Myocardial injury, defined as an increase in cardiac troponins (cTn), is a common syndrome in peri-operative high-risk surgical populations with an estimated pooled incidence of 19.6% (confidence interval [CI] 17.8−21.4) [1]. As the vast majority of patients with myocardial injury in the peri-operative period will be asymptomatic, reliable detection of myocardial injury is only possible with active surveillance strategies, most commonly done with serial cTn measurements. Myocardial injury during the peri-operative period is prognostically important for short- and long-term mortalities [2,3,4,5] and adverse cardiovascular outcomes [3,4,5] regardless of whether criteria for acute myocardial infarction are fulfilled [4, 5]. Although the prognostic value of perioperatively increased cTn has been established, its ability to distinguish at individual level between patients with and without later events (predictive value), remains under-investigated [6].

Etiology

Myocardial injury during the peri-operative period is a heterogeneous syndrome reflecting different pathophysiologies (ischemic and non-ischemic, cardiac and extra-cardiac) and carrying different prognoses. Relevant peri-operative cardiac complications are type 1 and 2 myocardial infarction, arrhythmias, heart failure, or pulmonary embolism, which are associated with acute myocardial damage [4, 7]. Therefore, etiological distinction of the causes of peri-operative myocardial injury (PMI) is the key for management. In a large, prospective study among patients with increased cardiovascular risk undergoing major inpatient non-cardiac surgery (NCS), the etiology of PMI was extra-cardiac (e.g., sepsis) in 11% of patients, while acute myocardial infarction (AMI), tachyarrhythmias, and acute heart failure (AHF) occurred in 7%, 5%, and 4% respectively [4]. A majority of PMI were attributed to ‘likely Type II myocardial infarction (lT2MI)’. While the classification process in this paper requires confirmation, the main finding was that outcomes differ according to etiology: major adverse cardiovascular events occurred in 51%, 41%, 57%, 64%, and 25% of patients with extra-cardiac PMI, Type 1 AMI, tachyarrhythmia, AHF, and lT2MI respectively and one-year mortality was 38%, 27%, 40%, 49%, and 17%, compared to 7% and 9% in patients without PMI.

Management

Since peri-operative myocardial injury is attributable to multifactorial causes, personalized, etiology-driven management of myocardial injury rather than a ‘one-size fits all’ management strategy seems reasonable. Pending evidence-based alternatives, the diagnostic algorithms proposed by the European Society of Cardiology [8] offer a pragmatic approach for clinicians. Increased levels should prompt an etiological investigation. A suggested hierarchical algorithm [4] is to exclude extra-cardiac causes followed by identification of cardiac pathology. Pathologies, such as sepsis, AMI, tachyarrhythmias, and AHF, have specific management pathways, and these should be adhered to with special consideration for specific risks such as post-surgical bleeding. A proposal for management of patients with confirmed myocardial injury is shown in Fig. 1.

Fig. 1
figure 1

Suggested management strategy in patients with myocardial injury. Myocardial injury is defined as an increase in high-sensitivity cTn above the 99th percentile upper reference limit (URL) of a normal health population. The increase may be preoperative, which should prompt the perioperative physician to determine the acuity of the illness (e.g., by symptoms and signs, electrocardiography, echocardiography, further testing). Acute increases due to some pathologies e.g., acute myocardial infarction, acute heart failure, sepsis, acute pulmonary embolism have established treatment guidelines which should be followed. If the cTn increase is deemed to be chronic (no dynamic changes), pre- and peri-operative optimization of cardiovascular pharmacotherapy, cardiology consultation, anemia management, reconsideration of anesthesia, surgery, and peri-operative management should be considered. A decision to implement post-operative surveillance in high-risk patients may also be made for early detection of peri-operative myocardial injury. Perioperative myocardial injury is defined as an increase in post-operative cTn above baseline values. Increased levels should prompt an etiological investigation. A suggested hierarchical algorithm [4] is to exclude extra-cardiac causes, then specific cardiac pathology. After these have been excluded, Type 2 myocardial infarction (T2MI) is considered likely if the patient has suffered from hypoxia, hypotension or tachyarrhythmias. AMI acute myocardial infarction, AHF acute heart failure, CV cardiovascular, PE pulmonary embolism, T1MI type 1 myocardial infarction, T2MI type 2 myocardial infarction

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To date, only one randomized controlled trial has been conducted in patients after non-cardiac surgery and diagnosed with myocardial injury after non-cardiac surgery due to presumed ischemic causes (MINS) [9]. Dabigatran for 24 months after MINS reduced the incidence of major vascular complications without increasing the risk of life-threatening, critical or major bleeding. However, the incidence of less severe bleeding increased, and 45% of patients discontinued the drug. In a case–control study, patients who suffered peri-operative myocardial infarction or isolated troponin elevation and treated with intensified cardiovascular therapy (antiplatelet drugs, β-blockers, statins, or angiotensin-converting enzyme (ACE) inhibitors) had better one-year survival without a major cardiac event than controls [10]. Conversely, patients who did not receive intensified therapy had an increased hazard of death (hazard ratio [HR] 1.77, CI 1.13–2.42). Retrospective studies suggest that early cardiological intervention may benefit patients with MINS [10, 11]. Among thoracic surgical patients, early cardiology intervention (consultation, pharmacological intervention and risk factor modification) was associated with a reduced risk of early death, but this was no longer significant at 30 days after surgery [11]. Similar results were shown in a large, propensity-matched study of patients undergoing NCS with acute increases in cTn [12]. Cardiology consultation and associated interventions decreased the risk of 30-day mortality, an effect largely driven by a group of patients without cardiac symptoms. Although myocardial injury is prognostically significant, there is insufficient evidence to recommend specific pharmacotherapy or procedures such as directed hemodynamic management, routine high-dependency unit, or admission to the intensive care unit (ICU).

Prevention and early identification of acute peri-operative myocardial injury are at least as important as its treatment. Some centers have already implemented active cTn surveillance in patients with cardiovascular risk factors undergoing intermediate to high-risk surgery [8]. Others have not implemented routine surveillance due to lack of robust data on predictive values, patient-related outcome measures, and biomarker-led management [6]. Regardless of the adopted strategy (active surveillance vs. individualized approach), the final goal is to detect peri-operative complications as early as possible.

A Cochrane review suggested that preoperatively increased cTn provides additional predictive value over validated risk prediction scores [13]. Preoperative cTn may be used for informing patients, for peri-operative planning including cardiovascular optimization, modification of anesthesia and surgical techniques, and to flag at-risk patients where increased post-operative surveillance may be useful. To date, no intervention has demonstrated effectiveness for the prevention of myocardial injury, including transdermal bisoprolol 7 days pre- and post-surgery [14], avoidance of hypo- and hypertension [15], or normothermia maintenance [16].

Studies establishing the discriminatory value of cTn are still lacking. Until such information becomes available, a reasonable plan of action may consist of cTn surveillance among patients with known high-risk of adverse cardiovascular events identified by current risk scoring systems. Early detection should prompt the clinician to look for causes of elevated cTn, (e.g., acute myocardial infarction, acute heart failure, sepsis) some of which will be amenable to treatment using current evidence-based strategies (Fig. 1). Prospective studies of management strategies based on peri-operative cardiac troponin surveillance are currently underway (IMPLEMENT-PMI, NCT05859620).

Take-home message

Increased cardiac troponins are prognostically important for mortality and adverse cardiovascular outcomes in patients undergoing NCS. PMI may be considered as a marker of complications and its early detection should prompt clinicians to look for cardiac and non-cardiac causes. Treatment should be tailored according to etiology.