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Eur J Cardiothorac Surg 2003;24:260-269
© 2003 Elsevier Science NL
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Department of Cardiac Surgery, Centro Cardiologico Monzino IRCCS, University of Milan, via Parea 4, 20138 Milan, Italy
Received 30 July 2002; received in revised form 15 April 2003; accepted 24 April 2003.
* Corresponding author. Tel.: +39-02-58002558; fax: +39-02-58011194
e-mail: aparolari{at}cardiologicomonzino.it
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Abstract |
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 Top Abstract 1. Introduction2. Historical background (Table...3. Inflammation, hemostasis and...4. Discussion5. Limitations of the...6. ConclusionsReferences |
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Key Words: Cardiopulmonary bypass • Coronary surgery • Beating heart surgery • Inflammation • Hemostasis • Oxidative stress
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1. Introduction |
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TopAbstract1. Introduction2. Historical background (Table...3. Inflammation, hemostasis and...4. Discussion5. Limitations of the...6. ConclusionsReferences |
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After the recent development of effective devices for target vessel exposure and stabilization, beating heart techniques, e.g. off-pump coronary artery bypass grafting (OPCAB) and minimally invasive direct coronary artery bypass (MIDCAB) have gained widespread diffusion as alternative techniques to conventional on-pump coronary artery bypass grafting (CABG). The avoidance of CPB and myocardial ischemia-reperfusion has been proposed to significantly reduce the postoperative systemic complications which negatively affect the perioperative course after surgical myocardial revascularization [1,2].
The aim of this study is to review possible differences between on-pump and off-pump coronary surgery in the perioperative activation of inflammation, hemostasis and oxidative stress markers.
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2. Historical background (Table 1) |
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TopAbstract1. Introduction2. Historical background (Table...3. Inflammation, hemostasis and...4. Discussion5. Limitations of the...6. ConclusionsReferences |
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3. Inflammation, hemostasis and oxidative stress: CABG vs. OPCAB or MIDCAB |
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TopAbstract1. Introduction2. Historical background (Table...3. Inflammation, hemostasis and...4. Discussion5. Limitations of the...6. ConclusionsReferences |
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(Table 2)
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(TNF-) is a potent proinflammatory cytokine produced mainly by monocytes–macrophages, but also by B and T cells and by fibroblasts. The myocardium subjected to ischemia-reperfusion cycle during conventional CABG is a major source of TNF- [15], particularly if the left ventricle is dysfunctioning [16]. The systemic release of TNF- is limited during aortic cross-clamping, but it becomes striking after aortic declamping [17]. Diegeler et al. documented in a nonrandomized study, a significant increase in the release of TNF- soluble receptors, p55 and p75 soon after surgery in CABG, which persisted up to 48 h; conversely, there was an early significant postoperative increase in the circulating levels of TNF- soluble receptors in OPCAB group and no change in MIDCAB [14]. Two randomized studies comparing the kinetics of TNF- in CABG vs. OPCAB [10,18] showed somehow conflicting results. Significant increases in the circulating levels of TNF- in both groups of patients were observed [18], which were significantly greater in the CABG group throughout the study period. In contrast, in another study, no changes in TNF- levels were observed in OPCAB, and a trend towards TNF- increase in the early hours, reaching statistical significance only at 48 h postoperatively, was observed in CABG patients [10]. This discrepancy may be explained by the fact that, in this latter study, CABG patients underwent on-pump surgery on beating heart without aortic clamping, a condition in which the contribution of perioperative myocardial ischemia-reperfusion might have been relatively small in terms of inflammation.
3.2. Interleukins (Table 3)
3.2.1. Interleukin-6
Interleukin-6 (IL-6) is a pleiotropic cytokine produced by several cells, such as T cells, monocytes–macrophages and fibroblasts. Experimental [20] and clinical [15–17] studies documented that myocardium exposed to cardioplegic arrest is one of the major sources of IL-6. The exclusion of the lungs from circulation may play a role in explaining the elevated levels of IL-6 levels during CPB [21]. IL-6 participates and contributes to the acute inflammatory reaction as well as to the activation of T cells, stimulation and growth of hematopoietic precursor cells and fibroblasts [22]. Finally, there is evidence that IL-6 blunts the release of other proinflammatory cytokines [22].
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3.2.2. Interleukin-8
Interleukin-8 (IL-8) is a proinflammatory cytokine produced by several cell types, such as monocytes/macrophages, endothelial cells and T lymphocytes. This cytokine plays a major role in the control of neutrophil trafficking [29]. Similar to TNF- and IL-6, the myocardium and the lungs are among the major sources of IL-8 during CPB [15–17,21,30].
Nonrandomized studies indicate that in CABG, OPCAB and MIDCAB, the perioperative levels of IL-8 increase over time, mostly in CABG compared with MIDCAB patients [12,14].
Ascione et al. [9] in a randomized study showed increased plasma levels of IL-8 in CABG patients from 1 to 24 postoperative hours, whereas no relevant changes in the levels of this proinflamamtory cytokine were detected over time in OPCAB. Another study [10] showed no major differences in the time course of IL-8 between CABG and OPCAB patients. In the latter, there was a significant increase of IL-8 over baseline in CABG early postoperatively. In the OPCAB group, a similar trend, although not statistically significant, towards an early perioperative increase of IL-8 was observed. Indeed, in this study, CABG patients were operated on a beating heart during CPB. In this way, the avoidance of myocardial ischemia induced by aortic cross-clamping might prevent the release of IL-8 [30] and other cytokines from the myocardium. Also, other nonrandomized studies documented higher levels of IL-8 in the early hours after surgery in CABG patients, with similar levels between CABG and OPCAB at later times [25,26].
3.2.3. Interleukin-10
This cytokine is produced by monocytes–macrophages, B and T cells, and it possesses anti-inflammatory properties [31,32]. Both randomized [23] and nonrandomized studies [25,26] have shown rapid and significant increases of interleukin-10 (IL-10) levels in CABG just after reperfusion, which return to baseline within 2–4 h after surgery. Instead, no statistically significant changes in IL-10 levels are observed in OPCAB [14,23,25,26] or MIDCAB [14] patients. The mechanisms responsible for the increases in the levels of IL-10 in plasma in CABG are somehow uncertain.
3.2.4. Other interleukins
Evidence concerning the kinetics of the levels in plasma of other interleukins in the different surgical approaches to coronary artery disease is still limited. The receptors for IL-2, a proinflammatory and immunostimulatory interleukin involved in the initiation of inflammatory response, have been shown to be increased in both CABG and OPCAB procedures, with relatively higher levels in CABG [18]. Finally, the kinetics of the proinflammatory IL-1 was not different in CABG, OPCAB, MIDCAB and on-pump MIDCAB [28].
3.3. C-reactive protein, leukocytes and elastase (Table 4)
C-reactive protein (CRP), one of the major acute phase reactants, enhances phagocytosis of bacteria, viruses and parasites and also activates complement. In nonrandomized studies, similar CRP levels both in CABG and OPCAB up to 24 h after surgery were observed [27,33]. In contrast, in a randomized study, levels of CRP were found to be increased in the early days after surgery both in CABG and OPCAB; the increase of CRP levels was greater and persisted for longer time after CABG with respect to OPCAB [18].
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Nonrandomized studies showed significant increases over time of leukocytes [13,34] and neutrophils [34] in the postoperative period in CABG and MIDCAB with no differences between these two surgical techniques. Concerning elastase behaviour, only one randomized study [11] reported levels of elastase higher in CABG than in MIDCAB.
3.4. Coagulation, platelets and adhesion molecules (Table 5)
To our knowledge, only one recent nonrandomized study has investigated coagulation and fibrinolysis variables in CABG vs. OPCAB up to 24 h after surgery [35]. Both in CABG and OPCAB, remarkable changes in some of the coagulation and fibrinolytic variables occur perioperatively. CABG, however, is associated with early (<24 postoperative hours) lower platelet counts, lower plasminogen and higher D-dimer levels soon after surgery, whereas after 24 h, these differences are no more detectable.
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It is noteworthy that a randomized trial comparing one-vessel CABG and MIDCAB showed, even in this case, considerable changes in terms of activation of coagulation and fibrinolytic pathways in both groups. This study, however, reported no differences between the two study groups [37]. On the other hand, some controversy exists concerning effects of CABG or MIDCAB on platelet activation. Gu et al. in a randomized study showed that CABG is accompanied by increased platelet activation at the end of surgery [11]. A later randomized study, however, from the same group did not confirm this finding [37].
3.5. Oxidative stress
Oxidative stress is the result of imbalance between local antioxidant defenses and the formation of reactive oxygen species. This is known to occur during myocardial reperfusion. Off-pump procedures are associated with lower degrees of oxidative stress than on-pump coronary surgery. Gerritsen et al. [38] in a prospective, although not randomized study comparing patients with similar preoperative clinical features showed that OPCAB was associated with significantly lower levels of urinary excretion of hypoxanthine, xanthine and malondialdehyde during the first 24 h after surgery. Even if the burst of oxidative stress that occurs during CABG has been related to myocardial ischemia-reperfusion due to cardioplegic arrest of the heart [39,40], a separate contribution of CPB to oxidative stress has also been recently shown. In fact, Matata et al. [10] in a prospective randomized study comparing OPCAB with on-pump coronary bypass with the beating heart and without cardioplegia showed that, in the early hours after surgery, OPCAB patients display significantly lower levels of lipid hydroperoxides, protein carbonyls and nitrotyrosine, all markers of oxidative stress. In this latter case, both on-pump and off-pump procedures were performed on a beating heart and the coronary arteries target for revascularization were clamped only for the time necessary to perform the distal anastomosis in both groups, which suggests similar degrees of myocardial ischemia-reperfusion in both groups.
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4. Discussion |
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TopAbstract1. Introduction2. Historical background (Table...3. Inflammation, hemostasis and...4. Discussion5. Limitations of the...6. ConclusionsReferences |
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Consistent advantages of OPCAB over CABG are limited to some inflammatory markers and to the time span between the final steps and the very early hours after the surgical procedure. Some inflammatory markers (activated complement factors, TNF-, IL-8, IL-10 and elastase) increase with respect to baseline both in CABG and OPCAB, but the peak levels are highest in CABG; afterwards, the differences in terms of inflammatory profile progressively fade and finally cancel out (Fig. 1
). Indeed, in the early phase, CPB is the major determinant of the onset of the inflammatory reaction, but in the late phases, the surgical trauma itself is likely to play a predominant role. Evidence about other markers (IL-1, IL-6, some leukocyte subsets) is less consistent and in some cases, even contradictory. Overall, it can be hypothesized that CPB itself only minimally influences the circulating levels of these markers. Thus, the trauma derived from the surgical procedure may be likely the major determinant of inflammatory reaction. The activation of the inflammatory system, although less marked than that of CPB, documented during vascular and noncardiac thoracic surgery [6,7], further supports this hypothesis.
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, IL-6, IL-8) during CPB after organ reperfusion [15,17,21,30]. Moreover, levels of cytokines in plasma are positively related to the aortic cross-clamping duration [12,14], increasing exponentially after 60 min of cross-clamping [44]. Massoudy et al. [21] reported that the avoidance of the oxygenator from the CPB circuit, using the patient's lungs as autogenous oxygenator (i.e. maintaining lung perfusion, so called Drew circulation) significantly reduces the proinflammatory state compared with the conventional CPB circuit. It is still unclear, however, if the lack of increases in circulating levels of proinflammatory cytokines is secondary to the avoidance of reduction of in pulmonary blood flow or it is consequent to the preservation during CPB of the normal scavenger properties of the lungs, which eliminate from the circulation proinflammatory mediators by means of pulmonary enzymatic systems. One potential explanation for the limited difference between off-pump and on-pump techniques may be that, with the exception of the CPB and myocardial ischemia-reperfusion, both techniques share the necessarily invasive nature of the surgical access. Surgical incisions commonly adopted in open heart surgery, sternotomy and thoracotomy, are highly traumatic accesses, which impose a significant injury to the tissues and elicit a marked inflammatory response even before the institution of CPB. Gu reported that neutrophil preactivation occurs after the start of the cardiac operation before full dose systemic heparinization and institution of CPB; moreover, the capability of neutrophils to be preactivated is relatively low during and after CPB as compared with the time period before CPB [45]. In a recent study, Chello et al. [19] observed that the surgical stress itself (independently of the use of CPB) by decreasing neutrophil apoptosis in patients undergoing on-pump and off-pump coronary surgery prolongs the survival of activated neutrophils and, consequently, amplifies the inflammatory response.
Information concerning potential advantages of OPCAB with respect to CABG in terms of activation of the hemostatic system is still limited. During OPCAB, reduced platelet consumption as well as less activation of the fibrinolytic system than during CABG have been reported. These differences, however, can be perceived only up to 24 h after surgery. Interestingly, no differences in terms of endothelial or platelet activation markers were observed during the two surgical procedures. No information, however, is still available concerning potential differences in the activation of the coagulation pathway as well as in terms of thrombin generation in these conditions.
Previous studies by our group [46] and by others [47] showed that, during and early after cardiac surgery performed with CPB use, there is a massive activation of coagulation with elevated levels of prothrombin fragment, F1.2 and of thrombin–antithrombin complexes; activation of the fibrinolytic system follows [46]. Indeed, increased levels of cross-linked fibrin degradation products [8] and plasmin–antiplasmin complex [47] have been reported as a consequence of the activation of the coagulation system. If on one side, the interaction of blood with extensive nonendothelial surfaces of the bypass circuit is one of the causes of the activation of these pathways, on the other side, other mechanisms, e.g. surgical trauma and retransfusion of pericardial blood collected intraoperatively may significantly contribute to activation of the coagulation–fibrinolytic systems. This latter observation may explain the sensible activation of these pathways even during and early after off-pump procedures.
In fact, during the operation continuous oozing and bleeding from the cut edges and particularly from the sternal spongiosa into the surgical field, even after meticulous hemostasis, may activate monocytes after contact with the pericardium [48,49]. There is evidence of high levels of markers for thrombin and fibrin generation and inflammatory markers in mediastinal shed blood [49]. Activated shed blood may return into the circulation by suction from the surgical field after processing of cell-saver devices, and it is well known that washing of blood by cell-savers reduces but does not eliminate proinflammatory cytokines and the procoagulant properties of the blood returned to the patient [50,51]. It is noteworthy that blood-saving devices may be used also in off-pump surgery [35,41], and this can justify the changes that occur even during these procedures.
Finally, surgical chest wound is a major source of tissue factor and cytokines [48], which activates the extrinsic pathway of the coagulation cascade and contributes to the onset of a postoperative hypercoagulable state.
In addition, it should be stressed that during OPCAB, this potentially hypercoagulable state is unopposed by a full course of intravenous heparin and hemodilution as in CABG, and likely contributes to frequently reported reduction of mediastinal blood losses and blood transfusions, but also to early thrombotic complications [52–54]. Quigley et al. observed by means of thromboelastography, a twofold increase in coagulation index in patients undergoing OPCAB after 72 h after surgery, whereas in patients undergoing CABG, the coagulation index had returned to preoperative values.
Finally, for what oxidative stress is concerned, OPCAB seems to be associated with significantly lower degrees of oxidative stress with respect to CABG, and a separate contribution of CPB and ischemia-reperfusion injury is also likely. An increasing body of evidence suggests that oxidant stress is involved in the pathogenesis of many cardiovascular diseases, including hypercholesterolemia [55], atherosclerosis [56], hypertension [57], diabetes [58] and heart failure [59]. However, further studies in this field are warranted, in order to clarify pathogenetic mechanisms and to prevent and treat oxidative stress.
In summary, the analysis of the available data shows that in terms of biological impact, there are subtle differences between OPCAB and CABG and the general surgical trauma may play a even more significant role. Nevertheless, we have to recognize that in most of the studies quoted into the present review, the CPB was structured and conducted in a standard way, i.e. using mild or moderate systemic hypothermia, cold cardioplegia, uncoated circuits, without the administration of anti-fibrinolytic drugs or of any other inflammation modulating drug and using the cardiotomy suckers. However, during the last decade, the practice of the CPB has been subjected to major refinements and improvements in the field of biocompatibility like the introduction of warm heart surgery, coated circuits, anti-fibrinolytic drugs and the elimination of cardiotomy suckers. Warm cardioplegia seems to reduce the oxidative stress [60–62] and inflammatory response [63,64]. Routine use of heparin-coated circuits and the elimination of cardiotomy suction has been related to the reduction of thrombin generation, platelet activation and inflammation during CABG [65]; moreover, the use of both heparin-coated and phospholipid-coated circuits were associated to reduction to the release of proinflammatory molecules [66–68]. Also, these improvements to the routine CPB gained widespread diffusion in the clinical practice during the last years.
Few studies comparing CABG and OPCAB adopted in their protocol normothermic systemic perfusion [9,23,24,28], warm cardioplegia [9,14,25] and aprotinin [14,23,24,28,34]. It is noteworthy that in the studies adopting only normothermic techniques [9,25], the authors observed a significant increase in the inflammation and oxidative stress in the CABG group, as compared with the OPCAB group, whereas, in the studies adopting simultaneously both normothermic techniques and aprotinin [14,23,24,28,34], the inflammatory response was related to the general surgical trauma, derived by the surgical access, rather than the use of CPB. It is unknown if this difference is linked only to the administration of the aprotinin per se or to the combined use of normothermia and aprotinin. Strong and definitive evidences about the superiority of these techniques are still lacking probably because they are often adopted separately. Baufreton et al. [69] observed that the use of heparin-coated circuits reduced complement activation, whereas the administration of aprotinin resulted in the reduction of thrombin and D-dimer generation; they suggested that the combined adoption of heparin-coated circuits and aprotinin may be advisable in order to achieve maximal reduction of both pathways of blood activation during CPB.
We may thus speculate that the simultaneous and integrated use of warm surgery techniques, coated circuits, anti-fibrinolytic and anti-inflammatory drugs and the elimination of the cardiotomy suckers may enhance the biological compatibility of the CPB. Any reduction of the impact of the heart–lung machine on the inflammation, coagulation and oxidative stress may probably further minimize the differences, already subtle, between CABG and OPCAB.
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5. Limitations of the available evidences |
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TopAbstract1. Introduction2. Historical background (Table...3. Inflammation, hemostasis and...4. Discussion5. Limitations of the...6. ConclusionsReferences |
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6. Conclusions |
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TopAbstract1. Introduction2. Historical background (Table...3. Inflammation, hemostasis and...4. Discussion5. Limitations of the...6. ConclusionsReferences |
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References |
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TopAbstract1. Introduction2. Historical background (Table...3. Inflammation, hemostasis and...4. Discussion5. Limitations of the...6. ConclusionsReferences |
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