Why, then, are such patients almost automatically screened? Recent editorials [1-4] strongly recommend that patients with moderate risk (defined as the presence of one or two risk factors, such as age more than 70 years or diabetes, even in the absence of angina) have preoperative noninvasive testing. This has created a scenario wherein "defensive medicine" is practiced; in my experience, any desire to avoid testing meets with resistance from the cardiologist, the anesthesiologist, and the surgeon. In addition, preoperative noninvasive or invasive testing often reflects a lack of focus on the immediate question: "Can this patient reasonably have noncardiac surgery?" Instead, the consultant's preoperative opinion often concerns a different issue [3]: "Would coronary revascularization improve the long-term prognosis from a cardiac standpoint and protect the patient from adverse events during the necessary noncardiac surgery?" By modifying the question to include the definition of prognosis based on the presence and extent of coronary disease, the primary question—is the patient cleared for surgery?—becomes secondary.

The fallacy in this approach is twofold. First, it is assumed that this patient, who would otherwise have continued to receive medical therapy, now requires invasive management because of the need for major noncardiac surgery. This is assumed despite general agreement that data supporting the use of prophylactic coronary revascularization before noncardiac surgery are lacking [1-4] and that controlled trials on this question are needed [6, 7]. Second, although plaque rupture and thrombus formation are generally the mechanisms leading to myocardial infarction, the pathophysiology of infarction after noncardiac surgery may differ [8]. An alternative hypothesis is that although plaque rupture may be the final common pathway, postoperative ischemic events are preventable rather than random. If so, what question should the clinician consider? It should not be, Who among the population with or at risk for coronary artery disease needs further evaluation before noncardiac surgery? Rather, it should be, Why do patients experience adverse events and how might these events be prevented?

Overview of Studies Defining Postoperative Risk for Cardiac Events

Early studies of patients who are known to have had myocardial infarction on the basis of a history of infarction or an electrocardiogram [9] or who have a confirmed history [10] reported a postoperative rate of myocardial infarction of about 7%, with more than 50% of these patients dying as a result of the infarction. These investigators found that the risk was particularly high if the previous infarction had occurred within 6 months of the noncardiac surgery, if the patient was older than 65 years of age, and if surgery had involved the thorax or upper abdomen.

Goldman and colleagues [11] prospectively studied 1001 patients having various noncardiac operations to identify factors predicting increased risk. In addition to confirming that age (in their series, more than 70 years) and the occurrence of a myocardial infarction within 6 months were highly significant predictors of adverse postoperative events, Goldman and colleagues found that clinical evidence of heart failure and arrhythmias was a powerful predictor of adverse cardiac events. They developed a point system to help identify patients with a high likelihood of dying of a cardiac event or having a life-threatening complication. Detsky and coworkers [12] validated both these criteria and a modified version, which included the severity of angina pectoris. However, many events occurred in patients with low risk scores, and the proposed indices had limited discriminant value in many patients referred for vascular or other major surgery [13, 14].

Eagle and colleagues [13] retrospectively recorded the clinical variables of 200 patients having vascular surgery who had had dipyridamole thallium studies before surgery. By using simply acquired clinical data (age more than 70 years, Q waves, history of angina, history of ventricular ectopic activity, and diabetes mellitus requiring therapy), they could define an intermediate-risk group that had one or two of these variables and a dipyridamole thallium test that had incremental value. The presence of a reversible myocardial perfusion defect was associated with a 30% (16 of 54) event rate compared with a 3% (2 of 62) rate in patients without such thallium abnormalities. On the basis of these data and an extensive review of the literature, Wong and Detsky [2] concluded that patients with intermediate risk, including those with one or two of the risk factors described by Eagle and colleagues [13], should have noninvasive testing.

Recent large studies have raised questions about these conclusions. Baron and colleagues [15] reported on 457 patients referred for abdominal aortic surgery. All patients were evaluated clinically; noninvasive tests included a dipyridamole thallium single-photon emission computed tomographic study done 1 to 10 days before surgery. Although studies are always difficult to compare, the similar classification and frequency of adverse events suggested that the populations studied were comparable. For example, Baron and colleagues [15] reported a cardiac mortality rate of 4.4% and a nonfatal myocardial infarction rate of 3.7%, whereas Eagle and colleagues [13] reported rates of 3% and 4.5%, respectively. Baron and colleagues also found that age greater than 65 years and definite coronary disease (defined as a history of myocardial infarction, typical angina, or ischemic ST-T segments on an electrocardiogram) were predictive of events. However, in contrast to Eagle and colleagues, Baron and colleagues [15] found that thallium defects did not add to the model, with an odds ratio of only 1.1.

The use of clinical factors to define an intermediate-risk group has also been recently reevaluated. Ashton and coworkers [14] classified 1487 men who were older than 40 years of age and were having major surgery into those with high, intermediate, low, and negligible risk for postoperative myocardial infarction [14]. Those considered to be at high risk had coronary artery disease (established on the basis of either a history or electrocardiographic evidence of infarction), typical angina, abnormal coronary arteriography, or previous aortocoronary bypass surgery. Patients with intermediate risk had no evident coronary artery disease but had other vascular disease, such as stroke or a condition for which vascular surgery was scheduled. Patients in the low-risk group had risk factors such as older age, history of smoking, or diabetes that gave them a likelihood of at least 15% that a cardiac event would occur within 6 years, on the basis of Framingham criteria. Patients with negligible risk had none of these factors. The high-risk group had a myocardial infarction rate of 4.1% and a cardiac-related mortality rate of 2.3%. In contrast, the intermediate-, low-, and negligible-risk groups all had postoperative adverse event rates of less than 1%. These results and those of a recent meta-analysis of earlier studies [5] emphasize the difficulty of identifying which patients are at risk for an adverse cardiac event. In essence, the low prevalence of events severely limits the ability to predict which patients require intervention before having noncardiac surgery.

Mechanisms of Postoperative Myocardial Infarction

The rationale for intensive screening is based on the assumption that revascularization prevents postoperative myocardial infarction in patients with coronary artery disease. A review of older studies and several more recent studies in which Holter monitoring was used supports the concept that unstable angina and myocardial infarction are preceded by electrocardiographic evidence of ischemia, which in turn is related to a persistent sinus tachycardia. These data suggest that excess oxygen demand, not simply a random abrupt loss of oxygen supply, is a key component of the mechanism causing ischemic events after surgery.

It has been known for some time that the incidence of perioperative myocardial infarction after noncardiac surgery peaks on postoperative days 2 and 3 [9, 10]. Recently, Mangano and coworkers [16] showed that postoperative tachycardia peaked on postoperative days 1 and 2 and occurred before maximum postoperative ST-segment depression on days 2 and 3. Postoperative ischemia occurred 1 or more days before all five severe adverse cardiac events. In a separate report [17], these same investigators used multivariable analysis to show that the only variable that could predict ischemic events was ST-segment depression indicated on Holter recordings done after surgery.

Other researchers have shown similar results. Raby and colleagues [18] reported that patients who had cardiac events, compared with those who did not, had higher peak heart rates after surgery (106 beats/min compared with 99 beats/min), more ischemic episodes (mean, 6 ischemic episodes compared with 3 ischemic episodes; P < 0.05), and a longer cumulative duration of ischemia (136 min compared with 53 min). Of the 16 events, 11 occurred 24 to 48 hours after surgery, including 6 of 9 cases of myocardial infarction. Other recent reports [19, 20] have similarly shown that ST-segment depression detected after surgery predicts cardiac events.

Although these data support the concept that excess oxygen demand causes postoperative cardiac events, they do not provide enough evidence to argue against plaque rupture as the final pathway. Conversely, the increased stress and catecholamine levels could make the patient with coronary artery disease more prone to plaque rupture. For this discussion, it is important that the primary mechanism be preventable if it is not spontaneous plaque rupture but rather hours or days of excess and easily remedied stress that has led to increased oxygen demand with or without plaque rupture. Better anesthetic techniques, hemodynamic monitoring, and pain control, all of which decrease oxygen demand, may be critical in managing patients with coronary artery disease during the perioperative period and avoiding cardiac complications [10, 21]. For example, Rao and coworkers [10] prospectively studied 733 patients who had had myocardial infarction and were having major noncardiac surgery; the patients were carefully monitored, often invasively, during surgery and for 24 to 96 hours after surgery. Rao and coworkers found a perioperative myocardial infarction rate of 1.9%, which was significantly less than the 7.7% rate found in a historical control group even though patients in the study group were older and were having similar types of surgery [10]. Indeed, if one considers that a submaximal stress test lasting 6 to 8 minutes can induce ST-segment changes and myocardial ischemia, one can readily understand that having the heart rate exceed 100 beats/minute for 2 hours can induce myocardial ischemia in patients with obstructive disease.

Who Needs Preoperative Testing and What Form Should It Take?

If postoperative stress is accepted as the etiologic mechanism responsible for postoperative cardiac events, the optimal strategy becomes clear. Patients can be considered to belong to one of two groups. One group is defined by the presence of a clinical syndrome consistent with plaque rupture or a severely limited coronary flow. Postoperative management directed toward limiting myocardial oxygen demand is unlikely to sufficiently protect against myocardial ischemia and infarction. This includes the management of patients with new or unstable angina, patients who recently had a myocardial infarction with or without postinfarction angina, and patients with disabling angina that occurs with minimal exertion, such as walking one or two blocks. Indeed, such patients generally have been excluded from studies and are managed aggressively, often with cardiac catheterization and revascularization [7, 15]. Such findings are not seen in the second group, which comprises patients whose functional capacity is sufficient to determine that the angina developing with exertion is stable. These patients have a low likelihood of myocardial infarction and do not require testing. Indeed, exercise testing to more accurately quantify exercise capacity has not proved to be predictive [22]. Rather, the focus should be on detecting and managing postoperative stress and pain (often heralded by a sinus tachycardia) before myocardial ischemia ensues.

Thus, when called on to "clear" a patient with known or possible coronary artery disease, the consultant should focus on the question that relates to performing noncardiac surgery, not managing coronary artery disease. If the patient has clinically stable angina or has only risk factors for coronary artery disease, noninvasive testing adds little but confusion because of the poor positive predictive value. Moreover, no studies have shown that prophylactic revascularization will decrease the event rate after noncardiac surgery, particularly if complications of revascularization are included. On the other hand, if the clinician thinks that the patient has a syndrome consistent with plaque rupture, such as unstable angina, that makes the patient extremely sensitive to any stress, the patient's cardiac status does warrant evaluation in and of itself. Noncardiac surgery should be deferred in favor of an aggressive cardiac assessment that often includes invasive testing, and a staged or combined procedure should be considered. Otherwise, the tests should be skipped and the patient cleared.