In recent decades, intraoperative mortality has decreased by a factor of 10, even though we now care for much sicker and older patients.1 Preventable anesthetic-related intraoperative mortality is now so rare that it is hard to quantify.2 In contrast, postoperative mortality remains substantial. Overall, 30-day postoperative mortality after noncardiac surgery is about 1% in the United States and about 2% among inpatients (outpatients die much less frequently).3,4 To put this mortality in perspective, if the postoperative period were considered a disease, it would represent the third leading cause of death in the United States.5 Approximately half of all 30-day postoperative deaths are cardiovascular or consequent to cardiovascular events,—with myocardial ischemia being the most common by far.6
Worldwide, 8% of surgical inpatients >45 years of age sustain postoperative myocardial injury as defined by a troponin elevation that is attributable to an ischemic etiology, with only 42% of these events fulfilling the diagnostic criteria of the universal definition of myocardial infarction.7 Only 14% of patients who are experiencing a perioperative myocardial infarction will have chest pain, and 65% are entirely clinically silent, which means that they will go undetected without routine troponin screening.6,8,9
It is tempting to dismiss asymptomatic biomarker elevation as troponitis and assume that it is inconsequential; but this approach would be mistaken because 30-day mortality in patients with elevated postoperative troponin is similar with and without symptoms.10 The term myocardial injury after noncardiac surgery (MINS) recognizes that troponin elevations without a nonischemic explanation (eg, sepsis and pulmonary embolus) are clinically important, even in patients whose symptoms and signs do not meet the formal definition of a myocardial infarction.11
Mortality at 30 days in patients with MINS is a concerning 10%, which represents a 5-fold increase from background risk. Mortality increases exponentially as a function of peak postoperative troponin concentration, ranging from 9% for fourth-generation troponin T (high-sensitive cardiac troponin T) plasma concentrations 0.03 to 0.29 ng/mL to 17% for concentrations ≥0.3 ng/mL (Table). Moreover, it is not just mortality that is increased; a composite of nonfatal cardiac arrest, congestive heart failure, stroke, and death occurred at a rate of 2.4% in patients without MINS and 18.8% among those with MINS, a factor-of-8 increase.10
Among inpatients ≥45 years of age who are having noncardiac surgery, the number needed to screen to detect MINS that would otherwise be missed is only about 15 patients, fewer than for tests we conduct routinely for conditions that are far less deadly. Consistent with this logic, per the third universal definition of myocardial infarction guidelines: “routine monitoring of cardiac biomarkers in high-risk patients after major surgery is therefore recommended.”7 In fact, troponin screening should not be restricted to high-risk patients because the incidence of MINS is 8% among a representative cross-section of surgical inpatients selected only for being ≥45 years of age.11
Thus, troponin screening seems appropriate for most surgical inpatients ≥45 years of age. Troponin analysis can be included with routine morning blood sampling on the first, second, and third postoperative mornings while patients remain hospitalized. Screening thereafter is probably not necessary because about 75% of postoperative myocardial infarctions occur within 48 hours after surgery9 and because about 80% of all 30-day mortality occurs during the initial hospitalization.12 That being said, blood should immediately be sent for troponin analysis in any patients who has cardiovascular symptoms such as chest pain or shortness of breath. Nonischemic causes of troponin elevation include end-stage renal disease, sepsis, and pulmonary embolism7; preoperative plasma troponin assays might help clinicians interpret subsequently elevated values.
Postoperative fourth-generation troponin T concentrations ≥0.03 ng/mL in the absence of alternative explanations should prompt a medical or cardiology consult. This recommendation is supported by evidence that suggests that intensification of cardiovascular therapy in patients with elevated postoperative troponin concentrations reduces the risk of subsequent cardiac events by about 40%.13 Additional work is required to establish the optimal thresholds for non–high-sensitivity troponin I assays and troponin I and T assays.
However, there are no available randomized trial results that suggest specific treatments for MINS. Nonetheless, potential benefits of troponin screening include a cardiology consultation and patients: (1) being informed that they had myocardial injury and are thus at risk for future heart attacks; (2) potentially starting aspirin; (3) being considered for statin and/or ACE inhibitor therapy; (4) having improved hypertension control, as necessary; and (5) taking advantage of a teachable moment14 to promote lifestyle changes, including smoking cessation, sensible diet, and enhanced exercise.
Too many anesthesiologists still consider our work done when patients arrive safely in the postanesthesia care unit. Although patients rarely die during surgery, postoperative mortality remains high, with myocardial injury being a leading cause. Troponin screening is an opportunity to extend our influence as perioperative physicians into the postoperative period.
Name: Daniel I. Sessler, MD.
Contribution: This author helped write the manuscript.
Name: P. J. Devereaux, MD, PhD.
Contribution: This author helped write the manuscript.
This manuscript was handled by: Richard C. Prielipp, MD, MBA, FCCM.
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