New biomarkers in acute cardiac care

Professor C Mueller adressed the issue of new biomarkers in acute cardiac care on the ESC on Monday, 1st September. Read his comment in the following.

In conjunction with clinical assessment and the ECG, simple and rapid blood tests have become the standard for the detection of myocardial infarction. Starting in the year 2000, recommendations by the European Society of Cardiology and other major cardiology societies worldwide have begun to state uniformly that a rise in cardiac troponins – sensitive and specific markers for dying cells in the heart - is a prerequisite for the clinical diagnosis of myocardial infarction. 

Myocardial infarction is the major cause of death worldwide. With effective treatment within our grasp, accurate and rapid diagnosis is of major medical and economic importance. With the development of sensitive trials depicting either cardiac troponin I or cardiac troponin T, the only current biomarkers thought to be unique to the heart, the diagnosis of myocardial infarction has been revolutionised. In a patient presenting with chest pain, a rise in cardiac troponin has become a mandatory feature for the clinical diagnosis of myocardial infarction. Cardiac troponins are our current gold standard for the detection of myocardial necrosis. The more sensitive the cardiac troponin essay used, the smaller the number of dying myocardial cells necessary for this signal to be detected. This has enabled us to detect high risk acute coronary syndrome patients with only minor myocardial damage.

Unfortunately, current cardiac troponin essays have one major limitation in common with their predecessor (CKMB): it takes 3–4 hours after symptom onset until cardiac troponin becomes detectable. Ongoing large clinical multicenter studies, including the Advantageous Predictors of Acute Coronary Syndromes Evaluation (APACE), are assessing whether novel cardiac troponin assays with even higher sensitivity or other biomarkers reflecting different pathophysiological processes such as, for example, copeptin (reflecting endogenuous stress) or myeloperoxidase (reflecting plaque instability and inflammation) will significantly shorten the “troponin-blind” period. Obviously, this would constitute a major medical and economic improvement in clinical practice.

However, the development of high sensitivity cardiac troponin assays also poses dilemmas: First, many physicians are reluctant to use the term “myocardial infarction” in patients with unstable coronary artery disease and tiny elevations of cardiac troponin. As these patients still seem to be at increased risk of death as compared to patients without detectable cardiac troponin levels, the current ESC/AHA/ACC guidelines encourage us to do so. Second, elevations in cardiac troponin I and T reflect myocardial injury, but do not indicate its mechanism. Myocardial infarction can only be diagnosed when cardiac troponin I or T are increased in the clinical setting of myocardial ischemia – this means the myocardial cells suffer from a lack of oxygen and are “suffocating” due to reduced oxygen supply usually related to a clot in the coronary arteries or less commonly due to other causes of decreased supply such as coronary spasm or hypotension or due to increased oxygen demand such as septic shock. As we currently lack a biomarker that reliably detects clot formation in the coronary arteries, we are left with our basic clinical tools, including patient history, to differentiate myocardial infarction from other causes of myocardial injury. Third, once a diagnostic test is declared “gold standard”, it becomes virtually impossible to rule out definitely false positive test results. This is currently the case with cardiac troponins. We strongly believe that the heart is invariably the exclusive source of cardiac troponin elevations, regardless of the specific patient conditions. However, as both the ECG and imaging techniques have far lower sensitivity to myocardial necrosis than cardiac troponin, scientific proof cannot be provided. 


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