cross-clamping of the ascending aorta at the origin of the brachiocephalic artery. One liter of St. Thomas' cardioplegia (Plegisol; Abbott Laboratories), at 4°C was infused into the aortic root through a 16-gauge cannula, and the heart was vented by incising the superior vena cava and the right pulmonary veins distally. The heart then was immersed in 4°C normal saline solution. Transection of the superior and inferior venae cavae was done as distally as possible, and the ascending aorta was transected just proximal to the aortic cross-clamp. The left and right pulmonary veins were transected at their pleural aspect outside the pericardium.
The heart was stored in 4°C normal saline solution (control group and group 2) or protected for 4 hours in a 4°C preservation solution (groups 3 and 4). The preservation solution is based on an extracellular preparation with high osmolality (420 mOsm/L; sodium chloride, 138 mEq/L; potassium chloride, 25 mEq/L; calcium chloride, 0.7 mEq/L; magnesium chloride, 7.56 mEq/L; glucose, 15 g/L; mannitol, 20 g/L; hetastarch 6%; tromethamine to pH 7.4 to 7.5) formulated at Duke University Medical Center Pharmacy.
Preparation of Recipient
Two hours prior to transplantation, each recipient received triple immunosuppression therapy consisting of 10 mg/kg of oral cyclosporine (Sandoz Pharmaceuticals Corp, East Hanover, NJ), 2 mg/kg of oral azathioprine (Burroughs Wellcome, Research Triangle Park, NC), and 25 mg/kg of IV methylprednisolone (The Upjohn Company, Kalamazoo, MI). After anticoagulation with 350 IU/kg of heparin sodium, a 16F arterial cannula was inserted into the femoral artery, and venous drainage was performed through bicaval cannulation using a 28F cannula for the inferior vena cava and a right-angled 24F cannula for the superior vena cava, both inserted as distally as possible in preparation for cardiopulmonary bypass (Sarns 5000 heart-lung machine; Sarns Corp, Ann Arbor, MI; Cobe VPCML membrane oxygenator, Cobe Laboratories Inc, Lakewood, Co).
On bypass, the core temperature was reduced to 32°C before rewarming was initiated during anastomosis of the pulmonary artery. The flow rate was kept between 80 and 100 mL • kg-1 • min-1, and mean arterial pressure was maintained between 60 and 70 mm Hg. Occasionally, when systemic pressure and circulating volume were low, a bolus of 1 mg of norepinephrine was administered (Winthrop Pharmaceuticals, New York, NY). Throughout cardiopulmonary bypass, the lungs were maintained on full ventilation to prevent pulmonary cellular injury associated with total circulatory support in dogs.
Complete Orthotopic Cardiac Transplantation Technique
A complete orthotopic cardiac transplantation technique was used as described previously [12]. The superior and inferior venae cavae together with the ascending aorta and pulmonary artery were transected at their most proximal portions in the recipient. The anatomy of the pulmonary veins was delineated before the posterior wall of the atrium was divided into two Carrel patches containing the left and right pulmonary veins. On the donor heart, the pulmonary vein orifices were identified, and left and right orifices were fashioned for the anastomoses to the pulmonary veins. All the anastomoses were sutured with 4-0 Prolene in a continuous fashion and executed in the following order: left pulmonary veins, right pulmonary veins, inferior vena cava, pulmonary artery, aorta, and superior vena cava. The last anastomosis was performed after the heart was deaired and the aortic cross-clamp was released.
Data Acquisition and Analysis
Data were collected at baseline in every donor animal as well as 120 minutes and 240 minutes after brain death and 60 minutes after weaning from cardiopulmonary bypass and cardiac transplantation in recipients. Functional and hemodynamic data were digitized on-line, collected, and stored on a microprocessor (PDP 11/23; Digital Equipment Corp, Maynard, MA). Pressure data and cardiac output were analyzed with software developed in our laboratory as described elsewhere [10]. Briefly, all data were digitized at 500 Hz and filtered by a 50-Hz low-pass filter, stored on magnetic media, and analyzed on a Zenith Z-386/20 (Zenith Data Systems Corp, St. Joseph, MI).
Experimental Approval and Animal Care
The experimental setup and procedures conformed to the guidelines established by the American Physiological Society and the National Institutes of Health (Guide for the Care and Use of Laboratory Animals, National Institutes of Health publication no. 86-23, revised 1985). The experiments were approved by the Duke University Institutional Animal Care and Use Committee (DUIACUC Assigned Registry No. A477-93-10R3).
Statistical Analysis
Statistical analysis of data taken before and after brain death was performed on an IBM personal computer using commercially available software (Statistical Software Package; SAS Institute, Inc, Cary, NC). First, a linear multivariate analysis of repetitive measurements was used to test for an overall effect or trend over time. Because the analysis of repetitive measurements does not indicate which period or periods differ, follow-up paired Student's t tests were used to compare baseline values with data obtained after brain death and transplantation. Unpaired Student's t tests were used to compare left ventricular and right ventricular function after brain death and after transplantation. F tests were used to compare the means at each data point after brain death with baseline data. Each animal served as its own control. Bonferroni's method was used to compensate for the increased risk of a type I error with multiple comparisons. Multivariate analysis was implemented to assess the main effects of the factors brain death and preservation and their interaction. Mantel-Haenszel 
2 test was used to evaluate the requirement for inotropic agents in group 4. The results are expressed as the mean ± the standard error of the mean. A difference was considered significant at a p value of less than 0.05.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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. There were no significant differences between groups regarding body weight and hemodynamic and cardiac function baseline data.
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One donor animal each in groups 2 and 4 had development of circulatory arrest because of ventricular fibrillation after the induction of brain death, and they were excluded from the data analysis. Two of the 12 attempted transplantations in group 1 were excluded from the study because of a left-sided superior vena cava in 1 recipient and hypoxia secondary to aspiration during intubation in another recipient. One recipient in group 3 had sustained ventricular tachycardia with heart rates of greater than 190 beats/min after the discontinuation of cardiopulmonary bypass, making the acquisition of data impossible. There were eight successful transplantations in this group. One animal in group 4 could not be weaned from dopamine hydrochloride after transplantation and cardiopulmonary bypass and was also excluded from data analysis. This left eight successfully performed transplantations in this group.
Weaning From Cardiopulmonary Bypass
Weaning from cardiopulmonary bypass was done gradually with monitoring of left atrial and systemic pressures. Mean systemic pressure greater than 50 mm Hg in combination with a mean left atrial pressure of 5 to 12 mm Hg was acceptable. The total cardiac graft ischemic times and cardiopulmonary bypass times of the four groups are summarized in Figures 1 through 4.
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. In the control group, the short cardiac arrest and cardiopulmonary bypass times did not affect cardiac graft function after transplantation (see Fig 1). Cardiac arrest in combination with 4 hours of hypothermic cardiac graft preservation followed by subsequent cardiac transplantation (group 3) did not cause a significant change in right ventricular and left ventricular function (see Fig 2).
Brain death of the cardiac organ donor (groups 2 and 4) led to a significant decrease in right ventricular and left ventricular function by 30% ± 4.9% (p < 0.05) and 25% ± 1.9%, p < 0.05), respectively, 2 and 4 hours after brain death. Subsequent transplantation after brain death did not lead to a further significant change in right and left ventricular function in group 2 (see Fig 3). Preservation of the cardiac graft after brain death in group 4 caused a further significant decrease of 28% ± 4.0%, (p < 0.05) in right ventricular function after subsequent transplantation (from 15.6 ± 1.2 erg x 103 4 hours after brain death to 11.3 ± 0.9 erg x 103 [p < 0.0001 compared with baseline] after transplantation) (Fig 4).
Left ventricular and right ventricular x-intercept data (Emax, representing end-diastolic volume where zero stroke work is performed) increased significantly (p < 0.05) after brain death and after transplantation by 9.9 ± 2.7 mL and 5.9 ± 1.0 mL for the left and right ventricles, respectively, in group 2 and by 14.4 ± 2.7 mL and 15.6 ± 1.8 mL for the left and right ventricles in group 4. Left and right ventricular x-intercept data changed insignificantly after transplantation by 2.8 ± 2.5 mL and 2.3 ± 1.2 mL for the left and right ventricles, respectively, in the control group and by 4.5 ± 1.9 mL and 2.6 ± 1.9 mL for the left and right ventricles in group 3. Comparison of the percent changes in right ventricular and left ventricular function after brain death and after cardiac transplantation in groups 2 and 4 showed that right ventricular performance was significantly (p < 0.05) more impaired than left ventricular function.
Dopamine at a rate of 5 µg • kg-1 • min-1 was required to wean 4 animals in group 4 from cardiopulmonary bypass. This was significant (p < 0.0025) compared with the other groups, which required no inotropic support. The dopamine dosage was reduced to 2.5 µg • kg-1 • min-1 after 15 minutes and stopped 30 minutes after the discontinuation of bypass. In this group, posttransplantation data were acquired at 15 minutes, 30 minutes, and 60 minutes after weaning from cardiopulmonary bypass, which also allowed analysis of the inotropic effects of dopamine and the dose response–PRSW relationship in the myocardium of the transplanted cardiac grafts (Fig 5). In these animals, cardiac output decreased from 1,531 ± 486 mL/min to 1,233 ± 354 mL/min to 1,003 ± 272 mL/min and left atrial pressure increased from 6.7 ± 1.5 mm Hg to 8.0 ± 0.9 mm Hg to 8.3 ± 0.6 mm Hg after dopamine was reduced from 5 µg • kg-1 • min-1 to 2.5 µg • kg-1 • min-1 and then discontinued.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Using load-insensitive measurements to objectively analyze myocardial performance in a validated canine brain-death model, this study demonstrated that brain death has a significant impact on cardiac function in the organ donor. After 2 and 4 hours of brain death, biventricular systolic function and contractility, expressed by the linear relationship and regression of load-independent recruitable stroke work (or PRSW), were significantly decreased, more prominently in the right than in the left ventricle. This decrease in PRSW represents an objective loss of myocardial function for the left as well as the right ventricle and was 25% and 30%, respectively. Further, no inotropic support was given after brain death, and in this setting, any potential for recovery of biventricular function to baseline values was not observed over the course of 4 hours after brain death.
The goal of this investigation was to establish the feasibility of using hearts from brain-dead donors in a canine model of orthotopic transplantation. In this study, no further insult to the right and left ventricles was observed after transplantation with no significant change in posttransplantation right and left ventricular PRSW rates compared with pretransplantation brain-dead PRSW values. Injured hearts from brain-dead organ donors may therefore be used for orthotopic transplantation and can adequately support the recipient cardiovascular system without inotropic support when the total preservation and ischemic time is less than 90 minutes. These findings also document objectively that brain death has a significant impact on right and left ventricular function after cardiac transplantation.
Preservation of a donor heart from a non–brain-dead donor for a total ischemic time of 4 hours did not damage the myocardium, as biventricular function remained unchanged after transplantation compared with pretransplantation values. Overall, the preserved hearts performed equally well after transplantation as control hearts. These experiments also demonstrated that complete atrioventricular transplantation is a feasible technique that is able to maintain right and left ventricular function after transplantation. In the majority of transplants, sinus rhythm was resumed, and only 10 of 34 hearts required ventricular pacing for a short period after weaning from cardiopulmonary bypass.
As demonstrated in this study, a significant interaction exits between the effects of brain death on the myocardium and prolonged cardiac graft preservation. Dopamine infusion was required to wean 4 animals in this group (group 4) from cardiopulmonary bypass. One animal, which was not involved in this study, could not be weaned from bypass. Shivalkar and associates [19] used a similar canine brain-dead organ donor model and orthotopic cardiac grafting with bilateral atrioplasty and biventricular transplantation. In that investigation, the hearts were explanted after brain death, during the period of hemodynamic instability and metabolic derangement when the animals were still recovering from the Cushing phenomenon and hyperdynamic response, and preserved for 4 additional hours. Subsequently, high doses of inotropic drugs were required to wean all the recipients from cardiopulmonary bypass.
The results of this investigation also suggest that significant biventricular dysfunction after brain death may be a clinically important cause of acute cardiac failure after transplantation. However, these injured hearts do have the potential to support the circulatory system of the recipient. On the basis of these data, it is understandable that transplanted hearts have difficulty sustaining the circulation of recipients with elevated pulmonary vascular resistance because of both a decrease in right ventricular contractility and an increase in afterload. Increased pulmonary vascular resistance has been documented to be an incremental risk factor for acute death after cardiac transplantation [20]. The measured positive inotropic response, the increased biventricular function, and positive dopamine–PRSW relationship in four transplants indicate that these brain death–injured hearts do have a functional reserve; it may be due to the upregulated ß-adrenergic receptor system observed after brain death [7].
Future investigations will show whether early inotropic and hormonal interventions with agents such as thyroxine and vasopressin in brain death–injured hearts have major benefits. Recent prospective studies [21] have shown that thyroid hormone administration in the brain-dead organ donor may be beneficial to cardiovascular function and long-term graft survival. Subsequent data analysis after the discontinuation of dopamine showed a further significant reduction in right ventricular function after transplantation, which is superimposed on the reduction already caused by brain death. The right ventricle seems to be more susceptible to both brain death and preservation-related injury. The mechanisms contributing to more prominent right ventricular transplant dysfunction in hearts exposed to both brain death and prolonged preservation remain unclear. The results in group 2, where function was conserved despite brain death of the donor, demonstrated that a short period of cardiac arrest of less than 90 minutes is not sufficient to cause further decrease in right ventricular function. In group 4, however, the combination of brain death with its catecholamine-induced alteration in cardiomyocyte integrity [22], cardiac ischemia, and prolonged hypothermic preservation [23] led to additional cardiac injury.
In the validated canine brain-death model used in this study, a massive catecholamine storm is observed, occurring approximately 30 to 90 seconds after brain death [11]. The brain death model described here may not represent every clinical situation of brain death. It does replicate the clinical findings of most patients who sustain brain death from a sudden rise in intracranial pressure caused by acute intracranial hemorrhage or head trauma. Severe head injury is the cause of death in 56% to 77% of actual organ donors [13]. The importance of this catecholamine storm lies in its potential to cause cardiopulmonary damage. Many investigators [5, 11, 22, 24, 25] have associated the catecholamine increases occurring after brain death with myocardial injuries, ischemic insults, infarctions, and hemodynamic instability and death. However, the molecular basis for catecholamine-mediated cardiotoxicity is unclear at present and probably complex [26].
These findings have an important impact on current studies of enhanced cardiac graft preservation solutions, and future experiments of prolonged cardiac graft preservation should be carried out with hearts procured from brain-dead donors. Additional studies are required to determine whether intracellular-based cardiac graft preservation solutions are superior [27, 28] to the extracellular solution used in this study and therefore diminish the deleterious effects of brain death and preservation on cardiac function after transplantation. More work in this area is required to study the extent and the mechanism of reperfusion injury that occur after brain death and preservation on cardiac function after transplantation. More work in this area is required to study the extent and the mechanism of reperfusion injury that occurs after brain death and cardiac graft preservation in the transplant recipient.
In conclusion, a validated canine model of donor brain death in combination with orthotopic complete atrioventricular transplantation was used to study the effects of brain death and prolonged preservation on posttranplantation biventricular function in the recipient. The effects of brain death cause significant biventricular dysfunction in the donor. Donor brain death and prolonged cardiac graft preservation interact significantly to impair right ventricular systolic function after transplantation. These injured hearts can be used for cardiac transplantation if aggressive positive inotropic therapy is given to wean the hearts from cardiopulmonary bypass.
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Acknowledgments |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Presented at the Thirty-first Annual Meeting of The Society of Thoracic Surgeons, Palm Springs, CA, Jan 31–Feb 1, 1995.
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