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Ann Thorac Surg 2001;72:S2208-S2212
© 2001 The Society of Thoracic Surgeons
a Department of Surgery, VA Boston Healthcare System, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
* Address reprint requests to Dr Birjiniuk, Surgical Service (112), VA Boston Healthcare System, 1400 VFW Parkway, West Roxbury, MA 02132, USA
e-mail: vladimir.birjiniuk{at}med.va.gov
Presented at Monitoring and Improving Patient Safety During and Following Cardiac Surgery, San Diego, CA, May 5, 2001.
Abstract
In the absence of online methods for the intraoperative assessment of the adequacy of myocardial protection, patient outcomes remain the gold standard for determining whether a patient has sustained injury in the course of a cardiac operation. Properly risk-adjusted 30-day postoperative mortality and myocardial infarction are the most definitive indicators of perioperative injury. The definition and clinical assessment of irreversible ischemic myocardial injury continues to be problematic postoperatively. In most instances, deterioration in postoperative cardiac function and performance is indicative of intraoperative injury. Late postoperative mortality and long-term survival may be affected by intraoperative myocardial injury. Likewise, long-term graft patency may be affected by intraoperative injury to the conduit vascular endothelium. Proper assessment of outcomes, although it may not change the intraoperative course of an operation, can be useful in the comparative assessment of the efficacy of various operations, methods, and techniques.
There are several potential sources of injury to the heart during and after cardiac surgery, the most common of which is the interruption and subsequent restoration of coronary blood flow to the heart that occurs in the course of the vast majority of cardiac surgical operations, and that has the potential of causing myocardial ischemic and reperfusion injury [1]. Unfortunately, the clinical armamentarium of the cardiac surgeon today is devoid of a means by which this injury can be reliably monitored in real time. Hence, the clinical outcome of the patient, including the postoperative cardiac performance, remains the gold standard for determining whether a patient has sustained injury in the course of a cardiac operation. This communication reviews our current knowledge regarding the patient outcomes and postoperative functional indices that have been used in the assessment of myocardial injury that might be sustained in the course of cardiac surgery.
Postoperative mortality
Postoperative mortality remains the most definitive outcome that is reflective of patient injury in the perioperative period. To the surgeon, the medical tenant primum non nocere means that patients alive and functional before surgery should remain so and should continue to enjoy a good quality of life after surgery. Pursuing this endeavor, cardiac surgeons face significant challenges: We have to perform a technically adequate operation in parallel with protecting the heart from a variety of potentially injurious, factors including ischemia and reperfusion [1]. Hence, a patient’s failure to survive an operation that is electively undertaken can be an indication of inadequate perioperative protection from injury.
Postoperative mortality rates after cardiac surgery vary over a wide range, depending upon the type of procedure performed and the severity of illness of the patient [1]. Postoperative mortality is reported as either in-hospital or 30-day. The latter is a more accurate assessment, although more difficult to capture because of the cost-cutting push to discharge patients early after surgery.
The postoperative mortality rate has been used not only as an indicator of the degree of injury sustained by the patient perioperatively, but also as a comparative measure of the overall efficacy and quality of cardiac surgical care [2, 3]. In this context, as one compares the outcomes of specific patient populations to each other, it is imperative that the patients’ preoperative risk factors are accounted for. Since Parsonett and colleagues [4] first proposed a system for risk-adjustment of postoperative mortality after cardiac surgery; several such systems have been developed by various groups. These include the VA Continuous Improvement in Cardiac Surgery Program [3], the Society of Thoracic Surgery Database Committee [5], the State of New York Cardiac Surgery Program [2], the Northern New England Cardiovascular Group [6], the Cleveland Clinic [7], and the cardiac anesthesiology group [8]. These risk adjustment systems have been compared in several publications [9, 10]. Most of them use logistic regression analysis to identify, in multivariate models, the determinants of postoperative mortality in a specific patient population. The coefficients derived from these models are then used to calculate either a risk-adjusted mortality or an expected (E) mortality for that specific patient group. The expected mortality is then related to the observed (O) mortality rate, and the O/E ratio is calculated. A statistically significant high O/E ratio indicates a postoperative mortality that is higher than one would expect based on the severity of illness of the patient population. A low O/E ratio indicates a postoperative mortality that is lower than one would expect based on the severity of illness of the patient population, and it implies superior performance [11]. Nevertheless, most publications based on multicenter studies report unadjusted mortality rates that vary between the various studies. Some of the recent multicenter studies that report mortality rates for coronary artery surgery (Table 1) include the following: the Veterans Affairs Non–Q-Wave Infarction Strategies In-Hospital (VANQWISH) trial [12], in which patients with non–Q-wave infarction were randomized into revascularization versus medical therapy; the Platelet-Glycoprotein IIb–IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial [13], in which patients with acute coronary syndromes were treated with integrilin (IIb–IIIa inhibitor) or placebo within 72 hours of surgical revascularization; studies published by the Northern New England Cardiovascular Disease Study Group [14]; and the Angina With Extremely Serious Operative Mortality Evaluation (AWESOME) study [15], in which high risk patients were randomized into coronary artery bypass grafting or percutaneous coronary intervention.
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Myocardial infarction, or irreversible damage to the myocardial tissues, is the second most definitive outcome evidence of injury sustained in the course of cardiac surgery. In contrast to postoperative mortality (which is not difficult to define), there is a lack of consensus regarding the definition and quantification of myocardial infarction in the postoperative period [17]. Myocardial infarction sustained during this period has been defined in terms of three types of criteria: (1) electrocardiographic changes; (2) blood enzyme levels; and (3) new wall motion abnormalities evidenced by ventricular angiography or echocardiography.
A persistent new Q-wave on the electrocardiogram is generally accepted as singly indicative of, and the gold standard for, a definitive myocardial infarction. Although some authors have suggested that the development of a bundle branch block is also pathognomonic of postoperative myocardial infarction [18], non–Q-wave electrocardiographic signs of ischemia (such as ST segment elevation or depression, or bundle branch block) are not specific enough to provide definitive evidence of myocardial infarction. They often need to be combined with enzymatic or echocardiographic changes to provide such definitive evidence.
Blood enzymes that are indicative of myocardial damage include the following (with postinsult peak time given in parentheses): myoglobin (4 hours), total creatine kinase (CK) (16 hours), CK-MB isoenzyme (24 hours), troponin I and T (24 hours), and LDH (76 hours). CK-MB isoenzyme has been most widely used, but recent studies have suggested that troponin I is the most sensitive and specific in depicting myocardial ischemia [19]. Because of limited sensitivity and specificity, moderate elevations in enzymes alone do not provide a definitive evidence of myocardial infarction; they need to be accompanied by either ECG or echocardiographic changes to provide a definitive diagnosis of myocardial infarction.
The postoperative appearance of a new wall motion abnormality by angiography or echocardiography is highly suggestive, although not specific, of postoperative myocardial infarction [20]. Myocardial stunning, that is, postischemic transient ventricular dysfunction [21], is a common cause of postoperative new ventricular wall motion abnormalities. The appearance of a new ventricular wall motion abnormality in the postoperative period, whether due to irreversible myocardial infarction or to reversible myocardial stunning, is an indication of some form of inadequate myocardial protection during the intraoperative period.
Mangano and colleagues conducted several large clinical studies that showed that higher rates of adverse outcomes, such as myocardial infarction, might be encountered when attention is directed to both proper definition and collection of data [22]. For example, when Holter monitors were placed on cardiac patients postoperatively in the ICU, major ECG changes were observed in 58% of the patients, and myocardial infarction was diagnosed (based on ECG and enzyme criteria) in 25% of the patients [23].
Postoperative cardiac performance
Spontaneous defibrillation during reperfusion, before weaning from cardiopulmonary bypass, is thought to be a salutary indicator of adequate myocardial management, although there are no outcome studies that confirm its predictive validity in the assessment of the adequacy of myocardial protection. There are also no studies demonstrating that the need for repeated defibrillation or the need for high defibrillation voltage are indicative of poor intraoperative protection, although some surgeons assume them to be so [24]. New onset of ischemic ECG changes and ventricular arrhythmias during reperfusion are highly suggestive, but not definitive, of poor intraoperative myocardial protection.
Failure to wean from cardiopulmonary bypass, in the absence of systemic factors such as hyperkalemia and acidosis, is the earliest evidence of intraoperative myocardial injury or cardiac dysfunction. Adequate myocardial protection (particularly in the absence of preoperative ventricular dysfunction) as well as adequate surgical correction of cardiac abnormalities should allow normal weaning from cardiopulmonary bypass without the need for inotropic support. The need for significant inotropic support during weaning from cardiopulmonary bypass is an indication of poor cardiac performance. In the absence of technical problems, such as persistent valvular insufficiency or prosthetic valve dysfunction, the degree of inotropic support required to successfully wean the patient from cardiopulmonary bypass has been used as a measure of the adequacy of intraoperative myocardial protection [25, 26]. Unfortunately, there is no consensus on what pharmocologically constitutes "significant inotropic support." Cardiac surgery groups vary widely in their routine postoperative use of inotropic drugs. "Significant inotropic support" is thus dependent on local practice and is probably best defined as the degree of inotropic support exceeding that normally provided on a routine basis. For example, in certain centers, anesthesiologists routinely place every patient on a "renal dose" of dopamine (2 to 3 µg · kg-1 · min-1). During weaning from cardiopulmonary bypass at these centers, the need for 5 µg · kg-1 · min-1 or more of dopamine would thus be considered as constituting significant inotropic support, and would provide evidence of suboptimal intraoperative myocardial protection. The mere need for epinephrine during weaning from cardiopulmonary bypass has been considered by some to be indicative of significant inotropic support [26].
The need to insert an intraaortic balloon to facilitate weaning from cardiopulmonary bypass is a clear indication of compromised ventricular function. In most instances, it provides evidence of new myocardial injury (infarct or stunning) sustained in the course of the operation. The need for an intraaortic balloon during weaning from cardiopulmonary bypass may not indicate new myocardial injury. For example, in patients with severe mitral insufficiency and marked left ventricular dysfunction, valve replacement results in increased afterload. This would benefit from the prophylactic insertion of an intraaortic balloon during weaning from cardiopulmonary bypass. In this situation, a benefit would be realized by reducing the afterload of the left ventricle, and the insertion of an intraaortic balloon would not necessarily imply new damage to the myocardium.
A protracted state of low cardiac output, encountered in the postoperative course and the intensive care unit, is a frequent cause of operative mortality after cardiac surgery [25, 26]. Although there are no studies that have specifically related this condition to the adequacy of myocardial protection, the postoperative development of a low-output state that cannot be explained on the basis of a technical failure is a manifestation of poor intraoperative myocardial management.
In most cardiac operations, particularly those involving myocardial revascularization, an improvement in the left ventricular ejection fraction is expected postoperatively. This increase in ejection fraction may not be sustained beyond the first few weeks postoperatively, particularly in patients with relatively normal preoperative ejection fraction [27]. A postoperative decrease in the ejection fraction, particularly after coronary artery bypass graft procedures, is mostly indicative of suboptimal intraoperative myocardial management. An exception to this is those conditions that follow the repair of valvular insufficiency, where a decrease in the postoperative left ventricular ejection fraction is expected.
Clinical scores
Outcome scores have been devised to assess the efficacy of intraoperative myocardial management and protection from injury. Higgins and colleagues [25] proposed an ICU admission score that was both reflective of intraoperative management and predictive of risk of morbidity and mortality. Scores that combine weighted outcome variables can be useful at an institutional level. Their generalizability, however, is questionable, considering that the definition of some of the measurements contained in the score (such as the need for inotropic support) may vary widely between institutions. For example, a clinical myocardial preservation score was proposed by Khuri and associates [26] as part of the assessment of the predictive validity of myocardial tissue acidosis encountered in the course of cardiac surgery. The elements in the score were weighted in accordance with the author’s institutional practice and experience. They were validated by showing a direct relationship between the devised score and the duration of aortic clamping. Clinical scores can be useful in assessing the degree of injury sustained in the course of a cardiac operation; their applicability, however, should be institution-specific, and their validity needs to be demonstrated. Not surprisingly, the surgeon’s gut feeling can be a powerful predictor of postoperative outcome [28], and his or her subjective assessment of the adequacy of myocardial protection may be as accurate as any institutional-specific postoperative score.
Late postoperative outcomes
Are late postoperative outcomes and long-term survival reflective of the adequacy of intraoperative myocardial management? Recently appreciated determinants of long-term postoperative outcome, and evidence of intraoperative endothelial damage to implanted vascular conduits, suggest that the answer to this question is a definite "yes."
Two important variables are now known to be determinants of long-term outcome and survival after cardiac surgery: the degree of myocardial tissue acidosis during the period of aortic clamping, and the early postoperative left ventricular ejection fraction. In a study with an average follow-up of 10 years after complex cardiac surgery, Khuri and associates [29] observed a direct relationship between the lowest mean myocardial pH recorded both during and after the period of aortic clamping, and long-term patient survival. Patients who experienced acidosis (pH <6.5) had decreased survival compared with those who did not. Because myocardial acidosis has been shown to be reflective of both myocardial ischemia [30] and poor myocardial protection [31], the study by Khuri and associates relates, for the first time, the adequacy of intraoperative myocardial protection to long-term outcome, and indicates that prevention of intraoperative acidosis should improve long-term survival after cardiac surgery.
Systolic left ventricular function, assessed by the left ventricular ejection fraction, is an important determinant of long-term survival in patients with coronary artery disease [27, 32]. In patients undergoing coronary artery bypass grafting, a postoperative decrease in left ventricular ejection fraction compared with preoperative base line adversely affects long-term survival [32]. Because intraoperative myocardial injury can result in a postoperative decrease in ejection fraction, intraoperative myocardial protection can be assumed to be an important determinant of long-term survival after cardiac surgery.
Long-term graft patency has been related to size of recipient vessels and to the graft flow rate, and could be an indication of technical inadequacy of the anastomosis leading to reduced flow. It could also be due to failure to preserve the endothelium, as apparent in the work by Thatte [33].
Conclusion
Except for properly risk-adjusted postoperative mortality, outcome measures vary in their ability to reflect reliably the magnitude of ischemic and irreversible injury sustained in the course of cardiac surgery. Myocardial infarction and death remain the most definitive in assessing injury to the heart, although a single indicator of myocardial infarction has been elusive. Late postoperative outcome and survival may also be reflective of intraoperative events. Outcome, however, is an after-the-fact indication of perioperative injury. It may serve a purpose in assessing the comparative efficacy of various techniques in preventing myocardial damage, but it does not provide information that is useful in preventing the injury in real time.
References
This article has been cited by other articles:
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  I. S. Ali and K. J. Buth Preoperative statin use and in-hospital outcomes following heart surgery in patients with unstable angina Eur. J. Cardiothorac. Surg., June 1, 2005; 27(6): 1051 - 1056. [Abstract] [Full Text] [PDF]
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 R. M. Mentzer Jr, R. D. Lasley, A. Jessel, and M. Karmazyn Intracellular sodium hydrogen exchange inhibition and clinical myocardial protection Ann. Thorac. Surg., February 1, 2003; 75(2): S700 - 708. [Abstract] [Full Text] [PDF]
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