Abstract
Postoperative myocardial injury, as defined by troponin elevation, is strongly associated with adverse events in many non-cardiac surgery populations. The majority of such events, however, is silent and therefore difficult to diagnose. In order to facilitate risk stratification and early recognition of postoperative myocardial injury, routine troponin assessment was implemented.
In spite of its association with adverse events, one should acknowledge that this does not imply a causal relation. Indeed, ST-elevation myocardial infarctions are rare and cardiac interventions were deemed necessary in just 16% of patients with troponin elevation. Also, cardiac death within one year was infrequent in patients with troponin elevation. This suggests that most troponin elevations are a byproduct of prior coronary artery disease or a poor clinical condition rather than a primary cardiac event. Here, patient-specific characteristics (e.g. pre-existent cardiac, renal or cerebral disease) and procedure-specific characteristics (e.g. anemia, tachycardia, tachy-arrhythmia, stroke or sepsis) can be considered as the substrate and the trigger for myocardial injury, respectively. Of note, substrate and triggers vary significantly between different study populations. For instance, cerebral pathology and pulmonary embolism (which also correlate to a poor prognosis) proved to be highly prevalent in patients with postoperative troponin elevations. These events, however, were mostly silent and routine diagnostics (anamnesis, physical examination and electrocardiography) proved insufficiently sensitive and specific. Additional imaging modalities should therefore be considered more accessibly, which should consecutively be used for further interventional strategies.
In spite of its association with adverse events, one should acknowledge that this does not imply a causal relation. Indeed, ST-elevation myocardial infarctions are rare and cardiac interventions were deemed necessary in just 16% of patients with troponin elevation. Also, cardiac death within one year was infrequent in patients with troponin elevation. This suggests that most troponin elevations are a byproduct of prior coronary artery disease or a poor clinical condition rather than a primary cardiac event. Here, patient-specific characteristics (e.g. pre-existent cardiac, renal or cerebral disease) and procedure-specific characteristics (e.g. anemia, tachycardia, tachy-arrhythmia, stroke or sepsis) can be considered as the substrate and the trigger for myocardial injury, respectively. Of note, substrate and triggers vary significantly between different study populations. For instance, cerebral pathology and pulmonary embolism (which also correlate to a poor prognosis) proved to be highly prevalent in patients with postoperative troponin elevations. These events, however, were mostly silent and routine diagnostics (anamnesis, physical examination and electrocardiography) proved insufficiently sensitive and specific. Additional imaging modalities should therefore be considered more accessibly, which should consecutively be used for further interventional strategies.
Original language | English |
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Award date | 11 Oct 2016 |
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Publication status | Published - 11 Oct 2016 |
Keywords
- troponin
- postoperative myocardial injury
- non-cardiac surgery
- pulmonary embolism
- myocardial infarction
- coronary artery disease
- endovascular aortic repair