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Ann Thorac Surg 1997;64:1320-1324
© 1997 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Preconditioning Improves Myocardial Preservation in Patients Undergoing Open Heart Operations

Er-Xiong Lu, MD, Sheng-Xi Chen, MD, Ming-Dao Yuan, MD, Tie-Hui Hu, MD, Han-Cha Zhou, MD, Wan-Jun Luo, MD, Guo-Hu Li, MD, Liao-Mei Xu, BS

Department of Cardiac Surgery, Xiangya Hospital, Hunan Medical University, Changsha, Hunan, People's Republic of China

Accepted for publication May 14, 1997.


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background. Our previous work has shown that preconditioning can promote the recovery of cardiac function in patients having an open heart procedure. Because preconditioning is regarded as the most powerful form of endogenous myocardial protection, we tested the hypothesis that preconditioning protects against myocardial ischemia-reperfusion injury in patients undergoing prolonged cold crystalloid cardioplegic arrest.

Methods. Thirty patients who had rheumatic heart disease and required both aortic and mitral valve replacement were studied. Patients were randomly divided into two equal groups. Preconditioning was accomplished using two cycles of 2-minute occlusion of the vena cava and aorta followed by 3 minutes of reperfusion under cardiopulmonary bypass. All hearts were arrested with 4°C St. Thomas' Hospital cardioplegic solution. Myocardial protective effects were assessed by changes in myocardial levels of adenosine triphosphate, electrocardiographic activity, leakage of myocardial enzymes, and myocardial contractility.

Results. The adenosine triphosphate content in ischemic myocardium was higher in the preconditioning group than in the control group (p < 0.05 90 minutes after ischemia), and there was a significant reduction in release of the myocardial-specific isoenzyme of creatine kinase in the preconditioning group. Preconditioning improved the recovery of myocardial contractility (first derivative of left ventricular developed pressure, 1,490 ± 102 mm Hg/s versus 1,250 ± 97 mm Hg/s 30 minutes after reperfusion; p < 0.05), and there was also a protective effect on electrocardiographic activity.

Conclusions. Our results suggest that ischemic preconditioning protects the myocardium in humans from the severe ischemia-reperfusion injury produced after prolonged arrest with cold crystalloid cardioplegia.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Ischemic preconditioning was first described by Murry and colleagues [1] in 1986, and this phenomenon has been confirmed in various animal studies. Because preconditioning has provided protection against ischemia-reperfusion injury in every mammalian species studied to date, it is likely that human myocardium will also prove to be amenable to this form of protection [2].

There are increasing data that angina prior to an acute myocardial infarction preserves left ventricular function, reduces creatine kinase release, and improves the prognosis [3]. Also, the myocardial protective effects of preconditioning have been utilized during percutaneous transluminal coronary angioplasty [4]. However, all this evidence is indirect. During cardiac surgical procedures under cardiopulmonary bypass (CPB), the heart is subjected to global ischemia when the aorta is cross-clamped. This clinical situation offers the best chance to use the myocardial protective effect of preconditioning. The first clinical trial during cardiac procedures was done by Alkhulaifi and co-workers [5]. In their study, myocardial temperature was maintained at 37°C, and only the levels of adenosine triphosphate were evaluated. Although many studies have provided data suggesting that preconditioning can occur in humans, no results have yet provided definitive evidence [2].

To date, the most effective methods to preserve the heart remain hypothermia and cardioplegia. Recently, our initial studies [6] demonstrated that preconditioning reduces the leakage of myocardial enzymes and promotes the recovery of clinical cardiac function in patients having an open heart operation with cold crystalloid cardioplegia. In the present study, we evaluated the effects of preconditioning on myocardial salvage after prolonged cold crystalloid cardioplegic arrest in patients undergoing aortic and mitral valve replacement.


   Material and Methods
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 Footnotes
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
The clinical trial was approved by both the university scientific association and the local ethics committee. Written informed consent was obtained from each patient before the operation.

Patient Selection
From March 1995 to June 1996, 30 adult patients with rheumatic heart disease underwent aortic and mitral valve replacement with mechanical prostheses. The patients were randomly divided into two equal groups: the ischemic preconditioning group and the control group. Preoperative data are summarized in Table 1Go.


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  		Table 1. . Summary of Preoperative Patients Dataa,b
 
Operative Details
Anesthesia was induced with intravenous administration of fentanyl citrate and vecuronium bromide and was maintained with intravenously administered propofol and inhalation of isoflurane. Under endotracheal intubation, the lungs were ventilated with a volume-cycled respirator (Ohmeda Excel-210). The left radial artery and the right internal jugular vein were catheterized to monitor arterial pressure, central venous pressure, and pulmonary wedge pressure. The electrocardiogram and body temperature were also monitored. The patients were placed in the fully supine position. A midline thoracotomy was made. After heparinization, the aorta, the superior vena cava, and the inferior vena cava were cannulated. Left and right atrial drainage tubes were placed. Cardiopulmonary bypass was established with a crystalloid-albumin prime at a flow rate of 0.5 L • min-1 • m-2 to a maximum rate of 4.2 L/min (Sarns 7400 artificial heart-lung machine, 3M membrane oxygenator). The prime solution was prewarmed to 37°C.

Preconditioning was accomplished with two cycles of 2-min occlusion of the vena cava and aortic cross-clamping (with the left and right atria kept empty by intracardiac drainage) followed by 3 minutes of reperfusion (removing all occlusions) under CPB. The control group had only 10 minutes of CPB. All hearts were arrested by administering 15 mL/kg of 4°C St. Thomas' Hospital cardioplegia through a catheter in the aortic root. Throughout the period of ischemia, cardioplegic solution was given every 30 minutes. Blood temperature was maintained at moderate hypothermia (24° to 28°C) during the period of cardiac arrest. A total of 34 double-leaf and 26 single-leaf mechanical valves were replaced. There were no differences in the types of prosthetic valves between the two groups.

Measurement of Myocardial Contractility
Before CPB and at 30 minutes after reperfusion, a 3M 12-gauge needle attached to a pressure transducer (3M P23 XL) was inserted through the free wall of the left ventricle. Left ventricular developed pressure and its first derivative were recorded by inputting signals into a computerized polygraph system (RM-600; Nihon Kohden, Japan).

Assay of Myocardial Enzymes
Blood samples for measuring the myocardial-specific isoenzyme of creatine kinase (CK-MB) were withdrawn from the arterial line at baseline, 30 minutes after reperfusion, and 4, 12, and 24 hours postoperatively. The plasma was analyzed spectrophotometrically (Hitachi model 7170A) for determination of CK-MB levels (CK-MB kit; Sigma Diagnostic, St. Louis, MO). The CK-MB activity was expressed in international units per liter of plasma.

Analysis of Electrocardiographic Activity
A 24-hour electrocardiogram (HP 78354C) was used for recording ventricular arrhythmias and a standard electrocardiogram (NEC 8110K, Japan), for accurate measurement of ST-segment shifting before operation, 30 minutes after reperfusion, and 4, 12, and 24 hours after operation.

Adenosine Triphosphate Content in Myocardium
Myocardial tissue specimens were obtained from the right ventricular free wall with a Tru-Cut biopsy needle (Travenol Laboratories). The specimens were taken four times, ie, before CPB, 60 minutes and 90 minutes after ischemia, and 30 minutes after reperfusion, and were immediately frozen in liquid nitrogen. After homogenization in 3.6% ice-cold perchloric acid, the slurries were centrifuged, and the supernatants were neutralized with K2CO3 and KOH to pH 5.0 to 6.0 and frozen. The extracts were later centrifuged and assayed by high-performance liquid chromatography (model HP 1050).

Statistical Analysis
Data are expressed as the mean ± the standard error of the mean. An unpaired t test was used to compare the two groups. A p value of less than 0.05 was considered significant.


   Results
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
One patient in each group was excluded because of problems with the polygraph system. In addition, 1 patient in the control group was excluded for another technical reason. There were no operative deaths (to 30 days postoperatively) in either group. The CPB time and aortic cross-clamp time were 147.5 ± 12.5 minutes and 108.1 ± 10.9 minutes, respectively, for the control group and 155 ± 18.9 minutes and 110.3 ± 12.4 minutes, respectively, for the preconditioning group (p > 0.05).

Myocardial Contractility
There was no significant difference in left ventricular developed pressure or its first derivative between the two groups before myocardial ischemia. Thirty minutes after reperfusion, the difference in the first derivative of left ventricular developed pressure between the two groups was significant (Table 2Go).


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  		Table 2. . Changes in Myocardial Contractilitya
 
Leakage of Myocardial Enzymes
Preconditioning decreased the release of CK-MB after operation (Table 3Go). The difference in the leakage of CK-MB between the two groups was significant at 4, 12, and 24 hours after operation.


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  		Table 3. . Leakage of Myocardial Specific Isoenzyme of Creatine Kinasea
 
Changes in Electrocardiographic Activity
There was no significant difference between the two groups in auto-rebeating rate. However, preconditioning did reduce the incidence of ventricular fibrillation and the electric defibrillation time. The most significant change in the electrocardiogram was manifested in ST-segment shifting (Table 4Go).


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  		Table 4. . Elevation of ST Segmenta
 
Adenosine Triphosphate Content in Myocardium
The adenosine triphosphate content was higher in the preconditioning group. The difference between the two groups was significant 90 minutes after ischemia (Table 5Go).


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  		Table 5. . Adenosine Triphosphate Content in Myocardiuma
 

   Comment
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
Effective myocardial preservation is one of the keys to successful open heart operations, especially in human heart transplantation when the cardiac allograft must sometimes be transported great distances. Though modern myocardial preservation techniques have revolutionized cardiac surgery, continued refinements in the practice of myocardial protection are necessary to optimize postsurgical cardiac function. Many investigators have sought the ideal method for myocardial preservation in cardiac surgery. Modification of the myocardial response to ischemia during cardiac operations has focused on composition of the cardioplegic solution [7], methods of delivery of the solution [8], provision of external substrates [9], temperature manipulation [10], and other factors [11]. All of these studies, however, involve extraneous forms of myocardial protection.

Recently, it has been discovered that the heart has its own systems of protection against ischemia-reperfusion injury [12]. Can the inherent propensity of the cells for self-preservation be harnessed to protect the myocardium? It has been shown that pretreatment with heat-shock stress before prolonged cardioplegic arrest can improve postischemic recovery [13]. Similar results have been obtained by pretreatment with endotoxin [14], tumor necrosis factor [15], and mechanical stretching [16]. Nevertheless, preconditioning, to date the most powerful endogenous protection against ischemia-reperfusion injury, is more attractive because of its possible clinical use.

For surgical myocardial protection, many authors have examined the effects of preconditioning in conjunction with cold cardioplegia. Cave and Hearse [17] found that preconditioning plus cold St. Thomas' Hospital cardioplegia improved recovery of aortic flow and reduced leakage of creatine kinase in isolated rat hearts. We [18] noted the same protection in dogs. Ischemic preconditioning also improves preservation with crystalloid cardioplegia in isolated rabbit hearts [19].

Whether preconditioning can protect human myocardium is an important question that must be answered before clinical trials can be done. The increased evidence suggests that the human heart can be preconditioned. That antecedent angina may afford some degree of myocardial protection is highly relevant to preconditioning [20]. Studies during percutaneous transluminal coronary angioplasty confirmed that both subjective (angina) and objective (ST-segment shift, increased left ventricular filling pressure, reduced left ventricular ejection fraction) manifestations of ischemia were reduced during later balloon inflations even if the results were related to the collateral circulation [21]. Samples of human myocardium obtained during cardiac surgical procedures can be used to overcome some of the difficulties encountered when studying preconditioning in patients. With isolated strips of human atrial tissue, Walker and colleagues [22] found that repeated brief insults of hypoxia-reoxygenation protect the myocardium during a subsequent prolonged episode of hypoxia and result in improved recovery of contractile function after reoxygenation. Another study [23] of preconditioning revealed that two 3-minute ischemic periods each followed by 2 minutes of reperfusion produced a higher adenosine triphosphate content in the myocardium than no exposure to preceding brief ischemic periods after 10 minutes of aortic cross-clamping in a coronary artery bypass program. However, high-energy phosphate preservation does not provide conclusive evidence of preconditioning. In the present study, we found that preconditioning in conjunction with cold crystalloid cardioplegia offers better recovery of contractile function, reduces leakage of CK-MB and ST-segment changes, and maintains higher adenosine triphosphate levels in ischemic myocardium.

Many studies [24, 25] have investigated the mechanisms of preconditioning. Suggested mechanisms for the initiation of preconditioning-induced protection include reduced glycogen content prior to the sustained ischemic period, adenosine receptor stimulation, slower metabolism because of ischemia, and protein kinase C stimulation. Our previous study [26] showed that calcitonin gene-related peptide, a principal transmitter released from cardiac sensory nerves, may play an important role in mediating ischemic preconditioning. Although an experiment with strips of human atrial tissue [22] led to the suggestion that prior exposure to A1 adenosine agonists can mimic preconditioning, the mechanism of preconditioning in humans remains unclear. More data from studies of preconditioning in human myocardium are necessary.

There are a number of clinical situations for which a preconditioning-based intervention might prove beneficial. Preconditioning could increase safety during cardiac operation and percutaneous transluminal coronary angioplasty. Pharmacologic preconditioning might offer an alternative method to protect the myocardium under conditions in which ischemic preconditioning cannot be used [27]. More importantly, preconditioning can be used for protection during prolonged hypothermic storage of a donor heart, a measure that may increase the availability of donor organs and make transplantation of the heart even more safe [28].

In conclusion, the present study suggests that ischemic preconditioning can improve myocardial preservation after prolonged cold crystalloid cardioplegic arrest for open heart procedures.


   Acknowledgments
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
This work was supported by a grant from the State Scientific Commission of the People's Republic of China.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Address reprint requests to Dr Lu, Department of Cardiac Surgery, Xiangya Hospital, Hunan Medical University, Changsha, Hunan 410008, People's Republic of China (e-mail: erxiong{at}public.cs.hn.cn).


   References
Top
 Footnotes
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

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  9. Drossos G, Lazou A, Panagopoulos P, Westaby S. Deferoxamine cardioplegia reduces superoxide radical production in human myocardium. Ann Thorac Surg 1995;59:169–72.[Abstract/Free Full Text]
  10. Salerno TA, Houck JP, Barrozo CAM, et al. Retrograde continuous warm blood cardioplegia: a new concept in myocardial protection. Ann Thorac Surg 1991;51:245–7.[Abstract]
  11. Buckberg GD. Update on current techniques of myocardial protection. Ann Thorac Surg 1995;60:805–14.[Abstract/Free Full Text]
  12. Knowlton AA, Brecher P, Apstein CS. Rapid expression of heat-shock protein in the rabbit after brief cardiac ischemia. J Clin Invest 1991;87:139–47.[Medline]
  13. Sievers RE, Vissen FLJ, Welch WJ, Wolfe CL. Heat-shock protein induction in rat hearts: a role for improved myocardial salvage after ischemia and reperfusion? Circulation 1992;85:769–78.[Abstract/Free Full Text]
  14. Mattox ML, Day MJ, Adams HR, et al. Endotoxemia improves systolic and diastolic recovery after ischemia-reperfusion of isolated hearts. Circ Shock 1992;37:30–1.
  15. Brown JM, Anderson BO, Repine JE, et al. Neutrophils contribute to TNF-induced myocardial tolerance to ischemia. J Mol Cell Cardiol 1992;24:485–95.[Medline]
  16. Ovize M, Kloner RA, Przyklenk K. Stretch preconditions canine myocardium. Am J Physiol 1994;266(1 Pt 2):H137–46.[Medline]
  17. Cave AC, Hearse DJ. Ischemic preconditioning and contractile function: studies with normothermic and hypothermic global ischemia. J Mol Cell Cardiol 1992;24:1113–23.[Medline]
  18. Chen S-X, Lu E-X, Zhou H-Z, et al. Myocardial protective effects of ischemic preconditioning in the donor hearts during canine heart transplantation. Chinese J General Surg 1994;3:364–8.
  19. Illes RW, Wright JK, Inners-McBride K, Yang C-J, Tristan A. Ischemic preconditioning improves preservation with crystalloid cardioplegia. Ann Thorac Surg 1994;58:1481–5.[Abstract]
  20. Hirai T, Fujita M, Yoshida N, Yamanishi K, Inoko M, Miwa K. Importance of ischemic preconditioning and collateral circulation for left ventricular functional recovery in patients with successful intracoronary thrombolysis for acute myocardial infarction. Am Heart J 1993;126:827–31.[Medline]
  21. Cribrier A, Korsatz L, Koning R, et al. Improved myocardial ischemic response and enhanced collateral circulation with long repetitive coronary occlusion during angioplasty: a prospective study. J Am Coll Cardiol 1992;20:578–86.[Abstract]
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