The pathophysiology of peri‐operative myocardial infarction

Abstract

SummaryIt is generally believed that plaque rupture and myocardial oxygen supply-demand imbalance contribute approximately equally to the burden of peri-operative myocardial infarction. This review critically analyses data of post-mortem, pre-operative coronary angiography, troponin surveillance, other pre-operative non-invasive investigations, and peri-operative haemodynamic predictors of myocardial ischaemia and ⁄ or myocardial infarction. The current evidence suggests that myocardial oxygen supply-demand imbalance predominates in the early postoperative period. It is likely that flow stagnation and thrombus formation is an important pathway in the development of a peri-operative myocardial infarction, in addition to the more commonly recognised role of peri-operative tachycardia. Research and therapeutic interventions should be focused on the prediction and therapy of flow stagnation and thrombus formation. Plaque rupture appears to be a more random event, distributed over the entire peri-operative admission. Patients with or at risk of cardiac disease have a 3.9% (95% CI 3.3-4.6%) risk of suffering a major peri-operative cardiac event [1]. A peri-operative myocardial infarction has an associated in-hospital mortality of 15-25% [1] and an increased risk of subsequent cardiovascular death or myocardial infarction [2].Despite this important prognostic information, there are a number of controversial and poorly understood issues surrounding peri-operative myocardial infarction. There is well established evidence that an increasing heart rate is associated with peri-operative myocardial ischaemia and myocardial infarction [3]. However, substantial evidence suggests that hypotension, hypoperfusion and coagulation are important precipitants of early peri-operative myocardial ischaemia and infarction. Understanding peri-operative myocardial infarction pathophysiology is important in addressing appropriate peri-operative therapies, which in turn have important public health implications. Presentation of peri-operative myocardial infarctionTime of presentation Since the introduction of troponin surveillance, most perioperative myocardial infarctions are identified within the first postoperative day [4], compared with identification between 48 and 72 h when creatine phosphokinase was used. The day of presentation [5][6][7] of a peri-operative myocardial infarction is shown in Fig. 1.Although the majority of peri-operative myocardial infarctions present within the first 4 days of surgery, and nearly 90% by 7 days, the range of presentation is throughout the entire hospital admission [7]. After the seventh postoperative day approximately 1% of perioperative myocardial infarctions present per day [5][6][7].Pattern of presentation of troponin elevation A study of aortic surgical patients identified three patterns of troponin elevation [8]. The first pattern was characterised

Incidence of myocardial injury after non-cardiac surgery: Experience at Groote Schuur Hospital, Cape Town, South Africa

“…[2] Myocardial ischaemia with subsequent injury is strongly associated with perioperative mortality. [3,4] A large multicentre international study in 2012 investigated the mortality associated with perioperative elevated troponin levels in >15 000 patients from North and South America, Australia, Europe and Asia (Vascular Events In Non-cardiac Surgery Patients Cohort Evaluation (VISION) study). [3] The 30-day mortality was found to be independently associated with myocardial injury after non-cardiac surgery (MINS) in a subsequent analysis of the data.…”

Perioperative Implications of Vascular Endothelial Dysfunction: Current Understanding of this Critical Sensor-Effector Organ

“…These observations provide a plausible explanation for the peak incidence of myocardial infarction occurring in the postoperative period, when flow stagnation and increased thrombogenicity prevails; [20] and for lower cardiovascular complication rates observed for laparoscopy Fig. 2 The phenotypic expression of the endothelium can be described as a dynamic 'set point' that ranges between a quiescent, activated or dysfunctional state.…”

A Review of Cardiac and Non-Cardiac Causes of Troponin Elevation and Clinical Relevance Part I: Cardiac Causes

“…Of course, patients may be at risk for developing more than one type of MI, making identifying the exact mechanism in any specific patient very difficult. For example, there is a general concern for type 1 MI in peri-operative patients with known CAD; however, type 2 MIs are just as commonly noted on autopsy [14]. In the early post-operative period, the imbalance between oxygen supply and demand predominates, likely due to peri-procedural hypotension and platelet activation.…”

“…The mechanism for troponin release is ischemic in nature, despite it not being true ACS, or type 1 MI (due to plaque rupture). It tends to occur in patients with known CAD [2,14]. Many practitioners confuse this type of MI with non-ischemic myocardial injury and necrosis which can be caused by various mechanisms.…”