Eur J Cardiothorac Surg 2006;30:117-125
© 2006 Elsevier Science NL
Emergency re-revascularization with percutaneous coronary intervention, reoperation, or conservative treatment in patients with acute perioperative graft failure following coronary artery bypass surgery
Matthias Thielmann
a
,
*
,
Parwis Massoudy
a
,
Beate R. Jaeger
b
,
Markus Neuhäuser
c
,
Günter Marggraf
a
,
Stephan Sack
b
,
Raimund Erbel
b
,
Heinz Jakob
a
a Thoracic and Cardiovascular Surgery, West-German Heart Center Essen, University Hospital of Essen, Hufelandstraße 55, 45122 Essen, Germany
b Department of Cardiology, West-German Heart Center Essen, University Hospital of Essen, Essen, Germany
c Institute for Medical Informatics, Biometry, and Epidemiology, University Hospital of Essen, Essen, Germany
Received 25 October 2005;
received in revised form 15 March 2006;
accepted 31 March 2006.
* Corresponding author. Tel.: +49 201 723 4928; fax: +49 201 723 5451. (Email: matthias.thielmann{at}uni-essen.de).
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Abstract
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Objective: Perioperative graft failure following coronary artery bypass grafting (CABG) results in acute myocardial ischemia/infarction (PMI), which may necessitate an acute secondary revascularization procedure to salvage myocardium, in order to preserve ventricular function and improve patient outcome. Whether acute percutaneous coronary (re)intervention (PCI), emergency reoperation, or conservative intensive care treatment should be applied, is currently unknown. Methods: In order to identify the source of PMI and to pursue the appropriate re-revascularization strategy, coronary repeat angiography was emergently performed in 118 among 5427 consecutive isolated CABG patients with evidence of PMI. As a result, patients immediately underwent acute PCI (group 1), emergency reoperation (group 2), or were treated conservatively (group 3). Primary study endpoint was postoperative myocardial infarct size, as measured by peak cardiac troponin I (cTnI) serum levels. Secondary endpoints were perioperative left ventricular ejection fraction (LVEF%), assessed by transesophageal echocardiography, major adverse cardiac events, and short- and midterm mortality. Results: Repeat coronary angiography revealed early perioperative bypass graft failure in 67 among 118 patients and 84 among 214 bypass grafts after CABG. The number and type of failing bypass grafts were comparable between groups 1 and 2, but significantly different to that of group 3 (P
< 0.007). Acute PCI was applied in 25 patients, redo-CABG in 15 patients, and conservative treatment in 27 patients. Procedural peak cTnI serum levels were significantly different between groups 1 and 2 (81 ± 18 ng/ml vs 178 ± 62 ng/ml; P
< 0.001). Global LVEF was reduced during the acute ischemic event when compared with preoperative values (P
< 0.01). Thereafter, LVEF improved during follow-up within each group (P
< 0.001), but did not differ between the three groups. In-hospital and 1-year mortality were 12.0% and 20.0% in group 1, 20.0% and 27% in group 2, and 14.8% and 18.5% in group 3, respectively (P
= NS). Conclusions: Re-revascularization with emergency PCI may limit the extent of myocardial cellular damage compared with the surgical-based treatment strategy in patients with acute perioperative myocardial ischemia due to early graft failure following CABG.
Key Words: Coronary artery bypass grafting • Graft failure • Re-revascularization • Reintervention
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1. Introduction
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Perioperative myocardial infarction (PMI) with irreversible myocardial cell damage is one of the most serious and life-threatening complications after coronary artery bypass grafting (CABG), and are associated with substantially increased in-hospital morbidity and mortality rates. Postoperative rise of cardiac biomarkers after CABG, indicating irreversible myocardial cell damage, correlates with increased risk of subsequent congestive heart failure and adverse short- and long-term outcomes [1–3].
The pathogenesis of myocardial cell damage after CABG has been the subject of distinct clinical research and is based upon a variety of different bypass graft-related and nongraft-related mechanisms during the perioperative course [4,5]. The most common graft-related etiologies of myocardial cell damage after CABG are graft occlusion due to acute graft thrombosis, subtotal or hemodynamic relevant anastomotic stenosis, graft kinking or overstretching, and postoperative graft spasm [6,7]. Nongraft-related etiologies of myocardial cell damage after CABG are surgery-related, including inadequate cardioplegic perfusion and myocardial protection [8], incomplete revascularization [9], or distal coronary microembolization [10], possibly due to surgical manipulation on pre-existing microembolizing and disintegrating unstable plaques.
Although early graft failure after CABG appears to be a rare event, the recognition and diagnostic discrimination of graft-related PMI from other reasons of postoperative myocardial cell damage, as previously described [4], may help to minimize the time interval between the first clinical event of myocardial ischemia until a possible invasive reintervention procedure. Thus, the early identification of patients with PMI due to acute graft failure enables an adequate reintervention strategy for re-revascularization, such as percutaneous coronary (re)intervention (PCI) or reoperation with surgical graft revision to salvage reversibly damaged myocardium, in order to preserve ventricular function and improve patient prognosis. However, the possible benefit and the time-dependency of an immediate secondary revascularization procedure as compared with conservative treatment are currently unknown.
The purpose of the present study was, therefore, to study and analyze the impact of different treatment strategies (PCI, redo-CABG, conservative treatment) after CABG complicated by early bypass graft failure on (1) postoperative myocardial infarct size, (2) global left ventricular function, and (3) postoperative outcome.
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2. Patients and methods
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2.1 Patient population
Between January 1999 and January 2006, 118 (2.2%) out of 5427 consecutive patients undergoing isolated CABG were prospectively enrolled into this single-centre study with a confirmed diagnosis of early graft failure within the first 24 h after surgery. After a suspected diagnosis of PMI, patients were immediately subjected to repeat coronary angiography. When early graft failure was confirmed, patients were immediately assigned to any of the following treatment procedures: (1) catheter-based treatment strategy with subsequent PCI (group 1); (2) surgical-based treatment strategy readmitting patients to emergency redo-CABG (group 2); or conservative treatment (group 3).
2.2 Study endpoints and criteria
Primary study endpoint was postoperative myocardial infarct size, as measured by postoperative peak cardiac troponin I (cTnI) serum levels. Secondary endpoints were global left ventricular ejection fraction (LVEF), assessed by echocardiography, clinical outcome including major adverse cardiac events (MACE), as well as short- (in-hospital) and midterm mortality. In-hospital mortality was defined as any death within 30 days after surgery or during the same time period of hospital admission.
Emergency surgery and previous myocardial infarction (<4 weeks) at primary CABG were exclusion criteria. Institutional approval was obtained and all patients gave their informed consent.
2.3 Perioperative management
Standard cardiopulmonary bypass (CPB) technique with ascending aortic and two-stage venous cannulation, hemodilution, systemic mild hypothermia (>32 °C), and membrane oxygenation, as well as cold myocardial protection using antegrade crystalloid (Bretschneider) cardioplegia and topical cooling was used as previously described [5]. The left internal thoracic artery (LITA) and saphenous veins were the preferred grafts. Duration of CPB, aortic cross clamp time, and time of reperfusion were routinely assessed. Mean graft flow was assessed after CPB just before sternal closure by Doppler transit time flowmetry (Cardiomed, MediStim, Oslo, Norway) for each graft. Patients were hemodynamically monitored in the postoperative course, 12-lead ECGs were recorded and venous blood samples for cTnI measurement were collected preoperatively, 1 h, 6 h, 12 h, 24 h, 36 h, and 48 h after CABG. Echocardiography was carried out during the perioperative course and at follow-up by a cardiologist. A medication of 500 mg acetylsalicylic acid (ASA) was administered intravenously within the first 6 h after surgery in the absence of significant bleeding followed by an oral dose of 100 mg daily.
2.4 Repeat coronary angiography
Repeat coronary angiography was immediately performed, when PMI, as identified by one of the following criteria, was suspected: (1) a cTnI serum level >20 ng/ml within 24 h after surgery, (2) the appearance of ST-segment deviations at the J point in two or more contiguous leads with cut-off points 
0.2 mV in leads V1, V2, or V3 and 0.1 mV in other leads or T-wave abnormalities in two or more contiguous leads as previously described [4], or (3) hemodynamic instability despite intravenous inotropic support (>0.3 µg/kg–1/min–1). Repeat angiographies were performed in a standardized way by our colleague cardiologists as previously described [11].
2.5 Catheter-based secondary revascularization
When the respective decision was made, rescue PCI was carried out following diagnostic coronary angiography. The concept of the intention was to reintervene the native coronary artery system to which the failing graft belonged. After the PCI procedure patients routinely received a dual therapy of ASA and clopidogrel (300 mg clopidogrel loading dose, followed by 75 mg clopidogrel and 100 mg ASA daily for another month) according to the ESC/ACC guidelines.
2.6 Surgical-based secondary revascularization
When PCI was not feasible or not successful, the chances for surgical reintervention or conservative intensive care treatment option were discussed. When redo-CABG was proposed to be the most promising treatment option, patients were immediately readmitted to the operation theatre. Reoperations were performed with the same standard techniques as used for primary CABG. After resternotomy, all bypass grafts were again tested by Doppler transit time flowmetry. Unsatisfactory grafts were substituted with new graft material and thrombotic material was removed from the coronaries and bypass grafts. If LITA was the reason for myocardial ischemia, an additional vein graft was inserted. Inotropic medication and/or intraaortic balloon pump (IABP) was applied to wean patients from CPB. A veno-arterial heparin-bond extracorporeal membrane oxygenation (ECMO) system was applied in those patients refractory to inotropes and IABP with severe postcardiotomy myocardial dysfunction.
2.7 Conservative therapeutic strategies
Conservative therapy in patients with PMI due to early bypass graft failure consisted of (1) a medical therapy and (2) a temporary circulatory support, respectively. Medical therapy included aggressive pain control, beta-blocker therapy, antiplatelet therapy (500 mg ASA loading dose as soon as PMI was suspected, followed by 100 mg ASA daily) and intravenous heparin (if not contraindicated). Inotropic support was given, when ischemia had lead to hemodynamic compromise. Temporary circulatory support was given with either IABP or with veno-arterial ECMO implanted percutaneously. All patients were hemodynamically monitored as mentioned above and myocardial function was daily monitored by transesophageal or transthoracic echocardiography.
2.8 Statistical analysis
Data are reported as mean value ± standard deviation (SD) or median and 25–75% quartiles and categorical variables by their number and summarized as percentage. Comparisons of categorical variables between groups were performed by Pearson's 
2-test, whenever expected frequencies <5 occurred P-values were calculated exactly. Comparisons of continuous variables between groups were analyzed by Kruskal–Wallis test for one-way ANOVA. When a significant overall effect was detected, two group comparisons were performed with Fisher's exact test for categorical variables or the Mann–Whitney's U-test for continuous variables. In the current case of three groups this approach represents a closed testing procedure and, therefore, keeps the multiple levels 
without any multiplicity adjusted. The units for some analyses are grafts or anastomoses instead of patients. In these cases we assume that grafts and anastomoses, respectively, are independent even when at the same patient. Time course of LVEF was analyzed by repeated measures ANOVA, in which the correlation between time points was taken into account. Univariable and multivariable logistic regression analyses were performed to identify postoperative independent predictors for in-hospital mortality before repeated coronary angiography. All postoperative predictor variables that were identified as significant at a two-tailed nominal P-value of less than 0.10 in univariable regression analyses were then entered into a multivariable logistic regression analysis model. A P-value less than 0.05 was considered to indicate statistical significance. All statistical analyses between groups were performed using the StatXact 6.0 software (Cytel Software Corp., Cambridge, MA, USA) and the SAS System® (SAS Institute Inc., Cary, USA), version 8.
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3. Results
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Postoperative repeat coronary angiography revealed early graft failure in 67 among 118 patients, who had fulfilled the criteria of a PMI following CABG. As a result, 25 out of these 67 patients subsequently (13 ± 3 min; mean ± SEM) underwent acute PCI in group 1, 15 patients were referred (4.7 ± 0.4 h; mean ± SEM) to acute secondary surgical reintervention in group 2, whereas a conservative treatment strategy was applied in 27 patients in group 3 without any further secondary revascularization procedure.
3.1 Preoperative and intraoperative characteristics
Preoperative baseline characteristics and demographics of the patients were comparable between the three groups with the contemporary coronary surgery patient profile, except a significantly higher incidence of prior PCI procedures in group 2 compared with groups 1 and 3 (P
< 0.03; Table 1
). As demonstrated in Table 1, intraoperative results were also comparable between groups. Intraoperative transit-time graft flow measurement showed a significantly lower mean graft flow of the affected bypass grafts in group 3 (29 ± 17 ml/min) as compared with the graft flows in groups 1 (54 ± 21 ml/min; P
= 0.002) and 2 (59 ± 17 ml/min; P
< 0.001).
3.2 Angiographic findings
Repeat coronary angiography was immediately performed after suspected diagnosis of PMI, 13.5 ± 1.0 h (mean ± SEM) after primary CABG. Among a total number of 214 inserted grafts, 84 were identified as failing ones. The most common cause of graft failure was graft occlusion (n
= 70), followed by graft kinking (n
= 5) and anastomotic stenosis (n
= 9), which were identified by coronary angiography as subtotal (>75%) stenoses of the grafts and thus interpreted as functional occlusion. The localization, number, and distribution of failing grafts per patient were comparable between groups 1 and 2, but significantly different to group 3 (Table 2
). As a result, the myocardial region of secondary re-revascularization using a catheter-based reintervention strategy in group 1 was comparable to the regions, which were revascularized by surgical-based reintervention in group 2 (Table 2).
3.3 Postoperative myocardial cell damage
Peak cTnI levels indicating the extent of irreversible myocardial cellular damage were significantly increased in all three groups as compared with preoperative levels. Mean peak cTnI serum level was significantly higher in group 2 compared with groups 1 and 3 (P
< 0.001; Fig. 1
).
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Fig. 1. Postoperative peak maximum cTnI serum levels (mean ± SD) of the groups; P
< 0.001, one-way ANOVA.
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The comparison of the postoperative occurrence of ECG-changes revealed no significant differences between the three groups. Significant ST-segment deviations could be observed in 17 patients of group 1, 10 patients of group 2, and 23 patients of group 3 (P
= NS). New pathologic Q-waves during the further postoperative course were not significantly different between the groups and were observed in 12 patients in group 1, 5 patients in group 2, and 19 patients in group 3 (P
= NS).
3.4 Time course of global left ventricular function
The time course of global LV-ejection fraction was determined by echocardiography, preoperatively (LVEF-1), during ischemic event before angiography (LVEF-2), and at follow-up (LVEF-3). Preoperative LVEF was comparable between the three groups (59 ± 10%, 56 ± 11%, and 57 ± 11%, respectively). A significant reduction of LVEF could be seen during ischemic event compared with the preoperative values (37 ± 9%, 31 ± 9%, and 35 ± 10%; P
< 0.001), and at follow-up, again, a significant restoration (45 ± 12%, 43 ± 8%, and 42 ± 8%; P
< 0.001) was observed. However, a significant difference in terms of LVEF between the groups was not observed, neither during ischemic event (P
= 0.07) nor at follow-up (P
= 0.58; Fig. 2
).
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Fig. 2. Perioperative time course of global left ventricular ejection fraction (mean ± SD) of the groups; P
< 0.001 within each group; P
= NS between the groups, two-way ANOVA. LVEF-1, preoperative value; LVEF-2, at ischemic event before angiography; LVEF-3, at follow-up (298 ± 73 days).
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3.5 Secondary revascularization procedure
All postinterventional results of acute PCI of group 1 patients were found to be primarily successful by the interventionalist with TIMI III flows of the affected coronaries. The postoperative results of redo-CABG of group 2 patients were also found to be satisfying by the surgeon with a mean secondary graft flow of 85 ± 15 ml/min (mean ± SEM) of the substituted grafts. However, the secondary graft flow was not statistically associated with postoperative outcome.
3.6 Clinical outcome
Postoperative outcome data of the patients before decision of reintervention or reoperation at repeat angiography showed no differences, except a higher incidence of postoperative ST-segment deviations on the ECG in group 2 as compared with groups 1 and 3 (P
< 0.04). The time intervals from CABG to repeat angiography and from repeat angiography to reintervention or reoperation were significantly different between the groups 1 and 2 (Table 3
). The univariable logistic regression analysis identified some postoperative variables before repeat angiography to be significantly associated with in-hospital death (Table 4
). After risk adjustment, by using multivariable logistic regression analysis, only cardiopulmonary resuscitation remained independently associated with death. Postoperative clinical data like postoperative ventilation time, as well as ICU and hospital stay were similar between the three groups (Table 5
). Regarding MACE, a higher incidence for postoperative LCOS in group 2 compared with groups 1 and 3 occurred (P
< 0.01). The incidence of postoperative renal failure requiring temporary veno-venous hemofiltration or hemodialysis was also significantly different between the groups (P
< 0.01). IABP support was applied in 24%, 47%, and 37% in the groups, respectively (P
=
NS), and temporary veno-arterial ECMO support due to severely impaired ventricular function was necessary in one patient in group 1 and two patients in group 2 (Table 5).
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Table 4. Univariable and multivariable regression analyses of postoperative variables before repeat angiography associated with death
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3.7 Survival data
Cumulative 30-day and 1-year mortality were not significantly different between the three groups. All causes of death at 1-year follow-up were associated with major adverse cardiac events (Table 5). The comparison of the cumulative survival between the groups over the complete follow-up time of about 6.5 years revealed no significant difference between the groups (P
= NS; Fig. 3
).
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Fig. 3. Kaplan–Meier survival curve of the groups indicating the probability of survival at follow-up (P
= NS); (—) group 1, (— —) group 2, (- - -) group 3.
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4. Discussion
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The present study demonstrates that in a surgical population of patients undergoing CABG, the incidence of early graft failure within 24 h after CABG is about 1–3%, leading to early postoperative myocardial ischemia and irreversible myocardial cell damage, strongly associated with a higher mortality within 30 days and a higher incidence of major adverse events. The pathogenesis of myocardial cellular damage after CABG has been the subject of intensive clinical research and is generally based upon a variety of different bypass graft-related or nongraft-related mechanisms during the perioperative course of CABG [4,12]. When PMI is manifested by acute ST-segment elevation, rise of cardiac biomarkers, hemodynamic instability, or sustained ventricular arrhythmia, a sudden graft occlusion is frequently responsible. The most common reasons for graft-related myocardial cell damage after CABG are graft occlusion, subtotal or hemodynamic relevant anastomotic stenosis, graft kinking or overstretching, and postoperative graft spasm [6,7,12]. These graft-related mechanisms induce myocardial hypo- and/or malperfusion with subsequent regional myocardial dysfunction, leading to a wave front of myocardial damage extending from the subendocardium to the subepicardium in a time-dependent fashion. It is known to be reversible in the beginning, however, later leading to irreversible myocardial damage, reflected by the loss of cardiac myocytes and myocardial cellular necrosis.
Regarding the type of bypass grafts, LITA grafts achieve improved long-term patency compared with saphenous vein grafts, which have a 10–12% incidence of closure within the early (up to 60 days) postoperative period after CABG [13,14]. However, LITA graft failure even occurs due to injury during harvesting, technical problems with the anastomosis, mechanical kinking, or undetected subclavian artery stenosis [15,16] and thrombotic stenosis or occlusion of the LITA graft may be responsible for acute ischemic complications after CABG in at least a third [6,17] up to on half of the cases as observed in the present study.
Although early graft failure after CABG appears to be a rare event, the recognition and diagnostic discrimination of a graft-related ischemic event from other reasons of postoperative myocardial damage [4], may help to minimize the time interval between the first clinical event of myocardial ischemia to a possible reintervention procedure. Thus, the identification of patients with early graft failure enables adequate reintervention strategies, such as acute percutaneous coronary (re)intervention or reoperation with surgical graft revision. These reintervention measures may result in the salvage of reversibly damaged myocardium, thus preserving ventricular function and improving the patients outcome and prognosis after CABG [18,19].
However, the possible benefit of an emergency re-revascularization procedure like PCI or a reoperation in this clinical setting of myocardial ischemia and its time-dependency is currently unknown. To date, there are no guidelines clearly clarifying this issue. Although, the exact time point of graft failure and the onset of symptoms mostly remain uncertain in the early postoperative course, recent clinical trials have been hypothesized and demonstrated that even ‘delayed’ reperfusion (12–48 h after onset of symptoms) of infarcted myocardium may be beneficial by reducing myocardial infarct size, improving myocardial healing, and preventing electrical instability [20,21]. Moreover, the situation of coronary circulation after CABG and thus, the regional myocardial perfusion of an infarct-related coronary artery with additional early graft failure does not seem to be comparable to the theory of reperfusion of a native, infarct-related coronary artery without coronary artery bypass grafts [22]. Therefore, an adequate invasive reintervention strategy with immediate re-revascularization procedure by either a catheter-based reintervention strategy like PCI or surgical-based reintervention like redo-CABG may be useful even with a ‘delayed’ reperfusion after the initial graft failure to salvage as much myocardium as possible.
In the present study, a significant difference between PCI group 1 and reoperation group 2 could be observed with regard to postoperative myocardial infarct size and a higher incidence of postoperative LCOS in the reoperation group 2 compared with groups 1 and 3, indicating more myocardial cell damage after a secondary acute redo-CABG leading more frequently to a postoperative LCOS. The higher release of postoperative cTnI may additionally by associated with a longer time period between repeat angiography and reoperation in group 2 compared with group 1, which may be prevented or even shortened in the future with the installation of a combined ‘cathlab-OR’, where surgical interventions are possible directly after coronary angiography or even after unsuccessful PCI. Furthermore, in the present study a significant increase of postoperative hemodialysis-dependent renal failure could be observed in group 1 compared with group 2, which might be the result of a higher consumption of contrast agent leading to radiographic contrast material-induced nephropathy. On the other hand, there was no significant difference in the degree of myocardial restoration, as measured by echocardiography, and no difference in short- and midterm mortality between the reintervention groups 1 and 2. Furthermore, there was no significant difference between the reintervention groups 1 and 2, compared with the conservative treatment group 3. However, a selection bias in group 3 patients with exclusively single graft failures, predominantly with single vein grafts to lateral and posterior myocardial regions, and with significantly lower graft flows, and thus, a probably smaller myocardial ‘area at risk’ should be taken into account when compared with patients of reintervention groups 1 and 2.
Emergency reinterventions for early graft failure using a catheter-based revascularization strategy applying acute thrombolysis or PCI has been reported to have favorable results [18,23,24]. In a recent study of 45 patients, early postoperative PTCA was reported to be successful 49 days after CABG with reintervention in 95% of the native coronary artery lesions, 89% of vein graft stenoses, and 100% of LITA graft lesions [25]. Importantly, patent grafts were observed in 25–34% of the patients in these three series, suggesting that repeat coronary angiography should be applied, whenever PMI due to acute graft failure is suspected (except hemodynamically critical unstable patients) rather than performing a ‘blind’ redo-CABG. However, emergency PCI is only one of several possible treatment options in early graft failure after CABG surgery. Compared to acute redo-CABG, emergency PCI seems to be quicker and less invasive, as observed in the present study, but still offers the possibility for a complete re-revascularization in this situation. Acute thrombolysis, however, risks severe thoracic hemorrhage in the early postoperative period and does not reverse any technical problems of the failing graft anastomosis. Finally, conservative treatment of patients with early multiple graft failure and/or a large myocardial ‘area at risk’ undoubtedly fail to prevent the development of severe myocardial pump failure and the progression of fatal LCOS. Therefore, among the available treatment options, the catheter-based emergency reintervention strategy with PCI might be a promising treatment option in these patients.
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5. Limitations of the study
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The present study was prospective in design but not a randomized trial to compare the three treatment groups. The indication for acute PCI, redo-CABG, or conservative treatment was not prospectively defined, but the decision for a secondary revascularization strategy was made case by case during/after repeat angiography together with cardiologists and cardiac surgeons. Therefore, the present study may contain a study bias.
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6. Clinical implications
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Emergency reintervention with either catheter-based or surgical-based treatment strategies for postoperative ischemic complications after CABG requires an integrated approach that involves the cardiac intensive care physician, the interventional cardiologist, and the cardiac surgeon. Patient outcomes may be significantly improved as a result of this close collaboration and may lead to a new paradigm in which the cardiac cathlab or a combined ‘cathlab-OR/hybrid-OR’ is routinely available to help the surgeon when early postoperative ischemia is identified.
To date, the best approach for the treatment of acute graft failure after CABG is still unclear and remains controversial. Probably the majority of the European and International cardiac surgery centers prefer to treat those high-risk patients conservatively, whereas on the other hand the number of publications and institutions who prefer to reintervene in this clinical setting are increasing. Therefore, further multi-institutional clinical studies are needed to clarify the appropriate treatment strategy in these patients.
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Appendix A
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Conference discussion
Mr D. J. Wheatley
(Glasgow, United Kingdom): There must be a problem with randomizing this, because if you have a patient suspected of acute graft failure, the surgeon must have an idea whether this was something that you might well expect, a low graft flow or a poor vessel, or something that was totally unexpected and might therefore be a kinked graft, and this surely must have impacted on your decision to assign them to one of the three groups. Could you comment on that?
Dr Thielmann
: We have included in this study just those patients who were brought to the cathlab, and my suggestion would be to randomize the patients starting in the cathlab. If both, cardiologist and the cardiac surgeon together reach an agreement that the findings of coronary repeat angiography is worthy to reintervene, then the patient should be randomized to either a catheter-based reintervention or a surgical-based reintervention.
Dr M. Zembala
(Zabrze, Poland): Very interesting study, but I don’t agree with your conclusion. First, more general information. Preoperative infarction should be from 8.5% to 2%, not to 20%, otherwise we are not really partners with cardiologists. Maybe I am wrong, but I think that your long-term outcome is very much influenced by the type of strategy of reintervention, and what is more important is reangio in acute stage. That is where you made selection, relatively easy patient, so eventually one graft closed you put on the medical and stable. Don’t expect that it will be but long-term. The more sick patient you put in group II, which certainly had hemodynamic deterioration. That is one. I think the conclusion, in my mind, is quite wrong, despite the fantastic paper.
But would you change your strategy in retrospective analysis from historical group, ’99, 2005, when we involve preoperative flow measurement and a more invasive strategy? It was a very good paper but maybe we are different on the conclusion.
Dr Thielmann
: First of all, unfortunately I can’t agree with you, since the incidence of perioperative myocardial infarction is a complex issue and no universally valid definition exists, but in my opinion it depends on the type of measurement and the definition of PMI. If you are using MRI, for example, you have a much higher incidence of perioperative myocardial infarction between 30% and 40% up to 70%. If you use CK/CK-MB levels and/or Q-waves you might be right, but if you are using more sensitive cardiac biomarkers like cardiac troponins, it becomes a question of your definition, and should be somewhere between 10% and 30%.
Coming to your second comment: I tried to clearly point out in my talk that group III were those patients who were treated conservatively just because of one graft failure. These graft failures in group III seemed to be not as important as, for example, in group I and II patients, where more than one graft was occluded.
Indeed, this group III had a lower risk and should not be compared with groups I and II, but I tried to present all three groups and not just groups I and II. But I think, and the data indicate that, that groups I and II are absolutely comparable in regards to their preoperative and intraoperative characteristics as well as their comparable number and type of graft failure with a comparable myocardial ‘area at risk’.
Dr H. Azar
(Norfolk, Virgina): I think it is important to know the timing of investigation and intervention to draw the conclusion that you have. Also it appears that your two-year mortality is somewhat higher than expected in this kind of study.
Dr Thielmann
: Yes, I think the timing to reintervene is a major issue. The problem is that it is not very easy to discriminate between a graft-related and a nongraft-related perioperative myocardial infarction, and we tried to be as fast as possible after the diagnosis of a perioperative myocardial infarction, but the cardiac biomarkers and the ECG isn’t very sensitive, and it can last 12–24 h to discriminate a graft-related PMI.
Dr A. Al-Aulaqi
(Abu Dhabi, United Arab Emirates): Regarding group I and group II, I don’t think they are similar. We know that group III is not similar. Groups I and II are biased by the time of intervention. For the PCI group it is 1.5 h but in the surgical group it is an average of 5.4 h, and that is a major determinant I think in the revascularization of an ischemic or an infarcted area.
Dr Thielmann
: You are right, but this is a retrospective study of our patients and it is how it is. As I already mentioned, I think that the groups are comparable. The different time periods between repeat angiography and PCI on the one hand, and angiography and redo surgery on the other hand are due to the different methods of reintervention.
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Acknowledgments
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The authors wish to express their appreciations to the cardiologists and the staff at the cardiac catheterization laboratory for performing all acute repeat angiographic studies. We also thank Mrs Kitzroh, Mrs Kruse, Mrs Krykant, and Mrs Tebus, for their assistance in organizing and administering the study.
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Footnotes
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Presented at the joint 19th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 13th Annual Meeting of the European Society of Thoracic Surgeons, Barcelona, Spain, September 25–28, 2005.
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References
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- Fellahi J-L, Gue X, Richomme X, Monnier E, Guillon L, Riou B. Short- and long-term prognostic value of postoperative cardiac troponin I concentration in patients undergoing coronary artery bypass grafting. Anesthesiology 2003;99:270-274.[CrossRef][Medline]
- Steuer J, Horte LG, Lindahl B, Stahle E. Impact of perioperative myocardial injury on early and long-term outcome after coronary artery bypass grafting. Eur Heart J 2002;23:1219-1227.[Abstract/Free Full Text]
- Force T, Hibberd P, Weeks G, Kemper AJ, Bloomfeld P, Tow D, Josa M, Khuri S, Parisi AF. Perioperative myocardial infarction after coronary artery bypass surgery: clinical significance and approach to risk stratification. Circulation 1990;82:903-912.[Abstract/Free Full Text]
- Thielmann M, Massoudy P, Schmermund A, Neuhauser M, Marggraf G, Kamler K, Herold U, Aleksic I, Mann K, Haude M, Heusch G, Erbel R, Jakob H. Diagnostic discrimination between graft-related and non-graft-related perioperative myocardial infarction with cardiac troponin I after coronary artery bypass surgery. Eur Heart J 2005;26:2440-2447.[Abstract/Free Full Text]
- Thielmann M, Massoudy P, Marggraf G, Knipp S, Schmermund A, Piotrowski J, Erbel R, Jakob H. Role of troponin I, myoglobin, and creatine kinase for the detection of early graft failure following coronary artery bypass grafting. Eur J Cardiothorac Surg 2004;26:102-109.[Abstract/Free Full Text]
- Rasmussen C, Thiis JJ, Clemmensen P, Efsen F, Arendrup HC, Saunamäki K, Madsen JK, Pettersson G. Significance and management of early graft failure after coronary artery bypass grafting: feasibility and results of acute angiography and re-revascularization. Eur J Cardiothorac Surg 1997;12:847-852.[Abstract]
- Jain U. Myocardial infarction during coronary artery bypass surgery. J Cardiothorac Vasc Anesth 1992;6:612-623.[CrossRef][Medline]
- Franke U, Wahlers T, Cohnert TU, Koenig J, Rath NF, Wirsing M, Haverich A. Retrograde versus antegrade crystalloid cardioplegia in coronary surgery: value of troponin I measurement. Ann Thorac Surg 2001;71:249-253.[Abstract/Free Full Text]
- Onorati F, De Feo M, Mastroroberto P, Cristodoro L, Pezzo F, Renzulli A, Cotrufo M. Determinants and prognosis of myocardial damage after coronary artery bypass grafting. Ann Thorac Surg 2005;79:837-845.[Abstract/Free Full Text]
- Thielmann M, Dorge H, Martin C, Belosjorow S, Schwanke U, van de Sand A, Konietzka I, Buchert A, Kruger A, Schulz R, Heusch G. Myocardial dysfunction with coronary microembolization: signal transduction through a sequence of nitric oxide, tumor necrosis factor-alpha, and sphingosine. Circ Res 2002;19:807-813.
- Haude M, Baumgart D, Verna E, Piek JJ, Vrints C, Probst P, Erbel R. Intracoronary Doppler- and quantitative coronary angiography-derived predictors of major adverse cardiac events after stent implantation. Circulation 2001;103:1212-1217.[Abstract/Free Full Text]
- Holmvang L, Jurlander B, Rasmussen C, Thiis JJ, Grande P, Clemmensen P. Use of biochemical markers of infarction for diagnosing perioperative myocardial infarction and early graft occlusion after coronary artery bypass surgery. Chest 2002;121:103-111.[Abstract/Free Full Text]
- Fitzgibbon GM, Kafka HP, Leach AJ, Keon WJ, Hooper GD, Burton JR. Coronary bypass graft fate and patient outcome: angiographic follow-up of 5,065 grafts related to survival and reoperation in 1,388 patients during 25 years. J Am Coll Cardiol 1996;28:616-626.[Abstract]
- Bourassa MG, Fisher LD, Campeau L, Gillespie MJ, McConney M, Lesperance J. Long-term fate of bypass grafts: the coronary artery surgery study (CASS) and Montreal Heart Institute experiences. Circulation 1985;72:V71-V78.
- Massoudy P, Kim YY, Cetin M, Thielmann M, Herold U, Kamler M, Jakob H. Internal thoracic artery malperfusion: fast decision for an additional vein graft has impact on patient outcome. Ann Thorac Surg 2004;77:2061-2065.[Abstract/Free Full Text]
- Vajtai P, Ravichandran PS, Fessler CL, Floten HS, Ahmad A, Gately HL, Swanson JS, Starr A. Inadequate internal mammary artery graft as a cause of postoperative ischemia: incidence, diagnosis and management. Eur J Cardiothorac Surg 1992;6:603-608.[Abstract]
- Fabricius AM, Gerber W, Hanke M, Garbade J, Autschbach R, Mohr FW. Early angiographic control of perioperative ischemia after coronary artery bypass grafting. Eur J Cardiothorac Surg 2001;19:853-858.[Abstract/Free Full Text]
- Breuer M, Schutz A, Gansera B, Eichinger W, Weingartner J, Kemkes B. Intraoperative local fibrinolysis as emergency therapy after early coronary artery bypass thrombosis. Eur J Cardiothorac Surg 1999;15:266-270.[Abstract/Free Full Text]
- Mohl W, Simon P, Neumann F, Moidl R, Chevtchik O, Zweytick B, Kupilik N, Wolner E. Analysis of left ventricular function after emergency coronary artery bypass grafting for life-threatening ischaemia following primary revascularisation. Eur J Cardiothorac Surg 1998;13:27-35.[Abstract/Free Full Text]
- Schömig A, Mehilli J, Antoniucci D, Ndrepepa G, Markwardt C, Di Pede F, Nekolla SG, Schlotterbeck K, Schuhlen H, Pache J, Seyfarth M, Martinoff S, Benzer W, Schmitt C, Dirschinger J, Schwaiger M, Kastrati A. Beyond AlternatiVe Evaluation (BRAVE-2) Trial Investigators. Mechanical reperfusion in patients with acute myocardial infarction presenting more than 12 hours from symptom onset: a randomized controlled trial. J Am Med Assoc 2005;293:2930-2932.[Free Full Text]
- Pfisterer ME, Buser P, Osswald S, Weiss P, Bremerich J, Burkhart F. Time dependence of left ventricular recovery after delayed recanalization of an occluded infarct-related coronary artery: findings of a pilot study. J Am Coll Cardiol 1998;32:97-102.[Abstract/Free Full Text]
- Kim CB, Braunwald E. Potential benefits of late reperfusion of infarcted myocardium: the open artery hypothesis. Circulation 1993;88:2426-2436.[Free Full Text]
- Piana RN, Adams MR, Orford JL, Popma JJ, Adams DH, Goldhaber SZ. Rescue percutaneous coronary intervention immediately following coronary artery bypass grafting. Chest 2001;120:1417-1420.[Abstract/Free Full Text]
- Dauerman HL, Cutlip DE, Sellke FW. Intracoronary thrombolysis in the treatment of graft closure immediately after CABG. Ann Thorac Surg 1996;62:280-283.[Abstract/Free Full Text]
- Kahn JK, Rutherford BDMDR, Giorgi LV, Johnson WL, Shimshak TM, Hartzler GO. Early postoperative balloon coronary angioplasty for failed coronary artery bypass grafting. Am J Cardiol 1990;66:943-946.[CrossRef][Medline]
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Abstract
1. Introduction
