Perioperative myocardial injury

Learning objectives.

By reading this article, you should be able to:

• •Describe the definitions of PMI and the proposed pathophysiological mechanisms leading to cardiac troponin release.
• •Discuss the importance of PMI as a postoperative complication and the challenges posed by preventative and therapeutic measures.
• •Review the current guidance on perioperative troponin surveillance and its impact on patients.

Key points.

• •Perioperative myocardial injury (PMI) is always diagnosed by increased postoperative troponin, but there is no standardised definition.
• •The underlying mechanism(s) are likely to be numerous and may interact, including supply and demand imbalance.
• •Perioperative myocardial injury is common, with an incidence of around 20% in high-risk patients undergoing non-cardiac surgery.
• •Perioperative myocardial injury is associated with increased postoperative morbidity and mortality.
• •There are no current definitive preventative or management strategies for PMI.

Perioperative myocardial injury (PMI) is a recognised cardiovascular complication of non-cardiac surgery associated with poor postoperative outcomes. Myocardial injury is diagnosed by a change in cardiac troponin (cTn) concentrations indicating cardiomyocyte damage. Despite recent attempts to determine a standardised definition, many different methods of identification exist with differing pathophysiological foundations. This article reviews the current definitions, pathophysiological mechanisms and outcomes of PMI, and also considers existing recommendations for surveillance and potential treatment.

Cardiac troponins

Within the cardiomyocyte contractile apparatus, the troponin complex consists of three proteins: troponin C, which binds to calcium; troponin T (TnT), which connects the troponin complex to tropomyosin allowing myosin and actin binding; and troponin I (TnI), which inhibits ATP activity when bound to actin. Through these actions the troponin complex facilitates the contraction and relaxation of cardiac muscle. Within the cardiomyocyte the majority of troponin is bound to the sarcomere, but a very small percentage is free. Cardiac troponins are encoded differently to skeletal muscle troponins, hence are a specific marker for cardiomyocyte damage.^1,2

Definitions and diagnosis

Although consistently described by perioperative increase in cTn concentrations indicating cardiomyocyte damage, the definition of PMI varies throughout the literature. The two most common definitions are ‘myocardial injury after non-cardiac surgery’ (MINS)^3,4 and ‘post/perioperative myocardial injury’ (PMI); however, within these definitions the specific assays, cut-offs and measurement time points vary between different study-specific definitions. In part, these cut-offs reflect underlying assumptions concerning the pathophysiology (Fig. 1).

Fig 1.

Flowchart indicating different criteria for the definitions of PMI/MINS. The difference in definitions whereby some mandate the demonstration of ischaemia whereas others mandate the exclusion of ischaemia reflects the variation within the literature where, depending on definition, potentially different mechanisms of increased cTn concentrations are being investigated. Figure created by the authors using BioRender®.

Myocardial injury after non-cardiac surgery as per VISION group

The largest study to investigate increased postoperative cTn and define MINS was the Vascular events In non-cardiac Surgery patIents cOhort evaluatioN (VISION) trial, an international prospective cohort study of more than 40,000 patients. The initial VISION report on the first 15,000 patients recruited demonstrated that peak cTnT in the first 72 h after surgery was an independent predictor of 30-day mortality.⁵ This definition of MINS was further updated in 2017 and defined as myocardial injury judged to result from ischaemia occurring within 3 days of surgery and identified by a high-sensitivity TnT (hs-TnT) assay > 20 ng L⁻¹.⁴ By this definition, to diagnose MINS, myocardial ischaemia does not necessarily need to be demonstrated, but there must be ‘no evidence of a non-ischaemic cause’ for the increased troponin. Non-ischaemic causes of increased troponin concentrations were described as including rapid atrial fibrillation, pulmonary embolus or sepsis, which were adjudicated by study investigators at the lead centre.

American Heart Association

The American Heart Association (AHA) released a scientific statement in 2021 with their definition of MINS including both myocardial infarction and myocardial injury that does not fulfil all criteria for the Fourth Universal Definition of Myocardial Infarction—a troponin increase without ischaemic symptoms, ECG changes or imaging evidence of myocardial ischaemia or thrombus.^6,7 Therefore, MINS as defined by the AHA includes a postoperative cTn (T or I) above the 99th percentile upper reference limit (URL) with an acute change occurring in the first 30 days (but typically within 72 h) of surgery, attributable to a presumed ischaemic mechanism in the absence of an overt non-ischaemic cause. Clinical signs of ischaemia are not required as (described by the AHA) they may be masked by sedation or postoperative analgesia.

Fourth Universal Definition of Myocardial Infarction

The Fourth Universal Definition of Myocardial Infarction provides a different definition of PMI, namely that PMI can have any cause, including extracardiac. Myocardial injury is defined as an increased troponin concentration with at least one value above the 99th percentile URL and is considered acute if there is an increase or decrease in cTn of ≥ 20% from baseline. To distinguish myocardial injury from myocardial infarction, the absence of myocardial ischaemia (e.g. no chest pain or ischaemic changes on ECG) needs to be demonstrated.⁷ This definition does not state a postoperative timeframe for increased cTn to be defined as perioperative.⁷

Conversely, acute myocardial infarction is diagnosed where there is an acute change in troponin with at least one value above the 99th URL plus clinical evidence of myocardial ischaemia,⁷ namely at least one of the following⁷:

• (i)symptoms of myocardial ischaemia;
• (ii)new ischaemic ECG changes;
• (iii)development of pathological Q waves on ECG;
• (iv)imaging evidence of new loss of viable myocardium or new regional wall motion abnormality (RWMA) consistent with ischaemic aetiology (echocardiography, MRI);
• (v)identification of coronary thrombus by angiography or autopsy (type 1 MI only)

Acute myocardial infarction is classified into three different types:

• (i)type 1: secondary to atherothrombotic coronary artery disease, usually precipitated by atherosclerotic plaque disruption leading to reduced blood supply to the myocardium;
• (ii)type 2: secondary to mismatch between the oxygen supply and demand of the myocardium;
• (iii)type 3: sudden cardiac death associated with symptoms or signs of myocardial ischaemia.⁷

BASEL-PMI definition

Puelacher and colleagues characterised perioperative MINS in 2018 as part of the BASEL-PMI study, a prospective diagnostic study involving 2018 consecutive patients undergoing non-cardiac surgery with a planned postoperative stay > 1 day and at increased cardiovascular risk.⁸ Differing from the other definitions, they define PMI as an absolute increase in hs-TnT of ≥ 14 ng L⁻¹ above baseline within 7 days of surgery without the need for consideration of the mechanism, that is, injury could be diagnosed regardless of whether the mechanism was perceived to be ischaemic or non-ischaemic.

Standardized Endpoints in Perioperative Medicine

The Standardized Endpoints in Perioperative Medicine – Core Outcome Measures in Perioperative and Anaesthetic Care initiative (StEP-COMPAC) advocate the use of the term PMI to describe a troponin increase in excess of the 99th percentile URL (in the absence of overt ischaemia) regardless of mechanism.⁹ This delineates between recognising infarction, which has clearly defined management strategies, and injury, which is recognised to be a marker of higher postoperative risk but without proven treatment options. There is no postoperative timeframe specified. Most of the increased postoperative troponin concentrations may occur within the first 2 days of surgery with early (within 24 h) increases associated with morbidity as defined by the postoperative morbidity survey within 72 h of surgery.¹⁰

In the perioperative period, clinical symptoms of myocardial ischaemia may be masked by analgesia or sedation. Therefore, there may be more of a reliance on cardiac imaging techniques to identify potential infarction (if myocardial injury has been identified via cTn surveillance). None of the definitions for PMI rely on the ruling out of infarction by performing invasive imaging techniques. This is likely to be related to the high incidence of PMI and limited resources for definitive cardiac imaging, plus potential risks to patients such as with coronary angiography. With the increasing use of perioperative transthoracic echocardiography, there could be the potential to rule out RWMA in patients with increased perioperative cTn. However, currently no guidelines support the routine use of perioperative transthoracic echocardiography in these patients, and with a lack of large-scale prospective imaging studies describing ‘normal’ postoperative appearances, nor the significance of RWMA after surgery, and a lack of tested therapies in this situation, caution must be urged; in the absence of evidence suggesting benefit, there is real potential to do harm by pursuing diagnosis and management of perioperative infarction in all patients with PMI. Perioperative right ventricular dysfunction, for example, appears to occur not uncommonly, but the implication for patients are unclear.¹¹ Throughout this article, PMI will be used as an umbrella term for increased cTn within the perioperative period. Specific definition terms will be used where applicable and as described within the literature reported.

Incidence

The pivotal VISION study defining MINS demonstrated an incidence of 8% (95% confidence interval [CI] 7.5–8.4%) in patients aged ≥ 45 yrs undergoing a range of non-cardiac surgeries.³ As the definition of PMI has become arguably looser, without necessarily demonstrating myocardial ischaemia (as with MINS) or excluding cases where there is evidence of extracardiac causes of increased cTn values, the incidence of PMI in the perioperative literature has increased. However, there is significant variability depending on the population and surgical risk studied. A recent systematic review and meta-analysis investigating MINS as defined by the AHA demonstrated an overall pooled incidence of 17.9% (95% CI 16.2–19.6%) in 530,867 surgeries in 169 reports. The pooled incidence of MINS in a cohort of studies judged high quality was 19.5% (95% CI 17.8–21.3%).¹² Very few of these studies had preoperative troponin measurements, limiting their interpretation and generalisability.

Troponin assay

High-sensitivity assays measure cTn blood concentrations some five to ten times lower than non-high-sensitivity assays, so they can detect myocardial injury at lower troponin concentrations and also allow for identification of the 99th percentile URL.¹³ The sensitivity of cTn measured appears to alter the incidence of MINS. The pooled incidence of MINS when hs-TnT was measured was 24.7% (95% CI 19.7–29.9%, n = 10 studies), compared with 17.4% (95% CI 14.9–20.0%, n = 40 studies) and 20.1% (95% CI 16.8–23.6%, n = 79 studies) when (non-high-sensitivity) TnT or TnI were measured.¹² There also appears to be a difference in PMI incidence depending on whether TnT or TnI are measured: the incidence of PMI is 6.1% (95% CI 5.3–6.9%) when measured using hs-TnI (99th URL of 26 ng L⁻¹) but higher when measured using hs-TnT (11.3%, 95% CI 10.2–12.4%) with a 99th URL of 14 ng L⁻¹.¹⁴

Risk factors

Patients with MINS tend to be older, male and more likely to have hypertension, coronary artery disease, prior myocardial infarction, heart failure and kidney disease, which are typical cardiovascular risk factors. Patients undergoing emergency surgery are also more likely to experience MINS (RR 1.74; 95% CI 1.35–2.25). There is also variation in the incidence of MINS in patients undergoing different surgical specialties: general surgical patients have the highest incidence (25.9%; 95% CI 15.1–38.4%), whereas orthopaedics have the lowest (18.0%; 95% CI 12.1–24.7%).¹²

Mechanism

Release of cardiac troponin

For cTn to be detectable within blood, there needs to have been a degree of cardiomyocyte damage leading to cTn release. There are different potential pathways through which this may occur.² Cardiomyocyte necrosis caused by either type 1 or type 2 myocardial infarction leads to the release of large covalent cTn complexes as there is complete disruption of the sarcolemma. However, non-necrotic pathways such as intracellular proteolysis or increased sarcolemma permeability cause smaller cTn fragments to be present in the blood. Inflammation is also a proposed mechanism for intracellular proteolysis of cTn complexes. Increased sarcolemma permeability has been demonstrated in cases of cardiomyocyte stress and inflammation via TNF-α pathways. Current cTn assays cannot distinguish between large covalent troponin complexes released after cell necrosis and the smaller cTn fragments.

Ischaemic mechanisms

Postoperative myocardial infarction

Myocardial ischaemia is defined as inadequate blood supply to cardiac tissue. It may be inadequate because of reduced blood flow (type 1 mechanism) or result from tissue hypoxia with blood supply not matching the oxygen demand (type 2 mechanism). Infarction is the loss of cardiac tissue and is predominantly classified into that with a type 1 mechanism (e.g. atherothrombosis) or a type 2 mechanism (e.g. pathological tachycardia). Myocardial ischaemia may or may not lead to infarction. There cannot be myocardial infarction without myocardial injury, but there can be myocardial injury without infarction; accordingly, the incidence of postoperative MI is relatively low (4.1%; 95% CI 1.8–6.4% in men with coronary artery disease) when compared with the incidence of PMI.¹⁵

In the non-operative setting, atherothrombosis is the primary cause of MI. However, more than 70% of perioperative MI is attributed to a type 2 mechanism secondary to intraoperative hypotension, hypoxia, tachycardia or anaemia.¹⁶ A recent angiographic study in 30 patients with postoperative MI and 30 matched patients with non-operative MI found a thrombus at the culprit lesion in only 13.3% of the postoperative MI group compared with 66.7% of the non-operative MI group.¹⁷ The Coronary CTA VISION study showed that perioperative myocardial infarction occurred in patients both with and without preoperative coronary artery disease.¹⁸

Myocardial injury

Myocardial injury after non-cardiac surgery is presumed to be caused by an ischaemia (the majority attributed to type 2 ischaemia), with no evidence of an overt non-ischaemic cause. Similar rates of coronary artery disease have been demonstrated in patients with and without MINS who underwent cardiac computed tomography after major non-cardiac surgery.¹⁹ Also, trials investigating potential therapies for PMI using conventional acute coronary syndrome management, such as aspirin or statins, have not demonstrated improvements in outcome, which might have been anticipated if coronary artery disease were the underlying cause.^12,20

The hypothesis of type 2 ischaemia being the main mechanism behind PMI is being challenged however, with recent studies demonstrating the robustness of coronary artery autoregulation and myocardial perfusion–contraction coupling.² For type 2 ischaemia to occur, these compensatory mechanisms need to fail. This is certainly a risk in the perioperative period, but a more complex, systemic process has been suggested as discussed below.²

Non-ischaemic mechanisms

There are multiple mechanisms through which cardiomyocytes may release cTn in the absence of ischaemia. Via the cTn release pathways described above, the non-ischaemic causes can be classified into systemic inflammation, haemodynamic strain and autonomic dysfunction, with complex interactions between these mechanisms (Fig. 2).

Fig 2.

Proposed mechanisms of PMI. Dashed lines indicate detrimental interaction between mechanisms. Figure created by the authors using BioRender®.

There is increasing interest in the role of systemic inflammation in the perioperative period. An increased preoperative neutrophil–lymphocyte ratio (a marker of established systemic inflammation) was associated with PMI (OR 2.56; 95% CI 1.92–3.41) in more than 1600 patients undergoing elective non-cardiac surgery.²¹ In addition to preoperative inflammation, the surgical stress response elicits a state of hyper-catabolism and pro-inflammation via sympathetic stimulation. Bioinformatic interrogation of circulating microRNAs associated with acute coronary syndrome in the postoperative period suggests that PMI is a consequence of deficient cardioprotective mechanisms in the face of adrenergic stress and calcium overload.²²

Other mechanisms that may cause increased cTn in the absence of oxygen deficit include increased mechanical stress on the heart, including both increased preload and afterload. Increased preload, such as excessive intraoperative fluids, cause myocardial stretch, and acute heart failure is associated with PMI.¹⁶ Increased left ventricular afterload may be caused by catecholamine release secondary to the surgical stress response. Pulmonary embolus, increasing right ventricular afterload, is a common perioperative complication found in 33% of patients with postoperative MI and 20% of patients without postoperative MI.²³ During the perioperative period, increased pulmonary vascular resistance resulting from mechanical ventilation, lung injury, hypoxia or hypercarbia could potentially exert mechanical stress contributing to PMI.

Autonomic dysfunction has detrimental effects on coronary microvascular tone, worsens baroreflex function, causes tachycardia and is proinflammatory, all of which can lead to cardiomyocyte damage. There is increasing evidence that autonomic nervous system dysfunction is associated with PMI.^24,25 Preserving or restoring vagal function can limit myocardial injury (in laboratory models).²⁶

Overall, the mechanisms behind PMI are complex and likely to incorporate both the systemic effects of surgical stress and local cardiac effects, such as increased mechanical stress and a degree of oxygen supply and demand mismatch. All of these interlinking mechanisms (Fig. 2) are likely to have a detrimental effect on patients predisposed to myocardial injury.

Outcomes

Perioperative myocardial injury has been consistently associated with poor postoperative outcomes, regardless of mechanism. In-hospital mortality was reported in 25 studies as 8.1% (95% CI 4.4–12.7) in patients with MINS vs 0.4% (95% CI 0.2–0.7) in patients without (p < 0.001). Furthermore, 30-day and 1-yr mortality were also significantly higher in patients with MINS than in patients without MINS (8.5% [95% CI 6.2–11.0%] vs 1.2% [95% CI 0.9–1.6], p < 0.001 and 20.6% [95% CI 15.9–25.7] vs 5.1% [95% CI 3.2–7.4], p < 0.001, respectively).¹² Longer-term data are lacking but pooled mortality incidence from 11 studies ranging from 2- to 7-yr follow-up demonstrated mortality of 42.7% (95% CI 33.8–51.8) among patients with MINS vs 19.7% (95% CI 10.6–30.9) in patients without MINS (p < 0.001).¹² It is important to remember that within the literature reporting MINS, there may be conflation between PMI and MI. A secondary analysis of the Evaluation of Nitrous Oxide in Gas Mixture of Anesthesia (ENIGMA-II) trial evaluated the incidence of postoperative complications for patients with PMI (defined as increased postoperative troponin concentrations). Logistic regression models showed that PMI was associated with reduced disability-free survival at 1 yr (OR 1.6; 95% CI 1.2–2.0).²⁷

The BASEL-PMI study is an ongoing programme of active PMI surveillance for high-risk patients undergoing major non-cardiac surgery. Over a 1-yr period they found that 9.8% (95% CI 6.8–14.0) of patients with PMI died 30 days after surgery compared with 1.6% (95% CI 1.1–2.4) who did not develop PMI (p < 0.001). At 1 yr, 22.5% (95% CI 17.9–27.8) of patients who developed PMI had died compared with 9.3% (95% CI 8.0–10.8, p < 0.001) of patients who did not develop PMI (Fig. 3).⁸ Recently the BASEL-PMI investigators aimed to characterise the outcome of PMI (as per BASEL-PMI definition) by the perceived cause of PMI. All patients diagnosed with PMI (1016/7754) underwent investigations and clinical adjudication to identify the cause of the PMI. Postoperative outcomes differed by aetiology: PMI caused by acute heart failure demonstrated the highest incidence of postoperative major adverse cardiovascular events at 1 yr (56% [38–70%]) and 1-yr mortality (49% [30–62%]), followed by tachyarrhythmias (49% [34–75%] and 40% [25–53%], respectively), extracardiac causes (30% [20–47%] and 35% [22–46%], respectively), type 1 MI (37% [24–47%] and 28% [17–38%], respectively) and type 2 MI (17% [14–20%] for both).¹⁶ In this study over 70% of PMI was adjudicated as type 2 MI, as expected within the perioperative period.

Fig 3.

Mortality of PMI. Cumulative all-cause mortality within 30 days (A) and 1 yr (B), shown for patients with (red) and without (black) PMI.⁸ Reproduced with permission.

Prevention of PMI

The patient-related risk factors for PMI appear to be the same for other perioperative cardiovascular complications. Preoperative optimisation of these risks such as cardiovascular disease optimisation, lifestyle interventions such as increased exercise, alcohol and smoking cessation may reduce the risk of PMI, as recommended by the European Society of Cardiology/European Society of Anaesthesiology (ESC/ESA) guidelines on cardiovascular assessment and management might therefore reasonably be expected to confer reduced risk.²⁸ However, there is no evidence that these interventions specifically reduce the risk of PMI. Similarly, the proposed mechanisms for PMI development include autonomic dysfunction, systemic inflammation and oxygen supply and demand imbalance. Therefore, anaesthetic conduct may also have an impact on the development of PMI, and avoidance of hypotension, anaemia, hypoxia and tachycardia would be expected to reduce the risk in vulnerable patients, again however there is no evidence to suggest this is the case. Good postoperative analgesia might also be hypothesised to have a positive impact on these processes. Proposed preventative strategies are predominantly focussed on prevention of perioperative myocardial ischaemia, with medications commonly used in the secondary prevention of acute coronary syndromes most studied:

Aspirin

There are a few small studies investigating the effect of aspirin on MINS with variable and inconclusive results.¹² The PeriOperative ISchaemic Evaluation (POISE)-2 trial demonstrated that aspirin did not reduce the incidence of postoperative myocardial infarction compared with placebo (HR 1.08; 95% CI 0.93–1.26) but did not investigate PMI as an outcome.²⁹

Statins

Despite a potentially positive subanalysis of the VISION study and suggestive smaller observational studies indicating that statin use may be beneficial in preventing MINS, Smilowitz and colleagues did not find any association between statin use and MINS in a pooled analysis of 25 studies.^12,30

Angiotensin-converting enzyme inhibitors/angiotensin-II receptor blockers

In a pooled analysis of 18 observational non-randomised studies, an association was reported between perioperative use of angiotensin-converting enzyme inhibitors (ACE-I) or angiotensin-II receptor blockers (ARBs) and increased incidence of MINS (pooled RR 1.29; 95% CI 1.11–1.51). However, the Stopping Perioperative ACE-inhibitors or angiotensin-II receptor blockers (SPACE) study, a recent randomised controlled trial (RCT), found no difference in PMI incidence (defined as an acute change in cTnT within 48 h of surgery with no investigation of underlying cause) between patients randomised to continue their ACE-I/ARBs and patients randomised to discontinue these medications before surgery (OR 0.77; 95% CI 0.45–1.31).

Beta-blockers

Beta-blocker use was associated with an increased risk of MINS in a pooled analysis of 27 observational studies.¹² However, there were conflicting findings between these studies. The largest study, a case-control analysis in patients undergoing vascular surgery, found that acute preoperative beta-blockade was an independent predictor of increased cTnI (OR 6.0; 95% CI 3.1–11.5). A recent prospective cohort study in more than 10,000 patients by the BASEL-PMI group sought to clarify the role, if any, of preoperative beta-blockade on PMI.³¹ Established preoperative use of beta-blockers was not associated with PMI (judged to result from cardiac causes) within 3 days of major cardiac surgery (weighted OR 0.97; 95% CI 0.87–1.04). There was also no association with beta-blockers and longer-term cardiovascular complications, including death at 365 days. The impact of acute perioperative block was not investigated.

Haemodynamic management

Intraoperative hypotension, specifically a systolic blood pressure <90 mmHg, has been associated with PMI³² theoretically caused by reduced coronary artery perfusion. Hypotension itself may not cause PMI (unless very severe) as cardiac autoregulation can maintain coronary blood flow despite low perfusion pressure and that reduced left ventricular afterload reduces myocardial oxygen demand.² The POISE-3 trial randomised more than 7000 non-cardiac surgery patients to either undergo a hypotension-avoidance strategy or a hypertension-avoidance strategy.³³ The primary outcome was a composite of vascular death and MINS (not defined), stroke and cardiac arrest within 30 days of surgery. There was no difference in primary outcomes between the two groups (HR 0.99; 95% CI 0.88–1.12) and no difference in any secondary or tertiary outcomes.

Management of PMI

The only trial to investigate potential treatment of MINS is the Management of Myocardial Injury After Non-cardiac Surgery (MANAGE) trial, a large international RCT that recruited more than 1700 patients.³⁴ Patients diagnosed with MINS (as per VISION) were randomly assigned to either dabigatran 110 mg twice daily or matched-placebo within 35 days of MINS diagnosis, and followed up for up to 2 yrs. The primary endpoint was a major vascular complication (vascular mortality, myocardial infarction, non-haemorrhagic stroke, peripheral arterial thrombosis, amputation and venous thromboembolism [VTE]). The investigators describe choosing dabigatran as it is an oral direct thrombin inhibitor shown to prevent perioperative VTE, potentially reducing the risk of other postoperative cardiovascular complications. Dabigatran was associated with a 28% reduction in the primary endpoint with no associated increase in bleeding after a mean of 16 (sd 7) months. A potential limitation to the generalisability of the study is the strict exclusion criteria, including patients whom the surgeon was concerned about bleeding risk. The composite primary outcome was very broad with VTE and amputation added during recruitment, with a revised recruitment target and a high number of patients in both groups discontinuing the treatment. When the primary outcome was divided into its composite parts, non-haemorrhagic stroke demonstrated the only significant difference between the two cohorts; however, the incidence of VTE was also twice as high in the placebo group compared with the dabigatran group. Although indicative that dabigatran is safe to use in a carefully selected cohort of postoperative patients, more work is required to ascertain both the longer-term effects and specific mechanism through which it reduces postoperative vascular complications and whether it has any specific therapeutic effect on PMI.

The AHA recommends postoperative coronary angiography only in very high-risk patients diagnosed with MINS (e.g. those with markedly increased cTn concentrations or confirmed postoperative myocardial infarction).⁶ As discussed above, most PMI is attributed to a type 2 mechanism rather than atherosclerotic plaque rupture and studies have shown that only a small proportion of patients with postoperative myocardial infarction require either percutaneous coronary intervention or coronary bypass grafting.³⁵ Because of the risks of bleeding with invasive angiography, the indication and timing of this procedure after surgery need to be carefully considered. However, a diagnosis of PMI does highlight that patients are at high cardiovascular risk, and so should act as a trigger for subsequent investigation and management of cardiovascular risk factors once out of the immediate postoperative period.⁶

Current recommendations

There are currently three international association guidelines recommending routine measurement of perioperative cTn for PMI surveillance; within these there is variation between the recommended timings of cTn measurement and limited discussion, if any, of action recommended in the event of PMI diagnosis.^6,28,36 Broadly, the European Society of Anaesthesiology and Intensive Care recommends consideration of cTn measurement in high-risk patients both before and after surgery.²⁸ The Canadian Cardiovascular Society recommends cTn measurement in high-risk patients with a raised NT-ProBNP and then daily cTn measurement up to 3 days after surgery with a postoperative ECG in these patients.³⁶ The AHA recommends postoperative cTn measurements in the first 2–3 days of surgery.⁶ A recent review by Chew and colleagues³⁷ provides discussion of the rationale and current implementation of perioperative troponin surveillance.

The Canadian Society is the only body to make recommendations regarding therapy in the event of PMI diagnosis. They recommend starting aspirin and a statin after PMI is diagnosed. However, as detailed above, there is little evidence to support this recommendation.

Conclusions

Perioperative myocardial injury is associated with poor postoperative outcomes but is potentially preventable to some degree. However, research and practice are confounded by differing definitions and different theorised aetiological mechanisms. International guidelines recommend perioperative troponin surveillance in order to recognise PMI, but unfortunately evidence for pharmaceutical interventions is currently lacking. A standardised definition will help future studies investigate the underlying mechanisms and potential therapies for this important perioperative complication.

Declaration of interests

The authors declare that they have no conflicts of interest.

MCQs

The associated MCQs (to support CME/CPD activity) will be accessible at www.bjaed.org/cme/home by subscribers to BJA Education.

Biographies

Cara Hughes MSc FRCA is a clinical research fellow at the University of Glasgow, completing an MD by research on perioperative risk prediction with perioperative myocardial injury as the primary outcome.

Gareth Ackland PhD FRCA FFICM is a reader in perioperative medicine and NIHR advanced fellow in translational medicine and therapeutics at the William Harvey Research Institute, and an honorary consultant in anaesthesia and perioperative medicine at the Royal London Hospital, London. He has published extensively on PMI.

Ben Shelley FRCA FFICM MD is a consultant in cardiothoracic anaesthesia at the West of Scotland Heart and Lung Centre, which includes the Scottish Pulmonary Vascular Unit, the Scottish National Advanced Heart Failure Unit (including mechanical circulatory support and cardiac transplantation).

Matrix codes: 1A01, 2A03, 3A03