Perioperative myocardial infarction or injury after noncardiac surgery

INTRODUCTION — The stress of surgery can lead to myocardial ischemia or infarction via multiple mechanisms including coronary artery plaque rupture and myocardial demand ischemia. Due to the effects of anesthesia and analgesia, patients with myocardial injury may not present with the usual symptoms of myocardial ischemia or infarction (eg, chest discomfort, electrocardiogram [ECG] changes); many patients only exhibit an elevated troponin level.

This topic will focus on the evaluation, diagnosis, and distinct aspects of management of patients with perioperative myocardial infarction or myocardial injury after noncardiac surgery (MINS). This topic also reviews surveillance for these disorders.

Other topics on cardiovascular complications of surgery include:

●(See "Evaluation of cardiac risk prior to noncardiac surgery".)

●(See "Management of cardiac risk for noncardiac surgery".)

●(See "Perioperative management of heart failure in patients undergoing noncardiac surgery".)

PATHOPHYSIOLOGY — In patients with myocardial injury after noncardiac surgery (MINS), myocardial injury is either due to a supply-demand mismatch, often in the presence of underlying obstructive coronary artery disease (CAD), or an acute thrombus [1-3]:

●In a study that included patients with perioperative acute coronary syndromes (ACS) or "spontaneous" (ie, nonoperative) ACS who underwent coronary angiography, unstable CAD or plaque rupture were present in 45 percent of patients with perioperative ACS [4].

●A study that evaluated patients who had perioperative myocardial infarction (n = 30) with matched cases who had a spontaneous myocardial infarction (n = 30) identified coronary thrombus with optical coherence tomography as the culprit lesion in 13 percent of patients with perioperative myocardial infarction and 67 percent of patients with spontaneous myocardial infarction [5].    

●Three large prospective cohort studies in which adjudicators attempted to evaluate each case of elevated troponin found that most patients (over 85 percent) with troponin elevations after surgery did not have evidence of a nonischemic etiology (eg, sepsis, pulmonary embolism) and thus elevated troponin was likely due to myocardial ischemia mediated by chronic obstructive CAD or acute thrombus [6-8].  

EPIDEMIOLOGY

Incidence — In adults ≥45 years of age who undergo inpatient noncardiac surgery (ie, spent at least one day in the hospital), myocardial injury after noncardiac surgery (MINS) occurs in 15 to 20 percent. Among patients who fulfill the diagnosis of MINS, 20 to 30 percent will also fulfill the diagnostic criteria of perioperative myocardial infarction as defined by the fourth Universal Definition of Myocardial Infarction criteria. Only a minority of patients (<15 to 20 percent) with perioperative myocardial injury have nonischemic causes of myocardial injury (eg, sepsis).

However, the exact incidence of perioperative myocardial injury and MINS varies based on the risk of myocardial injury in the populations studied, different criteria used to establish the presence of MINS, and the changing sensitivity of troponin assays. For example, among patients with MINS, perioperative myocardial infarction accounts for approximately 40 percent of cases when a non-high-sensitivity cardiac troponin (cTn) assay is used and 20 to 30 percent of cases when a high-sensitivity cardiac troponin (hs-cTn) assay is used [6,7]. The apparent decrease in the fraction of patients with perioperative myocardial infarction results from an increase in the number of patients diagnosed with elevated troponin but without other signs or symptoms of myocardial infarction.

The risk of myocardial injury after outpatient surgery is not well studied.

Large prospective cohort studies that evaluated the incidence of postoperative myocardial injury, MINS, and postoperative myocardial infarction using high-sensitivity assays (the standard assay in most of the world) include [6,8-11]:

●In a prospective study of 2018 patients (2546 noncardiac surgeries) undergoing noncardiac surgery who were ≥65 years of age or ≥45 years with history of CAD, peripheral artery disease, or stroke, high-sensitivity cardiac troponin T (hs-cTnT) was prospectively measured before and after surgery [8]. Perioperative myocardial injury (defined as an absolute increase in hs-cTnT of ≥14 ng/L above the preoperative value) occurred in 397 patients (16 percent), MINS occurred in 342 patients (13 percent), and perioperative myocardial infarction occurred in 117 patients (5 percent). At 30 days, mortality in those with elevated hs-cTnT was 8.9 percent and in those without elevated hs-cTnT was 1.5 percent.  

●In the second VISION cohort of 21,842 patients ≥45 years old, hs-cTnT was measured during the first three postoperative days [7]. Based on the association between hs-cTnT and mortality identified in the data, the authors defined an elevated postoperative hs-cTnT as a value 20 to <65 ng/L with an absolute change of at least 5 ng/L between measurements or a single hs-cTnT level ≥65 ng/L. Using this definition, perioperative myocardial injury was detected in 4385 patients (20 percent), MINS was detected in 3904 patients (17.9 percent), and perioperative myocardial infarction was detected in 846 patients (3.9 percent).

Among patients with MINS, 3633 patients (93 percent) did not experience an ischemic symptom. Among patients who had a perioperative myocardial infarction, 575 patients (68 percent) did not experience an ischemic symptom. These patients would have likely gone undetected without perioperative troponin screening.

Risk factors — Risk factors for myocardial injury after noncardiac surgery include [5,8,12-15] (see "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Using risk assessment tools'):

●Age ≥65 years

●History of coronary artery or peripheral arterial disease

●History of diabetes or kidney dysfunction

●Elevated N-terminal pro-B-type natriuretic peptide level

●Baseline ST-T wave changes

●Major perioperative hemorrhage

●Type of surgery (eg, emergency)

The Revised Cardiac Risk Index can be used to estimate the cardiovascular risk of surgery from multiple variables (table 1).

CLINICAL MANIFESTATIONS — Patients with perioperative myocardial infarction may have symptoms (rarely) and signs similar to the broad group of patients with an acute coronary syndrome. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'Clinical presentation'.)

However, due to the influence of agents with anesthetic, analgesic, or amnestic effects, symptoms of myocardial infarction are often muted, atypical, or absent. Due to variable ECG monitoring, ECG signs of myocardial infarction are often not recorded. As an example, in the international POISE-1 trial, among 415 patients who had a perioperative myocardial infarction, approximately 65 percent of patients did not experience ischemic symptoms [16].

EVALUATION

Signs or symptoms of myocardial infarction — In patients who present with typical signs or symptoms of myocardial infarction after surgery, the evaluation of these findings is similar to patients who present with typical signs or symptoms of myocardial infarction in other settings. (See "Evaluation of the adult with chest pain in the emergency department".)

Since patients undergoing surgery are at risk for complications that mimic myocardial infarction (eg, pulmonary embolism), patients with undifferentiated signs or symptoms that may represent a new cardiovascular diagnosis (eg, chest discomfort, arrythmias) should undergo appropriate testing for alternative diagnoses as appropriate. (See 'Differential diagnosis' below.)

Elevated surveillance troponin — In patients who underwent postoperative screening and have an elevated troponin level, the approach to evaluation is similar to that in patients who have other signs or symptoms of myocardial infarction. The following tests are obtained:

●ECG

●Repeat troponin in two to three hours

To confirm or exclude the presence of acute perioperative myocardial injury, we compare multiple troponin values and any preoperative values available. (See 'Diagnosis' below.)

In addition to these tests for myocardial infarction or injury, other tests may be required to evaluate for other causes of elevated troponin (eg, pulmonary embolism) appropriate for patients who recently had surgery. (See 'Differential diagnosis' below.)

Additional testing — In patients in whom the diagnosis remains uncertain after evaluation of symptoms, ECGs, and repeat troponin assays, additional noninvasive studies (eg, echocardiography, radionuclide myocardial perfusion imaging, cardiovascular magnetic resonance imaging [CMR]) may be required to confirm or exclude the presence of myocardial infarction. The approach to additional testing in patients who recently underwent surgery is similar to that in patients in the general population, which is discussed separately. (See "Noninvasive testing and imaging for diagnosis in patients at low to intermediate risk for acute coronary syndrome", section on 'Patients with ongoing symptoms' and "Noninvasive testing and imaging for diagnosis in patients at low to intermediate risk for acute coronary syndrome", section on 'Patients whose symptoms have resolved'.)

In patients diagnosed with myocardial injury after noncardiac surgery who recover from surgery, it is reasonable to obtain stress or anatomic imaging to assess for obstructive CAD unless another clear explanation for an elevated troponin level is present. However, there are no prospective studies that describe the yield of such testing.

DIAGNOSIS

Myocardial injury after noncardiac surgery — The diagnosis of myocardial injury after noncardiac surgery (MINS) requires that two criteria are met [6]:

●The presence of noncardiac surgery in the last 30 days with an elevated troponin level indicative of acute injury (eg, fall, rise).

●Nonischemic causes (eg, sepsis, pulmonary embolism, cardioversion) of troponin elevation were reasonably excluded.

Caveats to making the diagnosis include the following:

●The diagnosis of MINS is ideally based on the difference between a preoperative and postoperative troponin, though a change in serial postoperative troponin values can be used to differentiate between an acute event and a chronic troponin elevation in most patients.

●Abnormal troponin values are those levels above the 99^th percentile of the established upper reference limit or those above a value established as prognostically important for the specific assay in perioperative settings.

●Due to the masking of symptoms and the inability to obtain timely ECG analyses, patients with myocardial infarction may only meet the definition of MINS after further evaluation is performed.

Notably, the diagnosis of MINS is broader than perioperative myocardial infarction; it includes perioperative myocardial infarction (non-ST-elevation myocardial infarction [NSTEMI], ST-elevation myocardial infarction [STEMI]) and other causes of perioperative myocardial injury due to ischemia.

Differential diagnosis — Other potential causes of an elevated troponin after noncardiac surgery include pulmonary embolus, sepsis, rapid atrial fibrillation, and chronic elevation.

PERIOPERATIVE SURVEILLANCE

Risk assessment — For the purposes of perioperative surveillance, patients with one or more of the risk factors above are at high risk of myocardial injury after noncardiac surgery (MINS). The risk factors for MINS include:

●Age ≥65 years.

●Patients ≥45 years of age who will undergo in-hospital surgery and who have one or more other risk factors from the revised cardiac risk score (table 1).

●Patients with known atherosclerotic disease.

In patients with these factors, the risk of cardiovascular death or MINS is >20 percent [8].

High-risk patients — In patients with one or more risk factors for MINS, we suggest postoperative surveillance with troponin levels obtained 6 to 12 hours after surgery and on postoperative days 1, 2, and 3.

The contributors to this topic have different approaches to preoperative testing as it relates to postoperative detection of myocardial injury. Some contributors to this topic do not obtain a preoperative troponin level or ECG, while other contributors to this topic do obtain a preoperative troponin level and ECG.

Our approach is consistent with the approaches described by professional societies. Though the societies' approaches differ slightly, there is agreement that high-risk patients should have perioperative troponin measurements:

●The fourth Universal Definition of Myocardial Infarction international expert consensus document recommends measuring troponin before and up to 48 to 72 hours after noncardiac surgery in high-risk patients [17].

●The Canadian Cardiovascular Society Guidelines for patients undergoing noncardiac surgery recommend obtaining daily troponin measurements for 48 to 72 hours after noncardiac surgery in patients with a baseline risk of death or nonfatal myocardial infarction >5 percent within 30 days of surgery (eg, Revised Cardiac Risk Index [RCRI] score ≥1, age 45 to 64 years with significant cardiovascular disease, or age ≥65 years) [18].

●The American Heart Association scientific statement on the diagnosis and management of patients with myocardial injury after noncardiac surgery states, "high-risk individuals having noncardiac surgery should have serial cardiac troponin measurements during the first 48 to 72 hours postoperatively while hospitalized" [19].

●The European Society of Cardiology guideline on cardiovascular assessment and management of patients undergoing noncardiac surgery recommends measurement of high-sensitivity troponin before intermediate- and high-risk noncardiac surgery and at 24 and 48 hours after surgery in patients who have cardiovascular risk factors (including age ≥65 years) [20].

Our approach to surveillance is motivated by studies that suggest that perioperative surveillance detects subclinical postoperative myocardial injury in more than 20 percent of patients undergoing inpatient surgery, the important prognostic relevance of these events and the need to identify these patients for long-term follow-up, and our experience that detection of such events alters patient management. There are no trials of perioperative screening that establish its efficacy. However, without perioperative troponin screening, >90 percent of patients with MINS and >65 percent of patients with perioperative myocardial infarction would escape detection. Patients with MINS should be evaluated for cardiovascular risk factors, treated for any contributing conditions (eg, anemia), considered for medical therapy, and appropriately evaluated for obstructive CAD (eg, stress echocardiography, stress radionuclide myocardial perfusion, coronary computed tomographic angiography).

The evidence on each aspect of surveillance is discussed elsewhere in this topic:

●Yield of perioperative surveillance (see 'Incidence' above and 'Risk assessment' above and 'Prognosis' below)

●Acute management related to MINS detection (see 'Acute treatment' below)

●Long-term management of MINS (see 'Long-term management' below)

Other patients — In patients who will undergo outpatient surgery (ie, will not stay in the hospital for at least one day) or will undergo inpatient surgery but who do not have high-risk features for postoperative myocardial injury, we do not perform postoperative surveillance. In this group of patients, we only obtain tests for myocardial ischemia or infarction if signs or symptoms are present.

Some experts suggest that lower-risk patients, such as those with risk factors for cardiovascular disease (eg, smoking, hypertension, or dyslipidemia) not included in the RCRI, should undergo surveillance given the worse short- and long-term outcomes associated with perioperative myocardial infarction [11]. As with any screening program, the costs, risks, and benefits are relevant. Cost-consequence data only support screening in a high-risk patient population [21].

ACUTE TREATMENT

ST-elevation myocardial infarction — In patients with perioperative STEMI in whom the risk of bleeding with anticoagulation is acceptable, the approach to STEMI management is similar to that in other patients with STEMI. In patients whose risk of bleeding is excessively high, medical therapy (eg, anticoagulation) and the use of angiography and percutaneous coronary intervention (PCI) are individualized.

In most patients with perioperative STEMI, fibrinolytic therapy is not safe.

The general approach to the management of patients with STEMI is discussed separately. (See "Overview of the acute management of ST-elevation myocardial infarction".)

Non-ST-elevation myocardial infarction — In patients with perioperative NSTEMI, the choice of treatment strategy is individualized. In particular, the decisions to anticoagulate, treat with a P2Y₁₂ inhibitor, or proceed with invasive coronary angiography with appropriate PCI each depend on the patient's risk of bleeding. Additional factors that influence the approach to treatment include:

●The degree of any ongoing instability attributable to an acute coronary occlusion or stenosis.

●The likelihood that acute thrombosis or plaque rupture is present.

●The patient's ability to undergo ischemia imaging (using nuclear, echocardiography, or CMR imaging) or direct imaging of the coronary arteries (using cardiac computed tomography [CT] or magnetic resonance imaging) to identify obstructive CAD.

●The risks and benefits of any appropriate medical therapy.

The details on the strategies and therapies for NSTEMI are described separately:

●Approach to revascularization. (See "Non-ST-elevation acute coronary syndromes: Selecting an approach to revascularization" and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction", section on 'Pharmacologic therapy'.)

●Anticoagulation. (See "Anticoagulant therapy in non-ST elevation acute coronary syndromes", section on 'Conservative approach' and "Anticoagulant therapy in non-ST elevation acute coronary syndromes", section on 'Invasive approach'.)

●Antiplatelet therapy. (See "Acute non-ST-elevation acute coronary syndromes: Early antiplatelet therapy".)

●Other components of medical therapy. (See "Overview of the acute management of non-ST-elevation acute coronary syndromes", section on 'Initial medical therapy'.)

The approach to management is largely based on expert experience and the expected risks and benefits of usual therapy for NSTEMI (eg, anticoagulation) among patients who recently underwent surgery. There are no large trials in patients with perioperative NSTEMI to guide the choice of revascularization strategy. There is indirect evidence from patients with "spontaneous" NSTEMI and small studies from single centers:

●In trials that included patients with NSTEMI that examined the effect of reperfusion strategy, an invasive strategy was associated with a lower risk of recurrent myocardial infarction and a higher risk of bleeding compared with selective angiography. The approaches to choosing a revascularization strategy and medical therapy for patients with NSTEMI are discussed separately. (See "Non-ST-elevation acute coronary syndromes: Selecting an approach to revascularization", section on 'Evidence of infarction (NSTEMI)' and "Overview of the acute management of non-ST-elevation acute coronary syndromes", section on 'Initial medical therapy'.)

●Outcomes in the subset of perioperative myocardial infarction patients who are referred for coronary angiography within seven days of noncardiac surgery were evaluated in a 2016 report from the Cleveland Clinic [22]. In this study, 1093 such individuals were referred for angiography for marked elevations of cardiac troponin (>5-fold). Of these 1093 patients, 281 (40 STEMI and 241 NSTEMI patients) underwent PCI. Mortality at 30 days was 11.3 percent; the 30-day death rates in the STEMI and NSTEMI cohorts were 31.2 and 8.5 percent, respectively.

Overall mortality at 30 days and one year was 5.2 and 15 percent, respectively. Risk factors for 30-day mortality after PCI were a bleeding event after PCI (odds ratio [OR] 4.33), peak troponin T level (OR 1.2), and underlying peripheral artery disease (OR 4.86). Important risk predictors for long-term mortality were bleeding after PCI, renal insufficiency, and vascular surgery. The small sample size and retrospective nature of this study limit its external validity.

Myocardial injury after noncardiac surgery — The management of patients with myocardial injury after noncardiac surgery (MINS) consists of the following:

●General measures – In patients diagnosed with MINS who do not have myocardial infarction, we typically increase the frequency of vital signs and manage any conditions that could exacerbate MINS (eg, hypoxia, anemia, hypotension). In patients with tachycardia or hypertension that may be causing MINS, beta blockers and renin-angiotensin-aldosterone system (RAAS) inhibitors (eg, angiotensin converting enzyme [ACE] inhibitors) are options for therapy.

We suggest consultation with a cardiologist to assist with diagnosis and management.

●Pharmacologic therapy – In patients with MINS who do not have NSTEMI or STEMI, we suggest treatment with aspirin and a statin rather than no therapy or a regimen containing other agents. Some contributors to this topic give an initial dose of 75 mg of aspirin, while others give a higher dose (up to 325 mg) if the risk of bleeding is low. After the initial dose, we begin long-term therapy with aspirin 75 to 81 mg daily. We initiate therapy with a high-dose statin (eg, atorvastatin 80 mg, rosuvastatin 20 to 40 mg) and alter the dose based on tolerance.

In addition, some experts treat patients with MINS who have a low bleeding risk with low-dose dabigatran for two years, while others do not routinely treat with an anticoagulant. In patients with perioperative myocardial infarction treated with aspirin and a P2Y12 inhibitor, we do not treat with dabigatran or another anticoagulant unless indicated for another condition (eg, atrial fibrillation).

P2Y₁₂ inhibitors are not used to treat patients with MINS who do not have myocardial infarction and did not undergo PCI.

Professional guidelines do not specify a specific treatment regimen and give a relatively weak recommendation for use of low-dose dabigatran [20].

The rationale and evidence to support the use of specific therapies in patients with MINS includes the following:

●Aspirin and statins – The evidence for aspirin and statin therapy in patients with MINS is based on indirect data from patients with "spontaneous" (ie, nonoperative) acute coronary syndromes (ACS) and observational data in patients with MINS. In an observational sub-study of POISE-1, aspirin and statin use were each associated with a reduction in the risk for 30-day mortality among patients who had suffered a perioperative myocardial infarction (adjusted OR for aspirin 0.54, 95% CI 0.29-0.99 and adjusted OR for statins 0.26, 95% CI 0.13-0.54) [11]. The evidence on the efficacy of aspirin and statin therapy for acute MI is discussed separately. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy" and "Low-density lipoprotein-cholesterol (LDL-C) lowering after an acute coronary syndrome", section on 'Our approach to in-hospital therapy'.)

●Beta blockers and RAAS inhibitors – In patients with acute MI, beta blockers are routinely used and RAAS inhibitors are commonly used in patients with reduced left ventricular ejection fraction or heart failure, but there are only weak data to suggest efficacy with routine use of these agents in patients with MINS:

•One study included a propensity-matched sample of 66 patients with MINS and 132 patients without MINS who underwent major vascular surgery [23]. Among patients with MINS, 43 received therapeutic intensification of one or more of four cardiac medications (aspirin, statin, beta blocker, or ACE inhibitor) and 23 patients did not receive therapeutic intensification after MINS. The primary endpoint of 12-month survival without a major cardiac event (ie, death, myocardial infarction, coronary artery revascularization, or pulmonary edema requiring hospitalization) was lower in those receiving therapeutic intensification (hazard ratio [HR] 2.80, 95% CI, 1.05-24.2). However, the small sample size limits the broad application of this observation.

•In a retrospective study of 59,506 patients at risk of perioperative myocardial injury, troponin screening occurred in 20 percent and was elevated in 5 percent (n = 2793) [24]. Clinicians provided a new prescription for a beta blocker to 12 percent of these patients, an ACE inhibitor or angiotensin II receptor blocker (ARB) to 5 percent, and a statin to 8 percent. At six-month follow-up, a new prescription for either a beta blocker, ACE inhibitor, ARB, or statin was associated with lower risks of ACS and heart failure but not death. The retrospective nature of this trial limits its external validity.

●Oral anticoagulants – Our experts disagree on the role of the role of anticoagulation after MINS. The only trial specifically undertaken in patients who had MINS or perioperative myocardial infarction is the MANAGE trial [25]. The MANAGE trial randomized 1754 patients in 84 hospitals in 19 countries who had MINS to receive intermediate dose dabigatran 110 mg twice daily or placebo. The rate of the primary outcome (ie, a composite of vascular mortality and nonfatal myocardial infarction, nonhemorrhagic stroke, peripheral arterial thrombosis, amputation, and symptomatic venous thromboembolism) was lower with dabigatran than with placebo (11 versus 15 percent; HR 0.72, 95% CI 0.55-0.93). The rates of individual events that comprised the composite outcome were of varying severity (eg, death, venous thromboembolism). The rates of individual components of the primary outcome were similar (eg, all-cause mortality 11 versus 13 percent, myocardial infarction 4 versus 5 percent).

●Additional antiplatelet therapy – P2Y₁₂ inhibitors are not used to treat patients with MINS who did not undergo PCI or who have only an elevated troponin (ie, do not have NSTEMI or STEMI). There is no evidence that describes the efficacy of P2Y₁₂ inhibitors in such patients. In this patient population, P2Y₁₂ inhibitors may increase the risk of bleeding in patients who recently had surgery. In the MANAGE trial, 74 percent of patients received a single antiplatelet agent, usually aspirin, and 7 percent of patients took dual antiplatelet therapy [25].

LONG-TERM MANAGEMENT — In patients with myocardial injury after noncardiac surgery (MINS) who do not have evidence of NSTEMI or STEMI, we typically schedule the patient for follow-up in clinic within two weeks of discharge. This visit is used to manage any cardiovascular risk factors (eg, hypertension, diabetes), monitor any therapy (eg, low-dose oral anticoagulation, statin), and determine the need for imaging to detect obstructive CAD.

In most patients with MINS, we obtain noninvasive stress imaging or anatomic imaging of the coronary arteries (CT) to assess for CAD. This approach is based on our experience and our preference to exclude or identify the presence of CAD. The choice of test is discussed separately. (See "Selecting the optimal cardiac stress test" and "Clinical use of coronary computed tomographic angiography", section on 'Patients with acute symptoms'.)

There are no high-quality studies that describe the yield of imaging for CAD in this setting.

Patients with perioperative myocardial infarction should undergo long-term management appropriate for NSTEMI or STEMI, which is discussed separately. (See "Overview of the nonacute management of ST-elevation myocardial infarction" and "Overview of the nonacute management of unstable angina and non-ST-elevation myocardial infarction".)

PROGNOSIS

Myocardial injury — Short- and long-term mortality and morbidity are increased in patients with perioperative myocardial infarction or myocardial injury after noncardiac surgery (MINS):

●In a study of 2018 patients, crude 30-day mortality was 8.9 percent in patients with myocardial injury compared with 1.5 percent in patients without (adjusted hazard ratio [HR] 2.7, 95% CI 1.5-4.8) [8]. Importantly, the study also found similar 30-day mortality rates in patients with perioperative myocardial infarction and those with elevated troponin but no other criteria for acute myocardial infarction (10.4 versus 8.7 percent; p = 0.684). Both the absolute high-sensitivity cardiac troponin T (hs-cTnT) value and the increase from the baseline value (the "delta") were associated with higher mortality rates.

●A large United States database study (nearly 10,000,000 individuals) identified 8085 patients who were diagnosed with perioperative myocardial infarction [26]. Among patients diagnosed with a perioperative myocardial infarction during the index hospitalization, the absolute incidence of mortality was 13 percent higher and length of stay was six days longer than those without perioperative myocardial infarction. The rate of rehospitalization within 30 days was higher in those patients with myocardial infarction who survived the initial hospitalization compared with those without myocardial infarction (19.1 versus 6.5 percent; adjusted odds ratio [OR] 1.39, 95% CI 1.31-1.48). Approximately 25 percent of readmissions were due to cardiovascular complications, and an additional 16 percent of patients had an acute cardiovascular complication.

●In the MANAGE trial, all-cause mortality at 16-month follow-up was 13 percent in the placebo group [25]. (See 'Acute treatment' above.)

●In a report from the VISION study, death within 30 days occurred in 4.1 percent of patients with MINS, whereas it was 0.6 percent in patients without MINS [7]. An absolute change between any two postoperative hs-cTnT levels of 5 ng/L or more was independently associated with an increase in 30-day mortality (adjusted HR 4.69, 95% CI 3.52-6.25). Compared with a reference group (peak hs-cTnT <5 ng/L), patients with peak postoperative hs-cTnT levels of 20 to less than 65 ng/L, 65 to less than 1000 ng/L, and 1000 ng/L or higher had 30-day mortality rates of 3.0, 9.1, and 30 percent (adjusted HR 23.63, 70.34, and 227.01, respectively). Mortality at one year was significantly higher in patients with MINS (22.5 versus 9.3 percent, respectively).

●Similarly, in a 2011 meta-analysis of 15 studies (over 4000 patients) of various types of noncardiac surgery with follow-up ranging between 3 and 48 months, an elevation of either troponin or creatine kinase MB fraction was associated with a significantly increased risk of all-cause mortality (adjusted OR 3.4, 95% CI 2.2-5.2, and 2.5, 95% CI 1.5-4.0, respectively) [27].

Other markers of postoperative risk — Elevated perioperative B-type natriuretic peptide (BNP) level is also associated with cardiovascular outcomes after surgery:

●In a multivariable analysis of 10,402 patients who participated in a VISION substudy, higher N-terminal pro-BNP (NT-proBNP) values were associated with a higher risk of vascular death or MINS [15].

●In a 2013 meta-analysis of 18 studies (n = 2051) in which BNP was sampled less than seven days after surgery, a BNP level ≥245 pg/mL or an NT-proBNP level ≥718 pg/mL was associated with an increased risk of death or nonfatal myocardial infarction at 30 days (adjusted OR 4.5, 95% CI 2.74-7.4) [28].

A subsequent analysis of these 18 studies found that the addition of a preoperative BNP had increased prognostic value compared with isolated postoperative BNP levels [29].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Perioperative cardiovascular evaluation and management".)

SUMMARY AND RECOMMENDATIONS

●Evaluation

•Suspected myocardial infarction – In patients who present with typical signs or symptoms of myocardial infarction after surgery, the evaluation of these findings is similar to that in patients who present with typical signs or symptoms of myocardial infarction in other settings. (See "Evaluation of the adult with chest pain in the emergency department".)

•Elevated screening troponin – In patients who underwent postoperative screening and have an elevated troponin, the approach to evaluation is similar to patients who have other signs or symptoms of myocardial infarction. We obtain an ECG, chest radiography, and repeat troponin in two to three hours. (See 'Elevated surveillance troponin' above.)

In addition to these tests for myocardial infarction, we obtain other tests to evaluate for other causes of elevated troponin (eg, pulmonary embolism) appropriate for patients who recently had surgery. (See 'Differential diagnosis' above.)

•Role of additional testing – In patients in whom the diagnosis remains uncertain after evaluation of symptoms, ECGs, and repeat troponin assays, additional noninvasive studies (eg, echocardiography, radionuclide myocardial perfusion imaging) may be required to confirm or exclude the presence of myocardial injury. (See 'Additional testing' above and 'Long-term management' above.)

When patients diagnosed with myocardial injury after noncardiac surgery (MINS) recover from surgery, it is reasonable to obtain stress or anatomic imaging to assess for obstructive coronary artery disease (CAD) unless another clear explanation or an elevated troponin level is present.

●Diagnosis

•Myocardial injury after noncardiac surgery – The diagnosis of MINS requires that two major criteria are met (see 'Diagnosis' above):

-The presence of noncardiac surgery in the last 30 days and an elevated troponin level with a trend in troponin levels indicative of acute injury (eg, fall, rise) are required to establish the diagnosis of MINS.

-Nonischemic causes (eg, sepsis, pulmonary embolism, cardioversion) of troponin elevation were reasonably excluded.

●Perioperative surveillance

•Risk assessment – For the purposes of screening, risk factors for MINS include (see 'Risk assessment' above):

-Age ≥65 years.

-Patients ≥45 years of age who will undergo in-hospital surgery and who have one or more other risk factors from the revised cardiac risk score (table 1).

-Patients with known atherosclerotic disease (eg, CAD, aortic plaques, peripheral vascular disease).

•High-risk patients – Patients with any of the factors listed above are at high risk of MINS. In this population of patients, we suggest postoperative surveillance with troponin levels rather than no surveillance. Postoperative surveillance consists of troponin assays obtained 6 to 12 hours after surgery and on postoperative days 1, 2, and 3. (See 'High-risk patients' above.)

Other surveillance tests (eg, preoperative troponin levels, perioperative ECG and B-type natriuretic peptide [BNP]) are controversial.

•Other patients – In patients who will undergo outpatient surgery (ie, will not stay in the hospital for at least one day) or will undergo inpatient surgery but who do not have high-risk features for postoperative myocardial injury, we do not perform perioperative surveillance testing for MINS. (See 'Other patients' above.)

●Acute treatment

•ST-elevation myocardial infarction – In patients with perioperative ST-elevation myocardial infarction (STEMI) in whom the risk of bleeding with anticoagulation is acceptable, the approach to STEMI management is similar to that in other patients with STEMI. In patients whose risk of bleeding is excessively high, medical therapy (eg, anticoagulation) and the use of angiography and percutaneous coronary intervention (PCI) are individualized. (See "Overview of the acute management of ST-elevation myocardial infarction".)

In most patients with perioperative STEMI, fibrinolytic therapy is not safe.

•NSTEMI – In patients with perioperative non-ST-elevation myocardial infarction (NSTEMI), the choice of treatment strategy is individualized. In particular, the decisions to anticoagulate, treat with a P2Y₁₂ inhibitor, or proceed with coronary angiography with appropriate PCI depend on the patient's risk of bleeding. Additional factors influence the approach to treatment. (See 'Non-ST-elevation myocardial infarction' above.)

•Myocardial injury after noncardiac surgery – In patients with MINS who do not have NSTEMI or STEMI, we suggest treatment with aspirin and a statin rather than no therapy or a regimen containing other agents (Grade 2C). In patients with tachycardia or hypertension, beta blockers and renin-angiotensin-aldosterone system (RAAS) inhibitors (eg, angiotensin converting enzyme [ACE] inhibitors) are options for therapy. P2Y₁₂ inhibitors are not used to treat patients with MINS who do not have myocardial infarction and did not undergo PCI.

Some of the contributors to this topic treat patients with MINS who have a low bleeding risk with low-dose dabigatran for two years, while others do not routinely treat with an anticoagulant. (See 'Myocardial injury after noncardiac surgery' above.)

●Long-term management – In patients with MINS who do not have evidence of NSTEMI or STEMI, we typically schedule the patient for follow-up in clinic within two weeks of discharge. In most patients with MINS, we obtain stress imaging or anatomic imaging to assess or exclude CAD. (See 'Long-term management' above and "Selecting the optimal cardiac stress test" and "Clinical use of coronary computed tomographic angiography", section on 'Patients with acute symptoms'.)

ACKNOWLEDGMENTS — The UpToDate editorial staff acknowledges Jonathan B. Shammash, MD, Stephen E. Kimmel, MD, MS, and Scott Solomon, MD, who contributed to an earlier version of this topic review.