Troponin Is for Diagnosis, Not Screening

To the Editor In the recent Special Article “Perioperative Troponin Screening,”1 Sessler and Devereaux opine that “troponin screening seems appropriate for most surgical inpatients 45 years or older.” They also suggest that high-sensitive troponin T concentrations 0.03 ng/mL or greater should prompt a medical or cardiology consultation. Our reading of the current literature suggests that the likely result of screening every postoperative inpatient >45 years of age for high-sensitive troponins would be overtreatment of patients. The 2012 guidelines2 from the American College of Cardiology state that in cases of elevated troponin in patients with few or no risk factors, acute coronary syndrome is unlikely. Moreover, improvements in outcomes after non-ST–segment elevation myocardial infarction have occurred mostly in patients at moderate-to-high risk, not those without risk factors, and mostly from interventions rather than drug therapy.3 Over the past few years, our understanding of perioperative myocardial infarction has evolved from a type I (plaque rupture and thrombosis of coronary artery) to type II (demand ischemia). Now we know that any minor injury or stress to the myocardium may result in release of troponin4,5 and that low-level postoperative troponin elevations are associated statistically with an increased incidence of noncardiac complications. High-level elevations are associated statistically with an increased incidence of cardiac complications.6,7 We also recognize that intensification of therapy with angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, statins, β-blockers, nitrates, and/or aspirin reduced complications in high-risk vascular surgery patients with postoperative troponin elevation in an observational study, not a prospective one.8 Until we have stronger confirmatory evidence, would it not make more sense to limit screening to patients with risk factors for coronary disease undergoing operations that associate with increased risk of major adverse cardiac events? We also wonder whether screening troponin in the preoperative period would offer the greatest potential to improve outcomes. As has been shown by Maile et al,9 increased preoperative troponin concentrations are associated with increased morbidity and mortality in high-risk patients; thus, preoperative screening may be reasonable selectively in high-risk patients per the guidelines from the American College of Cardiology. Finally, no discussion of screening can ignore costs. Can we justify the added expense of screening to those who will pay for the testing? Drs. Sessler and Devereaux regret that too many anesthesiologists consider their work done when patients arrive safely in postanesthesia care unit. We agree; however, we find their recommendations for a “medical or cardiology consultation” equally unacceptable from those who regard themselves as “perioperative physicians.” What would we ask the internist or cardiologist to do? Even if we assume that every elevation of troponin T diagnoses a “non ST segment elevation acute coronary syndrome,” the standard initial treatment of this condition includes dual antiplatelet therapy and anticoagulation. Such treatment in an immediate postsurgical patient would usually not be feasible.10 In a postoperative patient with no symptoms or evidence on electrocardiogram, would we not maintain our goal-directed treatment plan whether or not there was troponin-leak? “Medical overtreatment” commonly has been criticized in the news media.11 To maximize patient safety and maintain the integrity of our profession, we should base our decisions on evidence and clinical practice guidelines when they are applicable. We would not favor routinely measuring troponin T in all patients who are 45 years or older who are recovering from surgery. The available evidence and published guidelines do not support this practice. We would emphasize that it is time that we sorted out the ambiguity regarding perioperative myocardial infarction versus myocardial injury, and we need to redefine type II myocardial infarction as has been suggested by Nagele.12 Nirvik Pal, MBBSJohn Butterworth, MDDepartment of AnesthesiologyVirginia Commonwealth University Richmond, Virginia[email protected][email protected]