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Division of Anesthesiology and Critical Care Medicine, The University of Texas M. D. Anderson Cancer Center, Houston, TX
To the Editor:
The study by Scott et al. (1) demonstrates that thoracic epidural analgesia (TEA) has beneficial effects on numerous organ systems in the setting of coronary artery bypass (CABG) surgery. However, despite these beneficial effects, which include a reduction in the incidence of supraventricular tachyarrhythmias, this study failed to demonstrate a reduction in the incidence of myocardial infarction (MI). Rather than a weakness of the epidural technique, we suggest that this observation reflects a more widespread failure to appreciate the true incidence of post-CABG MI.
Post-CABG MI has an often-quoted incidence of 
4% and corresponds with the incidence found by Scott et al. (1). We argue that this incidence reflects patients with clinically significant Q-wave (transmural) MI only and contend that ischemic myocardial injury is better considered a spectrum ranging from reversible ischemia through to irreversible infarction, which may be minor (suben-docardial/non-Q-wave) or major (transmural/Q-wave) in extent. Currently available diagnostic methods (such as technetium pyrophosphate scanning and cardiac-specific troponin isozyme levels) have higher sensitivity for detecting minor ischemic injuries and as a result have greatly improved our ability to diagnose perioperative MI. This has lead to some studies suggesting that the incidence of minor MI after routine CABG may be as high as 30% (3). The study of Scott et al. (1) may therefore have been adequately powered to demonstrate improved (or lack of) myocardial protection by TEA, as suggested by at least one other smaller study that showed a reduction in troponin levels by TEA (4). We would be interested to hear if these authors measured troponin levels in their patients.
Of greater importance is the observation that minor elevations in cardiac enzyme levels are predictive of poor long-term prognosis (myocardial infarction and death) after otherwise successful coronary interventions e.g., angioplasty/stenting (5–7). This suggests that even minor ischemic injury may be associated with poor long-term outcome. It is therefore probable that minor ischemic injury after CABG may also predispose to adverse long-term outcome. Potential mechanisms might include subendocardial injury, myocyte hypertrophy, and fibroblast proliferation with impaired systolic and diastolic (endocardial) reserve, and a humoral autoimmune response against intracellular proteins released during ischemic injury.
Despite showing significant reductions in the incidence of supraventricular arrhythmia, pulmonary infection, and renal dysfunction, the authors of the accompanying editorial state that Scott et al. (1) "fall short of demonstrating a dramatic change in postoperative outcome after CABG" (2). This view demonstrates our current tolerance of common adverse events and intolerance of potential rare adverse events e.g., epidural hematoma. We suggest that reduced postoperative morbidity is an important finding in its own right, but we agree that if this technique is to become more widespread it is important to demonstrate improved long-term outcome with TEA. In peripheral vascular surgery the use of regional anesthesia has been shown to reduce graft occlusion rates (8). We therefore encourage an appropriately powered, prospective, multicenter outcome study with clinically relevant early and late end points (e.g., improved graft patency rate, reduced perioperative MI, subsequent cardiovascular events, and death) to decide whether TEA in CABG surgery is ready for prime time or will remain forbidden territory.
References
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