Markers for perioperative myocardial ischemia: what both interventional cardiologists and cardiac surgeons need to
Johannes Mair1, Angelika Hammerer-Lercher
1Clinical Division of Cardiology, Department of Internal Medicine, Innsbruck Medical University, Innsbruck, Austria. Johannes.Mair@uibk.ac.at
Insights
Novel markers for myocardial ischemia lack specificity and do not surpass lactate testing. Cardiac troponins are key for diagnosing myocardial damage and necrosis, but interpretation requires care, especially after cardiac surgery.
Area of Science:
- Cardiology
- Biochemistry
- Clinical Diagnostics
Background:
- Novel myocardial ischemia markers like ischemia-modified albumin lack cardiac specificity.
- Current methods for diagnosing myocardial ischemia, such as lactate production, have limitations and lack comparative data with novel markers.
- Cardiac troponin I and T are the gold standard for myocardial damage, surpassing creatine kinase isoenzyme MB.
Purpose of the Study:
- To evaluate the diagnostic utility of novel myocardial ischemia markers.
- To compare novel markers with existing methods like lactate determination and troponins.
- To clarify the role and interpretation of troponin levels in various cardiac procedures.
Main Methods:
- Review of existing literature on myocardial ischemia and damage markers.
- Analysis of troponin levels in the context of percutaneous coronary interventions and coronary artery bypass grafting.
- Comparison of novel markers, lactate, and troponins for diagnostic accuracy.
Main Results:
- Novel ischemia markers lack specificity and require invasive sampling, limiting clinical use.
- No superiority of novel markers over lactate determination for myocardial ischemia has been proven.
- Troponin elevations after on-pump coronary artery bypass grafting are expected due to unavoidable tissue damage.
- Characteristic troponin time courses are crucial for diagnosing perioperative myocardial infarctions.
Conclusions:
- Novel markers are not a breakthrough for diagnosing myocardial ischemia in routine settings.
- Troponin monitoring is essential for diagnosing myocardial damage and necrosis, with specific interpretation guidelines for post-cardiac surgery.
- Troponin elevations >8-fold the upper reference limit after PCI indicate increased long-term mortality risk.
Abstract:
All novel markers of myocardial ischemia (ischemia-modified albumin, choline, unbound free fatty acids) lack cardiac specificity. Therefore, for the specific detection of myocardial ischemia selective blood sampling from an inserted coronary sinus catheter is needed, which limits the applicability of these markers in most clinical routine settings. In addition, the superiority of these novel markers over the calculation of myocardial lactate production, the current criterion standard for the laboratory diagnosis of myocardial ischemia, has not been demonstrated so far, and even comparative data is frequently lacking. Further the superiority of these new candidate markers over lactate determination for the diagnosis of myocardial ischemia in peripherally drawn blood samples has not been demonstrated either, and these novel parameters appear not to be a breakthrough for laboratory diagnosis of myocardial ischemia during or after percutaneous coronary interventions or coronary artery bypass grafting. The determination of cardiac troponin I or troponin T is the current criterion standard for the laboratory diagnosis of myocardial damage due to their higher sensitivities and specificities compared to creatine kinase isoenzyme MB. According to current knowledge, troponin increases in peripherally drawn blood samples must be regarded as an indicator of myocardial necrosis which, however, may be limited, only detectable by troponin and may be missed by creatine kinase isoenzyme MB determination. After on-pump coronary artery bypass grafting the generally applied troponin discriminator limits are not valid as there is limited, inevitable cardiac tissue damage occurring during the surgical procedure. Therefore, troponins are significantly increased after reperfusion of the arrested heart over values seen before bypass and also in patients without complications. Perioperative myocardial infarctions can be reliably identified by their characteristic troponin time courses, and both peak concentrations and time of peak values are diagnostic criteria. Troponin release is lower in off-pump compared to on-pump bypass surgery. Despite the controversy over the significance of troponin elevations after clinically uncomplicated and successful procedures, it is tempting to postulate that less myocardial damage as detected by troponin release is beneficial for the patient. After elective percutaneous coronary interventions, only troponin increases >8-fold the upper reference limit were associated with increased mortality in long-term follow-up.
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