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Ann Thorac Surg 2001;71:1198-1204
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Optimal timing of revascularization: transmural versus nontransmural acute myocardial infarction

^a Department of Surgery, Columbia University College of Physicians and Surgeons, New York, New York, USA

Address reprint requests to Dr Lee, c/o Dr Ting, 630 W 168th St, P&S 17-401, New York, NY 10032
e-mail: dcl64{at}columbia.edu
e-mail: wt60{at}columbia.edu

Presented at the Thirty-sixth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 31–Feb 2, 2000.

	Abstract

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Background. Higher mortality for emergency coronary artery bypass grafting (CABG) after an acute myocardial infarction (AMI) is well established. Whether it applies to both transmural and nontransmural AMI is unclear. This information may have different therapeutic implications for each cohort of patients.

Methods. A retrospective multicenter analysis of 44,365 patients who underwent CABG after myocardial infarction between 1993 and 1996 by 179 surgeons at 32 hospitals in New York State was performed.

Results. Overall hospital mortality for all patients with or without AMI was 2.5% versus 3.1% for patients who underwent CABG with history of myocardial infarction. Hospital mortality decreased with increasing time interval between CABG and AMI; 11.8%, 9.5%, and 2.8% (p < 0.001 for all values) for less than 6 hours, 6 hours to 1 day, and greater than 1 day, respectively. Patients with transmural and nontransmural AMI had identical mortality of 3.1%. However, different patterns emerged when comparing these two groups of patients with respect to time of operation. Mortality was higher in the transmural group if CABG was performed within 7 days after AMI. Multivariate analysis confirmed that CABG within 1 day and 6 hours of AMI are independent risk factors for mortality in the transmural and nontransmural groups, respectively.

Conclusions. Early operation after transmural AMI has a significantly higher risk, and surgeons should be prepared to provide aggressive cardiac support including left ventricular assist devices in this ailing population. Waiting in some may be warranted.

	Introduction

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More than 1 million individuals will have an acute myocardial infarction (AMI) annually with a mortality exceeding 30% in the United States [1]. Immediate surgical intervention among those with acute mitral regurgitation from the rupture of a papillary muscle or a ventricular septal defect are well established. However, the ideal timing of coronary artery bypass grafting (CABG) after an AMI remains controversial. Emergent CABG after an AMI is clearly associated with a higher perioperative mortality, which ranges from 4% to 32% [2–4]. Some studies have found early CABG to be an acceptable therapy [5–7], whereas others have recommended a waiting period [8–10]. Numerous interventions have also been suggested to improve the surgical outcome. Some of these recommendations have included better selection of patients [8, 11, 12], timing of the operation [5–10], and preoperative support with intraaortic balloon counterpulsation [10, 13]. However, whether patients with transmural and nontransmural AMI have different outcomes and should be treated differently remained unclear. The objective of this study is to compare the mortality and timing of CABG between these two cohorts of patients. The conclusions from this study may have important therapeutic implications.

	Material and methods

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Patients
The data for this report are obtained from the Bureau of Health Care Research and Information Services, New York State Department of Health. The New York State Cardiac Surgery Registry is a mandatory outcome reporting system that registers every patient undergoing a cardiac operation, including CABG, within the state. The data of 44,365 patients who underwent CABG as the sole procedure from 1993 to 1996 were identified and selected for analysis. These operations were performed by 179 surgeons at 32 hospitals in New York State. Mean age of patients was 65.2 ± 10.4 years (range, 22 to 95 years). There were 32,266 men (72.7%) and 12,099 women (27.3%). The mean left ventricular ejection fraction was 42.9% ± 14.6%. Mean number of vessels bypassed in each patient was 3.1 ± 0.9, with a mean aortic cross-clamp time of 58.2 ± 29.5 minutes and a mean cardiopulmonary bypass time of 97.3 ± 40.8 minutes. There were 3,545 (8%) cases that were redo CABG.

Statistical analysis
Data were analyzed with the SAS statistical analysis software (SAS Inc, Cary, NC). Mean values are expressed as the mean ± standard deviation unless otherwise specified. Data were first examined univariately by the Student’s t test for continuous variables and Fisher’s exact test for discrete data. Other categorical analysis included the ² test for trend and Mantel-Haenszel statistics. For the multivariable analysis, variables with a p value of less than 0.25 were entered into a logistic regression analysis model. The risk factor allowed into the final model with a p value of less than 0.05 is interpreted as an independent risk factor associated with in-hospital mortality over and above other potential risk factors included in the equation.

	Results

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Overall hospital mortality (not 30-day mortality) for all patients was 2.5% versus 3.1% and 1.6% (p < 0.001) for patients undergoing CABG with and without a history of myocardial infarction (recent or remote), respectively (Table 1).

	Comment

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Analysis of the New York State database showed a significant correlation between hospital mortality and time interval from AMI to time of operation, particularly if CABG was performed within one week of AMI. These results confirmed findings of many previous studies [2–4], although others reported conflicting data [10, 18, 19]. Hospital mortality returned to baseline range when the operation was performed 7 days after AMI.

Although overall mortality is identical between patients with transmural and nontransmural AMI (Table 3), these two groups have different trends in mortality when the time course is taken into consideration. Mortality for the nontransmural group peaked if the operation was performed within 6 hours of AMI, then decreased precipitously. On the other hand, mortality for the transmural group remained high during the first 24 hours after AMI before trending downward (Table 4). Correlation between time of operation and mortality in the transmural group is more striking as a result of these different patterns. Multivariate analysis of risk factors (Table 7) revealed timing of CABG as an independent risk that paralleled the mortality pattern in Table 4. Other studies have also indicated transmural AMI as a risk factor in early revascularization [5, 6, 20, 21]. No study to date, however, has shown the doubling of perioperative hospital mortality during the 6- to 23-hour interval after transmural AMI in comparison to the nontransmural group with a large patient population as illustrated in this analysis. Many have reported emergency surgery [13, 21], shock [2], low ejection fraction [2, 12], congestive heart failure [20, 21], and preoperative intraaortic balloon counterpulsation [20] as factors associated with mortality or predictors of perioperative mortality. However, these factors were also significantly more prevalent in the transmural AMI patient group (Table 7). One might argue that these factors were merely markers of transmural AMI as opposed to being independent risk factors.

Optimal timing of CABG in patients with AMI is a controversial subject. Early surgical intervention has the advantage of limiting infarct expansion and ventricular remodeling that may result in possible ventricular aneurysm and rupture [22]. However, there is the theoretical risk of reperfusion injury, which may lead to hemorrhagic infarction resulting in extension of infarct size, poor infarct healing, and scar development [23]. The data from this study cautions against early revascularization, particularly among patients with transmural AMI within 24 hours of onset. Some have advocated the use of mechanical support to stabilize and allow elective rather than emergent surgery [13]. To prophylactically use mechanical support instead of CABG to improve outcome, however, would require placement of such support in many unnecessary cases. If revascularization cannot be delayed, aggressive mechanical support such as left ventricular assist device must be available as mortality is most likely caused by pump failure. Furthermore, mechanical circulatory support has been shown to be efficacious as a bridge to ventricular recovery or transplantation for this patient cohort [24, 25]. A proposed scheme of patient management for those with AMI is summarized in Figure 1. It is based on the summary of results from this study and literature cited. Although emergent cases clearly cannot be delayed, nonemergent cases may benefit from delay of operation, particularly in patients with transmural AMI. Early operation after transmural AMI has a significantly higher risk, and surgeons should be prepared to provide aggressive cardiac support including left ventricular assist devices in this ailing population. Waiting in some cases may be warranted.

View larger version (28K): [in this window] [in a new window]   Fig 1. Proposed management algorithm for patients with acute myocardial infarction (MI). (CCU = coronary care unit; CABG = coronary artery bypass grafting.)

	Discussion

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Based on our understanding of the pathophysiology of acute myocardial infarction, revascularization strategies have evolved. We know that successful myocardial salvage drops rapidly with time, and irreversible damage is usually present within 4 to 6 hours. Doctor Lee and his colleagues have nicely presented a retrospective analysis from the New York State Cardiac Surgical Database. These data are reported, as he said, from 32 hospitals, representing the work of 179 surgeons from 1993 through 1996.

The New York State Database is a reservoir of extensive information for studies like Dr Lee’s, but is inherently plagued by the inability to know whether similar standards and protocols were followed for this difficult patient subgroup by all hospitals and surgeons. The patients operated on within the first 24 hours, or even within the first few days after infarction, were unlikely to fall into an aggressive primary surgical therapy group. Most likely these patients failed primary thrombolytic therapy, or percutaneous transluminal coronary angioplasty reperfusion, forcing the surgical option because of shock or postinfarction angina.

In 1983 Phillips and colleagues reported a low 1.3% operative mortality for primary surgical therapy within the first 24 hours of an acute myocardial infarction. But the mortality rate rose to 27% in patients who had uncontrolled reperfusion by thrombolytic therapy, or percutaneous transluminal coronary angioplasty, and then subsequently required emergency coronary artery bypass grafting. In fact, timing of operation was not an independent predictor of early outcome in a multivariate analysis. Advanced age, poor left ventricular function, anterior wall myocardial infarction, prior coronary artery bypass grafting, and shock were the significant predictors for death.

Surgical attempts to restore blood flow by performing primary coronary artery bypass grafting within 24 hours of an acute myocardial infarction achieved impressive results by the Spokane, WA, experience of 700 patients followed for a decade and reported by DeWood in 1983. They documented a lower hospital mortality for patients operated on within the first 6 hours of 3.8% versus those after 6 hours at 8%. They addressed nontransmural myocardial infarction and reported a hospital mortality of 3.1% versus 5.2% for transmural myocardial infarction. Most of the mortality was in patients with cardiogenic shock, and the surgical group enjoyed excellent late, event-free survival.

The slide illustrates a literature review published in 1984 of 1,098 patients operated on at 18 medical centers, confirming the low operative mortality with death rates of less than 5%, and most of the deaths occurred in patients with cardiogenic shock and significant time delays.

In spite of these compelling results, the adoption of an aggressive surgical approach for acute myocardial infarction has been restricted by limited surgical availability, logistical issues promoting procedural delay, and expense. Therefore, surgical therapy has been relegated to a secondary treatment option. Thrombolytic therapy and percutaneous transluminal coronary angioplasty have become the preferred initial strategies to achieve reperfusion except in emergency cases caused by the mechanical complications of myocardial infarction, the acute complications of percutaneous transluminal coronary angioplasty, and left main anatomy.

My final point is to emphasize that percutaneous transluminal coronary angioplasty and thrombolytic therapy can achieve but not control reperfusion. Surgically we can control reperfusion with warm substrate-enhanced blood cardioplegia given before releasing the cross-clamp, reducing reperfusion injury, and limiting infarct size. Substrate-enhanced blood cardioplegia as a warm induction followed by antegrade and retrograde cold blood cardioplegia provides maximal myocardial protection. Embracing these techniques has led to excellent clinical results suggesting that the surgical therapeutic option could be, and maybe should be, primary and not secondary. However, when surgeons play a secondary role, Dr Lee’s data suggest a delay in operation if possible for one week.

I have four questions for the authors: 1. How many patients, especially in the high-risk subgroups, had attempted thrombolytic or percutaneous transluminal coronary angioplasty interventions before operation?

2. Based on the New York State Database risk adjustment model, what is the odds ratio for preoperative cardiogenic shock and for surgery after acute myocardial infarction, especially within the first 6 hours?

3. Why did you not attempt to perform a multivariate analysis of all the preoperative risk factors available from the New York State Database, along with the time from infarct to operation and transmural versus nontransmural myocardial infarction, to determine which variables were the independent predictors of outcome?

4. Finally, did the patients who were operated on receive the myocardial protection protocol and controlled reperfusion techniques that I have described?

I want to compliment the authors on a fine study and a superb presentation. I thank The Society of Thoracic Surgeons for inviting me to discuss this paper. And thank you for your attention.

DR LEE: I would like to thank Dr Shemin for his insightful comments and questions.

Admittedly, a large multicenter database such as the New York State Cardiac Surgery Database is plagued by the problems suggested by Dr Shemin. However, a single center database also has its flaws. A more complete picture can be constructed, nevertheless, when these two types of databases are used to complement one another.

The data from the 1984 literature review cited earlier certainly supported Dr Shemin’s comments on our work. However, we must point out that the patient populations from those studies are significantly different when compared with the more contemporary patient population in our study. For example, only a minority of the patients in the Spokane data had three-vessel disease, whereas the mean number of vessels bypassed is greater than three in the patient population of this study. The improved capability of cardiologists to intervene has resulted in a more ailing surgical patient population in comparison with the 1970s and early 1980s. Furthermore, it is difficult for most of the medical institutions to follow the aggressive protocol proposed by the Spokane group given the logistical issues that Dr Shemin has pointed out.

In response to the specific questions raised, 5.1% of the patients had thrombolytic therapy and 2.4% of the patients had percutaneous transluminal coronary angioplasty before operation. Among patients received percutaneous transluminal coronary angioplasty, half had transmural myocardial infarction. The odds ratio for preoperative cardiogenic shock is approximately 10 and for operation after acute myocardial infarction in less than a day is approximately 3.

We did perform a multivariate analysis, which revealed timing of operation along with markers of end-organ perfusion such as shock and renal failure to be independent risk factors for hospital mortality. Inasmuch as these findings were comparable to many previously published results, we elected not to report them again in our presentation.

The myocardial protection protocol used by each surgeon may not be uniform. However, we would suspect that most of the medical institutions in the State of New York would mandate the use of the optimal myocardial protection technique as described by Dr Shemin.

The aim of this study is to emphasize the high mortality associated with early operation in this ailing population rather than focusing on the timing of operation in and of itself as a risk factor. If we must operate early, we must have mechanical circulatory support ready and be very aggressive with this group of high-risk patients.

DR JACK J. CURTIS (Columbia, MO): I congratulate the authors on their analysis of this difficult group of patients. At the University of Missouri, a few years back, we had the opportunity to look at a thousand such patients undergoing coronary artery bypass grafting after myocardial infarction. We found the same thing that you did, that the relative risk within the 24 hours after myocardial infarction is 6 times greater than that after that point in time.

We found something though that we did not expect when we analyzed our group by their anginal syndrome. In other words, those who had unstable angina had a mortality rate of 7%, whereas those who had stable angina, regardless of the interval after myocardial infarction, had a mortality rate less than 1%. And by stepwise logistic regression analysis, the interval to myocardial infarction ceased to be a risk factor.

That leads me to ask you a couple of questions. First, we know patients do not die of angina or chest pain, they die of myocardial ischemia, but I wonder whether you analyzed your groups by mortality risk comparing stable anginal syndrome versus unstable?

Second, I worry a little bit about the diagnosis of transmural versus nontransmural infarction, because I have been tricked many times by posterior infarctions that really do not show up that well on the electrocardiogram and when you see the heart you clearly have a transmural infarction.

And finally, I am not surprised that your group, which does so well with assist devices, would have a strong, aggressive recommendation of their use in this patient population, but you really did not show us any data to support that recommendation.

DR LEE: Thank you, Dr Curtis.

Unfortunately, our database does not contain information pertaining to the question of stable versus unstable angina. However, patients who were rushed to operation after diagnosis of acute myocardial infarction almost have to have unstable angina by definition. This is a very interesting point, but we do not have the information to confirm your data.

The diagnosis of transmural infarction can be challenging. We would assume that each center adhered to the criteria set by the New York State Department of Health, which included Q wave and enzyme elevation. We hope that the reporting would reflect the true diagnosis if these criteria failed to do so. However, we are not able to independently verify each diagnosis.

Finally, our recommendation of the use of ventricular assist devices in this patient group is based on our own data published in the June 1999 issue of the Journal of the American College of Cardiology by Jonathan Chen, MD, and Mehmet Oz, MD. This paper is a retrospective single-center analysis, which revealed that implantation of left ventricular assist device early after myocardial infarction achieved feasible outcomes as a bridge to transplantation or recovery.

I would like to thank the Society again for the privilege to present this study and thank you for your attention.

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Mehmet C. Oz Windsor Ting Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lee, D. C. Articles by Ting, W. Search for Related Content PubMed Articles by Lee, D. C. Articles by Ting, W. Related Collections Coronary disease Myocardial infarction