Clinical biochemistry

Reference range

S_TnT (99th percentile of reference population) 14 ng/L

S_NT-proBNP < 125 ng/L

S_BNP < 100 ng/L

CK males: < 3,2 µkat/L; females: < 2,4 µkat/L

Myoglobin males: 28 - 72 µg/L; females: 28 - 58 µg/L

D-dimers  < 0,5 mg/L FEU

For the diagnosis of structural myocardial damage, we mainly use cardiac troponins (cTn). These are proteins that are part of the contractile apparatus of the muscle. Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are sufficiently different in skeletal and cardiac muscle - we can reliably distinguish them analytically, so they are markers specific for cardiac muscle. We consider acute myocardial injury to be an increase in cTn above the 99th percentile of the reference population and a dynamic change in cTn values greater than 20% (increase or decrease). If signs of myocardial ischemia - e.g. ECG or clinical - are added to acute myocardial injury, it is acute myocardial infarction (AIM). Clinically, more complex algorithms are used, usually introducing two limits for absolute values and two limits for changes over time. One combination of absolute value and change is for exclusion of AIM, the other combination is for inclusion in AIM. cTn in this arrangement have a high NPV but a worse PPV (see above). However, acute myocardial injury itself is also found in other cardiac diseases, e.g. myocarditis or toxic myocardial injury.

We have mentioned above that during volume overload of the ventricles, brain natriuretic peptide type B (BNP) and a cleft of its precursor, N-terminal propeptide of natriuretic peptide type B (NT proBNP), are produced.Both are used as markers of heart failure and are incorporated into clinical diagnostic algorithms for the diagnosis of heart failure.

Skeletal muscle damage is best determined by an increase in the activity of the enzyme creatine kinase (CK). This is mainly a cytoplasmic enzyme composed of two subunits, M (muscle) and/or B (brain). Different isoenzymes contain different combinations of subunits: MM (predominant in skeletal muscle), MB (predominant in cardiac muscle) and BB (predominant in brain). The determination of CK isoenzymes is no longer used clinically, nor is the determination of CK-MB for the diagnosis of AIM. Total CK activity is useful for the diagnosis of skeletal muscle damage as well as for monitoring progress and treatment monitoring. Among the causes of rhabdomyolysis are excessive physical stress, convulsions, trauma, multi-organ failure (e.g. in sepsis), alcohol and some drugs (cocaine). Myoglobin is a relatively small muscle protein that is also released when striated muscle is damaged. Most of it is excreted by the kidneys, so a decrease in glomerular filtration rate increases its levels. Because it passes into the urine, it causes a positive blood result on an indicative test strip blood chemistry test (see above). Measurement of myoglobin levels is no longer relevant in the diagnosis of AIM, and even for the detection of rhabdomyolysis, CK is preferable due to its independence of GFR. The only advantage of myoglobin is its short half-life, so it can respond very quickly to changes.

D-dimers are formed by fibrin degradation and are used as a marker of thromboembolic conditions (e.g. deep vein thrombosis, pulmonary embolism). Their high NPV is valuable - if they are negative, the probability of the presence of disease is low. However, they also rise in a range of other conditions - e.g. in pregnancy or inflammation. A positive result is therefore of little predictive value.