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Troponin - Myocardial Injury After Non-Cardiac Surgery


Troponin - Myocardial Injury After Non-Cardiac Surgery

                                        K.Ruetzler, N.Smilowitz, J.Berger, P.Devereaux, B. Maron, et al. 

                                                     Circulation; vol 144 (19); Oct 2021 0:CIR.0000000000001024 

                                                  A Scientific Statement from the American Heart Association



Perioperative mortality after noncardiac surgery is ≈1% to 2% among inpatients ≥45 years of age.1 Approximately half of these deaths are attributed to cardiovascular complications of surgery.2 Substantial efforts have been made to investigate the causes, pathophysiology and consequences of cardiovascular complications in postsurgical patients.
Cardiac biomarkers indicative of myocardial damage such as cardiac troponin (cTn) are frequently elevated after noncardiac surgery. Historically, these biomarker abnormalities were ignored because associated clinical symptoms, such as chest pain and shortness of breath were rare in the postoperative setting. However, even clinically silent cardiac biomarker elevations after noncardiac surgery are associated with mortality and major vascular complications.3–5 
Based on the prognostic importance of postoperative cardiac biomarkers, a new clinical diagnosis, myocardial injury after noncardiac surgery (MINS), has been established. MINS includes myocardial infarction and ischemic myocardial injury that do not fulfill the Universal Definition of Myocardial Infarction (myocardial injury with a rise or fall of cTn above the 99th percentile of the upper reference limit and at least 1 of the following: ischemic symptoms, new ischemic electrocardiographic changes, development of new pathological Q waves on ECG, imaging evidence of myocardial ischemia, or angiographic or autopsy evidence of coronary thrombus).6
This American Heart Association scientific statement offers a clinical perspective of MINS, including a review of its definition, epidemiology, pathophysiology, prediction, surveillance, prevention, prognosis, and management.


MINS is defined by al least 1 postoperative cTn concentration that excess the 99th percentile upper reference limit of teh assay as result of a presumed ischemic mechanism (ie, supply-demand mismatch or atherothrombosis) in the absence of overt nonischemic causes.
Such elevations in cTn must be identified within the first 30 days after surgery but nearly always occur within the first 2 postoperative days. Clinical symptoms and electrocardiographic changes are not required to establish a diagnosis of MINS, wich includes myocardial infarction and myocardial injury.

TABLE 1. Diagnostic Criteria for MINS


* Elevated postoperative cTn with ≥1 cTn measurement above the 99th percentile of the URL for the cTn assay, with a rise/fall pattern indicative of acute myocardial injury*†

* Occurs in the first 30 d (and typically within 72 h) after surgery

* Myocardial injury is attributable to a presumed ischemic mechanism (ie, supply-demand mismatch or atherothrombosis) in the absence of an overt precipitating nonischemic cause (eg, pulmonary embolism)

* Clinical symptoms may be masked by sedation or analgesia in the perioperative setting, so an ischemic feature (eg, ischemic symptoms, electrocardiographic changes) is not required

  • Among patients with abnormal baseline troponin values, myocardial injury is considered acute if there is a ≥20% rise of cTnI or cTnT after noncardiac surgery, an absolute increase in high-sensitivity cTnT of ≥14 ng/L above preoperative values, or an increase in high-sensitivity cTnT ≥5 ng/L above the prior concentration and with a peak high-sensitivity cTnT >20 ng/L.
  • Prognostically important thresholds should be considered instead of the 99th percentile of the URL for specific cTn assays: non–high-sensitivity fourth-generation troponin T ≥30 ng/L (Roche fourth-generation Elecsys TnT assay), high-sensitivity troponin T of 20 to <65 ng/L with an absolute change of ≥5 ng/L, or a high-sensitivity troponin T concentration ≥65 ng/L.

Serial cTn concentrations are necessary to distinguish acute from chronic myocardial injury, and preoperative cTn concentrations inform the interpretation of postoperative measurements. For patients at high clinical risk for cardiovascular events such as adults ≥65 years or age or adults ≥45 years of age with established coronary or peripheral atherosclerotic cardiovascular disease, we recommend obtaining a preoperative baseline cTn measurement and then a repeat test within 48 to 72 hours after surgery if the results of testing would modify clinical management.4,7 When a postoperative cTn concentration is elevated but a recent prior cTn measurement (preoperative or postoperative) is not available, a second cTn measurement should be obtained to determine whether a rising or falling pattern indicative of acute myocardial injury is present. Among patients with a preoperative or initial postoperative cTn value exceeding the 99th percentile, myocardial injury is considered acute when there is a >20% rise or fall in a subsequent cTn concentration.6 This >20% threshold was originally proposed in the Universal Definition of Myocardial Infarction to identify a cTn change greater than the expected analytical variability of the assay in the assessment of reinfarction in nonsurgical cohorts.8 Although consistent with guidance for other myocardial infarction subtypes, a >20% threshold is based on expert consensus and has not been validated in the setting of surgery.6
When serial high-sensitivity cTnT (hsTnT) measurements are used, an absolute increase of ≥5 ng/L above the previous value was independently associated with an increased risk of 30-day mortality in a large international study.9 This study also demonstrated that a postoperative peak hsTnT >20 ng/L was associated with >3.0% mortality at 30 days. Therefore, an absolute change of >5 ng/L between 2 postoperative hsTnT concentrations with a peak value >20 ng/L identifies patients with an excess risk of postoperative mortality. Peak postoperative hsTnT >65 ng/L also was associated with 30-day mortality, regardless of the absolute change in hsTnT. In a separate single-center prospective study in which MINS was defined a priori as an absolute change of hsTnT >14 ng/L, a diagnosis of MINS was associated with 30-day mortality.10 In this study, even absolute increases >5 ng/L appeared to be associated with near-linear increases in 30-day mortality in unadjusted analyses.10 Although data for high-sensitivity cTnI assays are lacking, extrapolation might suggest that the use of a similar diagnostic threshold (ie, an absolute increase of >99th percentile of the reference limit for the cTn assay) may be reasonable for high-sensitivity cTnI assays, pending further investigation. A fourth-generation cTnT (TnT) threshold ≥30 ng/L was also associated with an adverse prognosis in a large prospective study.4 When these specific high-sensitivity and conventional cTn assays are used to detect myocardial injury, thresholds derived from large prospective cohort studies of MINS provide guidance for interpreting the clinical relevance and prognostic implications of cTn elevation Such data do not yet exist for all cTn assays.

TABLE 2 – Pronostic Threshold for MINS

* Troponin assay-specific thresholds for the diagnosis of MINS that are associated with adverse prognosis regardless of whether clinical signs and symptoms of ischemia are present

* Troponin four generation =/> 30ng/L

* Hs TnT =/> 20-65 ng/L or any elevation =/> 65 ng/L or any absolute change =/> 14 ng/L


NOTE: hsTnT indicates high-sensitivity troponin T;MINS, myocardial injury after noncardiac surgery.

Perioperative myocardial injury that has a documented nonischemic cause should not be
classified as MINS. Myocardial injury in the perioperative setting may be attributed to non
ischemic causes such as acute decompensated heart failure, sepsis, and pulmonary embolism.
In large, prospective cohort studies of representative patients having noncardiac surgery who had systematically measured postoperative cTn, 11% to 14% of elevated cTn measurements after surgery were adjudicated as myocardial injury as a result of a nonischemic or extracardiac cause such as sepsis or pulmonary embolism, chronic nonischemic cTn elevations, or nonatherothrombotic mechanism of myocardial supply-demand mismatch such as rapid atrial fibrillation or severe anemia.9,10 Nonetheless, the remaining 86% to 89% of perioperative hsTnT elevations are attributed to an ischemic mechanism and classified as MINS.


Myocardial injury after noncardiac surgery is common. In the international multicenter VISION study (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation) of 21 842 patients ≥45 years of age undergoing inpatient noncardiac surgery who had systematic hsTnT measurements, 18% developed MINS.9 When the conventional fourth-generation TnT assay was used, the incidence of MINS was 8%.11 In a single-center study of 2018 patients ≥65 years of age or ≥45 years of age with a history of vascular disease, 16% of the patients developed MINS.10 Overall, in a recent systematic review of 169 published studies reporting outcomes of 530 867 surgeries, the pooled incidence of MINS was 18% (95% CI, 16%–20%).12 In an analysis restricted to large, prospective series with systematic cTn measurement, 20% (95% CI, 18%–21%) of surgeries were complicated by MINS.4,9,10,12
Several factors influence the reported incidence of MINS. First, the definition of MINS has varied across studies. Some studies evaluating MINS excluded patients with presumed nonischemic causes of postoperative myocardial injury, whereas others included all patients with myocardial injury. Second, the incidence of MINS also depends on whether systematic postoperative cTn surveillance is performed because 84% to 93% of patients with MINS have no identifiable ischemic symptoms.9,11 Studies with and without systematic monitoring reported MINS incidences of 20% and 10%, respectively.12 The timing of surveillance also affects the frequency of MINS. According to data from VISION, 78% of MINS diagnoses were established on the day of surgery or the first postoperative day, and 94% occurred by the second postoperative day. Only 0.6% of MINS were diagnosed beyond the third postoperative day.9 Third, the type of cTn assay used affects the incidence of MINS, with a higher incidence associated with high-sensitivity cTn compared with conventional assays. In a systemic review of studies that implemented routine postoperative cTn surveillance, the incidence of MINS was 25% with hsTnT assays, 20% with conventional (third- or fourth-generation) cTnI assays, and 17% with conventional TnT assays.12 Finally, the surgical population also affects MINS incidence, which may vary according to age, sex, renal function, and the urgency of surgery.11


By definition, MINS has an ischemic origin (eg, supply-demand mismatch or atherothrombosis). Many factors can contribute to cTn elevations after noncardiac surgery.13 Anesthesia and surgical trauma can lead to surges in catecholamines, cortisol, and inflammatory cytokines. Perioperative hemodynamic fluctuations can lead to an ischemic imbalance in myocardial oxygen supply and demand that results in myocardial injury. Tachycardia decreases the duration of diastole and increases myocardial wall stress and oxygen requirements. Episodes of hypertension increase left ventricular afterload and increase myocardial oxygen demand. Increases in coronary artery sheer stress may destabilize preexisting coronary atherosclerotic lesions and provoke plaque disruption (erosion or rupture).14,15 Decreased coronary perfusion from hypotension or bradycardia in the setting of fixed stable coronary stenosis also may lead to profound mismatch in myocardial oxygen supply and demand. Increased platelet activation and hypercoagulability contribute to a thrombotic milieu. Vascular inflammation, endothelial dysfunction, and coronary microvascular disease also may contribute to myocardial injury. In combination, these substantial pathophysiological changes promote increased cardiovascular risk in the perioperative period.
In most cases, MINS is related to coronary artery disease (CAD). MINS may be caused by plaque disruption with or without thrombosis leading to type 1 myocardial infarction or injury or an imbalance between coronary perfusion and myocardial oxygen demand in the absence of an unstable plaque, causing type 2 myocardial infarction or injury.6 Myocardial injury may occur in the setting of stable obstructive CAD or nonobstructive plaque, with or without endothelial dysfunction and coronary microvascular disease. In a study of patients who had coronary computed tomography (CT) angiography before noncardiac surgery, obstructive CAD was present in 72% (51 of 71) with postoperative myocardial infarction, and only 4% of these patients had no CAD.16 Among patients having coronary angiography for perioperative myocardial infarction or MINS after noncardiac surgery, obstructive CAD was present in 77% to 94% of cases.17,18 Other angiographic series also suggest that MINS is frequently related to preexisting obstructive CAD or unstable coronary plaques.17,19–21 In an autopsy series, 46% of patients with fatal postoperative MI after noncardiac surgery had evidence of coronary artery plaque rupture.22
Several other cardiovascular risk factors prevalent in surgical cohorts with MINS may contribute to the pathogenesis of perioperative cTn elevation.23 Patients with obstructive sleep apnea are predisposed to cardiovascular events, possibly mediated by endothelial dysfunction, systemic hypertension, elevated circulating concentrations of vascular effector hormones, and episodic hypoxemia.24 Among 1218 patients at risk for obstructive sleep apnea followed prospectively for 30 days after major noncardiac surgery, severe obstructive sleep apnea was associated with MINS (adjusted hazard ratio [HR], 1.80 [95% CI, 1.17–2.77]).25 Other risk factors associated with MINS include diabetes, congestive heart failure, and established atherosclerotic heart disease.11 Anemia also may play a role in the mismatch of myocardial oxygen supply and demand.26–28 Renal failure is an independent risk factor for MINS, and there is a stepwise association between preoperative estimated glomerular filtration rate and incident events assessed by a conventional, non-hsTnT assay. Compared with individuals with an estimated glomerular filtration rate of ≥60 mL·min−1·1.73 m−2, those with an estimated glomerular filtration rate of 45 to 59, 30 to 44, and <30 mL·min−1·1.73 m−2 were associated with a 1.7 (95% CI, 1.4–2.0), 2.4 (95% CI, 2.0–2.9), and 7.9 (95% CI, 6.7–9.3) increased hazard of MINS, respectively.11 The precise mechanism by which renal function modulates myocardial injury is unknown, although the interpretation of biomarkers in patients with kidney disease may be challenging because of chronic cTn elevation in this group.29 As with other clinical situations, serial measures help to establish acute myocardial injury in patients with chronic kidney disease.
A number of conditions may confound the diagnosis of MINS through nonischemic myocardial injury. Sepsis can directly mediate myocardial injury and cardiomyopathy in the perioperative state, and in general, MINS should not be diagnosed in patients with sepsis.30 
In addition, right ventricular myocardial injury may occur in conditions in which afterload rises suddenly, as in patients with acute pulmonary embolism.31 Myocardial injury also is common in patients with acute decompensated heart failure.32


Preoperative cardiovascular risk assessment may identify patients with an increased likelihood to develop MINS. Estimates of perioperative risk can guide perioperative management and provide data for use during informed consent for surgery and anesthesia. Patients at increased risk of MINS may warrant modifications in intraoperative care, including invasive arterial pressure monitoring, hypotension avoidance strategies, and systematic preoperative and postoperative cTn surveillance.
Several risk factors for MINS (Table 3) were identified in prior cohort studies with systematic postoperative cTn testing, multivariable regression analyses, and reasonably large sample sizes (ie, ≥500 surgical patients, capturing ≥50 MINS events).11,21,25,27,33–45 These risk factors fall within several broad domains: demographics, functional capacity, atherosclerotic vascular disease, other cardiac disease, noncardiovascular comorbidities, results of preoperative testing, and operative characteristics (Table 3). Both male sex and older age (especially ≥75 years of age) are independently associated with the risk of MINS.11,25,33–37 Increased risk in select populations may be explained in part by age- and sex-based variation in upper reference limits for hsTnT concentrations.46 In VISION, there was no interaction between hsTnT thresholds associated with 30-day mortality and sex; interactions with age were not explored.9 This finding suggests that when men and women develop MINS, the association with subsequent mortality is similar, but men are more likely than women to develop MINS.11

TABLE 3 – Preoperative Risk Factors


 Increased age11,25,33–37

 Male sex11

Functional capacity

 Duke Activity Status Index score38,39

Atherosclerosis-associated comorbidities




 Peripheral artery disease11,25,34,40

 Cerebrovascular disease11

Other cardiovascular conditions

 Heart failure11

 Atrial fibrillation11

Other comorbidities

 Chronic renal insufficiency (eGFR <60 mL·min−1·1.73 m−2)11,25,35,36,40

 Untreated severe obstructive sleep apnea25

Composite risk indices

 Elevated Revised Cardiac Risk index score33,37,42

 High-risk STOP-Bang risk score25

Preoperative testing

 Elevated natriuretic peptide concentration33,38,42

 Neutrophil-lymphocyte ratio >437

 Elevated causal blood glucose concentration43

 Elevated reticulated platelet concentration36

 Reversibility on myocardial perfusion testing40,44

 Impaired postexercise heart rate recovery21,45

Surgery type

 Emergency surgery11,36

 Surgical procedure type11,35–37,44,45

When subjectively assessed by anesthesiologists during preoperative interviews, estimated functional capacity adds minimal additional information beyond the usual clinical factors to predict MINS.47 Similarly, maximal exercise capacity by standardized exercise testing is not associated with the postoperative risk of MINS.39 However, the self-reported standardized Duke Activity Status Index questionnaire is associated with MINS.39 Although further validation studies are necessary, Duke Activity Status Index scores ≤34 appear to identify surgical patients at greater risk for MINS.38
Known atherosclerotic cardiovascular disease, including CAD, cerebrovascular disease, or peripheral artery disease, and associated risk factors (ie, hypertension, diabetes) are strong predictors of MINS.11,34,35,40,41,48 Several other cardiovascular (heart failure, atrial fibrillation)4 and noncardiovascular (untreated severe obstructive sleep apnea, impaired preoperative renal function)11,35,36,40,48 comorbidities also are independent predictors of MINS.
Given the prognostic importance of individual cardiovascular comorbidities, it is not surprising that composite predictive indices that include these same comorbidities are also predictive of MINS. For example, the Revised Cardiac Risk Index, which includes CAD, heart failure, cerebrovascular disease, diabetes, and impaired renal function, is independently associated with MINS.37,42,49 Notably, high-risk classification based on the snoring, tiredness, observed apnea, hypertension, body mass index, age, neck circumference, STOP-BANG score, and male sex risk score,50 which was originally designed to screen for undiagnosed obstructive sleep apnea and includes some individual predictors of MINS (ie, older age, male sex, hypertension), was also independently associated with MINS in a large prospective cohort study.48
Aside from clinical features that can be readily identified during preoperative interviews, preoperative laboratory testing can inform risk assessment for MINS. Biomarkers with the strongest evidence for predicting MINS are natriuretic peptides, either BNP (brain natriuretic peptide) or NT-proBNP (N-terminal-proBNP).33,38 In a large prospective cohort study measuring preoperative NT-proBNP in 10 402 patients undergoing noncardiac surgery, 378 had MINS.42 Multivariable analysis demonstrated that compared with a preoperative NT-proBNP level <100 ng/L (reference group, 5% MINS incidence), patients with higher levels of NT-proBNP were at greater risk for MINS: NT-proBNP of 100 to <200 ng/L, 12% MINS incidence (adjusted HR, 2.29 [95% CI, 1.91–2.73]); 200 to <1500 ng/L, 20% MINS incidence (adjusted HR, 3.63 [95% CI, 3.12–4.21]); and ≥1500 ng/L, 36% MINS incidence (adjusted HR, 5.70 [95% CI, 4.69–6.92]).42 Furthermore, a systematic review of individual-patient data from 8 studies with 619 surgical patients with preoperative BNP measurement demonstrated that a BNP <92 ng/L was associated with low perioperative risk, whereas patients with higher BNP values had increased risks of perioperative death and nonfatal myocardial infarction.33
Several other laboratory tests predicted MINS in individual large cohort studies, including elevated blood glucose,43 elevated reticulated platelet concentration (a marker of platelet turnover),36 and neutrophil-lymphocyte ratio >4 (a marker of systemic inflammation).37 Among patients having vascular surgery, reversible defects identified by stress myocardial perfusion imaging were also associated with MINS.40,44 In addition, among patients who had preoperative exercise testing, impaired heart rate recovery (≤12-bpm decrease) during the first minute after exercise, a marker of parasympathetic dysfunction, was also associated with an elevated risk of MINS.45
In addition to patient-specific risk factors, both the urgency and type of planned surgical procedure are important determinants of the risk for MINS. Patients undergoing urgent or emergency procedures experience an ≈2- to 3-fold higher adjusted odds of MINS.11,36 Several surgery types are also associated with higher risks of MINS, including vascular procedures (especially open aortic or infrainguinal surgery)35,36,51 and intra-abdominal general surgical procedures.36 In the VISION study, the highest incidence of myocardial injury followed vascular (19%), orthopedic (12%), thoracic (9%), and general (9%) surgeries.4


Despite 3 large randomized trials that evaluated 4 preoperative interventions (β-blockers, α-2 agonists, aspirin, and nitrous oxide) to reduce cardiovascular risk, there are currently no known safe and effective methods for preventing perioperative myocardial infarction.52–54 Enrollment criteria for these trials were similar and included patients ≥45 years of age with known or suspected cardiovascular disease who were scheduled for inpatient noncardiac surgery. In each trial, myocardial infarction defined by the Third Universal Definition of Myocardial Infarction was the major component of a primary cardiovascular composite 30-day end point.8 Myocardial injury is a more recent concept, and to date, no published large multicenter randomized trial has used MINS as a primary end point. However, large ongoing perioperative trials include MINS in the primary outcome. Although MINS includes myocardial infarction, the effect of interventions on myocardial infarction may not inform the effect on the broader outcome of MINS.
The 3 randomized trials are:
1.- POISE (Perioperative Ischemic Evaluation Study) randomized 8351 patients.
2.- POISE-2 (Perioperative Ischemic Evaluation Study) trial randomized 10 010 patients 
3.- ENIGMA II trial (Evaluation of Nitrous Oxide in the Gas Mixture for Anaesthesia)
     randomized 7112 patients


Considering how central hemodynamic control is to anesthetic management, it is remarkable how little is known about appropriate hemodynamic targets and harm thresholds during surgery. A paucity of robust trials evaluating intraoperative hemodynamic management remains. Recent analyses of large electronic data sets suggest that even brief periods of intraoperative hypotension, at thresholds that until recently were generally considered acceptable, are associated with myocardial injury, acute kidney injury, and mortality.71–73
In 1 study, absolute mean arterial pressure ≤65 mm Hg and a relative decrease of ≈30% from baseline were associated with myocardial injury73 Thresholds were similar for acute kidney injury.73 Severity and duration of hypotension were key determinants of cardiac injury and mortality. For example, once mean arterial pressure decreased to 55 mm Hg, a duration of just a few minutes was associated with increased mortality.73 Systolic, diastolic, and mean arterial pressures were similarly predictive for MINS.75
Perioperative myocardial injury does not occur at random; it is largely restricted to patients with preexisting cardiovascular risk. Therefore, baseline risk factors are far stronger predictors of cardiovascular outcomes than intraoperative hypotension.73 Nonetheless, the association between hypotension and MINS is important because, unlike baseline patient characteristics, blood pressure can largely be controlled. For example, about one-third of all hypotension occurs as a result of anesthetic drugs between anesthetic induction and incision.76 Continuous intraoperative monitoring (including the use of arterial catheters) reduces the frequency and severity of hypotensive episodes. In 2 randomized trials, continuous blood pressure monitoring detected more hypotension and allowed clinicians to intervene earlier, thus reducing the number of episodes of hypotension and total hypotension exposure.77,78 Various noninvasive systems reliably estimate blood pressure continuously and, therefore, can be considered valuable alternatives to invasive arterial blood pressure monitoring.79
Despite the strong association between intraoperative hypotension and MINS, randomized trials of interventions to mitigate hypotension are necessary to confirm a causal link between hypotension and adverse outcomes. For example, some perioperative interventions that typically cause hypotension (eg, epidural anesthesia) have not been shown to increase perioperative cardiac risk.80 In addition, the treatment of intraoperative hypotension is not always straightforward. Uncertainty in the optimal approach to mitigate hypotension in clinical practice remains, including in the selection or quantity of intravenous fluids, the use or choice of vasopressor agents, and the management of depth of anesthesia.
There are currently no randomized trial data on the effect of blood pressure–management strategies on myocardial injury or infarction. A randomized trial compared tight intraoperative blood pressure control and minimal control in 298 high-risk surgical patients.81 The primary outcome, a composite of systemic inflammatory response syndrome or at least 1 organ failure, was reduced 25% in the group randomly assigned to tight intraoperative blood pressure control. These findings were mirrored by a randomized trial of 450 participants that compared usual clinical care against a hemodynamic management algorithm consisting of a minimum target mean arterial pressure of ≥65 mm Hg and guided fluid management.82 The hemodynamic management algorithm resulted in a 48% relative risk reduction for the composite of moderate to severe cardiac and noncardiac complications, but intraoperative blood pressures were not reported, and only 1 myocardial infarction occurred, precluding inferences about the effects of the algorithm on MINS.


Tachycardia, defined as a heart rate ≥100 bpm, increases myocardial oxygen demand, limits diastolic coronary perfusion time, and may contribute to myocardial injury.83 Given the contribution of tachycardia to nonoperative myocardial infarctions, clinicians might reasonably assume that intraoperative tachycardia contributes to MINS, which is also thought to be largely a consequence of myocardial oxygen supply-demand mismatch.19 Consistent with this theory, some studies have reported an association between preoperative ambulatory tachycardia and postoperative MINS.84,85 In a secondary analysis of the VISION study, myocardial injury was associated with tachycardia, with harm most apparent when heart rate exceeded 100 bpm for prolonged periods.86 However, in a separate study of nearly 3000 patients who had noncardiac surgery, heart rates >90 and >100 bpm were not associated with myocardial injury).83


Postoperative management of MINS remains an area of active investigation. Although short- and long-term risks of MINS are well established, few studies have prospectively evaluated management strategies in this high-risk cohort. Thus, considerable uncertainty surrounds the optimal management of patients with MINS.
Management of patients with MINS should be tailored to the suspected cause of the myocardial injury. Although myocardial injury is related to atherosclerotic cardiovascular disease in most cases, alternative causes of myocardial injury must be considered. Myocardial injury related to pulmonary embolism, valvular heart disease, and acute decompensated heart failure should not be treated as MINS because these diagnoses would substantially alter the approach to treatment. Vital signs, cardiovascular physical examination for murmurs, jugular venous distention, and lower extremity edema must be integrated with clinical risk factors to determine the likelihood of nonischemic causes of MINS. When there is doubt about the mechanism, additional cardiovascular testing may be warranted for further evaluation. For example, when the diagnosis of deep vein thrombosis or pulmonary embolism is suspected, transthoracic echocardiography to examine for right ventricular dysfunction, lower extremity venous duplex ultrasound, and CT of the chest with intravenous contrast or a nuclear medicine ventilation perfusion scan may be considered to confirm the diagnosis.
Medical therapy after MINS remains an area of uncertainty, but antithrombotic therapy appears to be beneficial. In a post hoc analysis of 415 patients enrolled in the POISE trial who developed perioperative myocardial infarction, aspirin prescribed at hospital discharge was independently associated with a reduced risk of 30-day mortality (adjusted odds ratio, 0.54 [95% CI, 0.29–0.99]).101 These data are consistent with the well-known benefits of aspirin for secondary prevention after spontaneous MI.102


MINS is an important clinical diagnosis defined by an elevation of cTn after noncardiac surgery, with or without ischemic symptoms or electrocardiographic abnormalities, after the exclusion of alternate nonischemic causes of cTn elevation. The MINS definition proposed herein should be used to standardize the assessment and reporting of ischemic events in clinical practice and future clinical trials. Additional investigation to determine specific mechanisms of MINS is necessary to develop targeted therapies. High-risk individuals having noncardiac surgery should have serial cTn measurements during the first 48 to 72 hours postoperatively while hospitalized. Troponin surveillance can avoid missed MINS and provides an opportunity to initiate secondary prophylactic measures and guide appropriate follow-up. At present, it is reasonable to intensify therapy for the secondary prevention of cardiovascular disease in patients with a diagnosis of MINS, particularly for patients with established cardiovascular disease or those who meet existing clinical practice guideline recommendations for therapy. Efforts to improve recognition and understanding of MINS will ultimately improve postoperative outcomes after noncardiac surgery.

NOTE: This is part of the article. Full text and references, tables, graphs, figures and charts in the original paper cited.


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