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Ann Thorac Surg 2001;72:S2212-S2213
© 2001 The Society of Thoracic Surgeons
a c/o Ms Diane Beatty, Ischemia Research and Education Foundation, 250 Executive Park Blvd, Suite 3400, San Franciso, CA 94134, USA
In the outline of the manuscript that I reviewed, there is an attempt to define outcomes as useful and consistent means with which uniform comparisons can be made across groups, databases, trials, and so forth. Specifically, the question of how to measure myocardial infarction was raised, and this obviously is a very complex question. We all struggle with it, inasmuch as we struggle with single-cell death versus patient death and the wide spectrum of changes that we see in between. I believe that in most practices, myocardial infarction is measured electrocardiographically, and I believe that we all have trepidation with respect to using enzymatic measures because we really do not know the exact thresholds that define myocardial infarction. What we lack, though, is consensus regarding how to measure injury; and this symposium, and the panel discussion that follows, is a step toward reaching such a consensus. As is evident from this symposium, there are many types of injury after bypass operations. There is the broad spectrum of degree of plaque stability with which patients present, and the potential for intraoperative ischemic and reperfusion injury, embolization, spasm, thrombosis, and death. Even for a common type of injury such as myocardial infarction, we all use a variety of definitions in our practices and specialties, lacking a consensus even among providers within a specialty.
The definition of myocardial infarction that we are most comfortable with is Q wave infarction on the electrocardiogram (ECG). It is our gold standard. Pathologically, it presents with a through-and-through infarction of the ventricular wall, as evident on this slide. When looked for meticulously, Q wave infarction is observed at rates ranging from 5% to 8%, and is accompanied by a higher incidence of mortality and a longer hospital stay than is non–Q wave infarction. However, some ECGs may be noninterpretable, and there is a certain false-positive rate. There is also some evidence that Q wave underestimates true infarction. We analyzed the perioperative deaths in a group of 4,000 patients who underwent bypass surgery. Twenty percent of the patients who died had Q waves before their cardiac deaths. Forty percent had significantly high enzymes (CK-MBs >125 or troponins >4 ng/mL. Another group of patients who died had no Q waves and only moderate enzyme release.
Non–Q wave infarctions occur at least as frequently as Q waves. How do we measure them, and what cutoffs do we use? What is the appropriate enzyme level and, in fact, what is the appropriate enzyme? One could make an argument for troponin because its normal circulating levels are low; it is at least as sensitive as CK-MB, with better specificity; and the elevations are persistent, allowing for more accuracy when single measurements are made postoperatively. Well, let us suppose that we accept troponin; can we come up with thresholds defining non–Q wave myocardial infarction? We attempted to identify such thresholds in studies based on about 4,000 patients in whom troponins were measured preoperative and three times postoperatively, and in whom CK-MBs were measured preoperatively and 10 times postoperatively. New Q waves were associated with a troponin level of 2.7 ng/mL, whereas serious events were associated with a troponin level of 3 ng/mL. A receiver operating characteristic curve constructed with this large data set revealed yet a different troponin threshold, indicating that there are a number of ways of correlating troponin levels with postoperative clinical events, and underscoring the difficulty of achieving consensus on a single, clinically relevant threshold level of a cardiac enzyme, even when one uses large population studies. When we compared, in these studies, patients with Q-wave myocardial infarction (MI) to patients with non–Q wave MI and troponin levels 
4 ng/mL, we observed a similar mortality rate and postoperative length of stay in both groups, as well as a higher incidence in the non–Q wave MI group of adverse postoperative events that we considered clinically important, including use of the intraaortic balloon. Hence we are now comfortable with defining postoperative myocardial infarction in terms of new-onset Q wave on the ECG or the combination of non–Q wave ECG changes indicative of MI and elevated cardiac enzymes, although we are still uncertain about the enzyme thresholds necessary for this definition. As was emphasized in the paper under discussion, this latter uncertainty contributes to the wide variation in the definition of nonfatal myocardial infarction among various clinical trials, registries, and databases, and has important implications in terms of how we evaluate drugs, quality of surgery, and so forth. We still need to sit down and try to get a better understanding of the clinical events that occur postoperatively in a hospital, and their associations with various enzyme levels. More importantly, we need to relate these specific enzyme levels to morbidity, survival, quality of life, and costs 6 months postoperatively and beyond, particularly as the incidence of adverse outcomes in these patients in the months after surgery may be very high.
So we do not have answers yet, but we have a lot of data from which we should seek to gain consensus and to achieve unifor-mity in definitions. A common understanding is imperative for our ability to adequately compare drugs, procedures, or anything else, including quality of cardiac surgical care.
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