Non-coronarogenic causes of increased cardiac troponins in clinical practice

Abstract

Cardiospecific isoforms of troponins are the most sensitive and specific biomarkers for the diagnosis of myocardial infarction. However, though elevated troponin levels indicate myocardial damage, they do not determine the cause and mechanism of the damage. With the new highly sensitive methods, very minor damages of the heart muscle can be detected. Myocardial damage can occur in many non-coronarogenic diseases. In this review, we discuss the mechanisms of elevation, the diagnostic value of cardiac troponins in the renal failure, tachyarrhythmias, endocarditis, myocarditis, pericarditis, sepsis, neurogenic pathologies (stroke), pulmonary embolism. In addition, we pay attention to the main reasons for a false-positive increase of the concentration of cardiac troponins: heterophilic antibodies, rheumatoid factor, alkaline phosphatase, cross-reactions with skeletal muscle troponins.

Cardiac Troponins: Contemporary Biological Data and New Methods of Determination

“…Due to the fact that any myocardial cell damage, even reversible, can be accompanied by an increase in cTnI and cTnT serum concentrations, these biomarkers cannot be considered specific biomarkers of ischemic myocardial damage characteristic of AMI and when making this diagnosis, should not be relied on laboratory diagnostic data only. 27,28,[32][33][34][35] To make a correct diagnosis, in addition to the laboratory diagnostic criteria, clinicians must necessarily consider the clinical picture, electrocardiogram and echocardiogram data; otherwise, the risk of misdiagnosis and incorrect treatment, which can cause harm to the patient, increases significantly. 35 Thus, cTnI and cTnT can be considered as specific biomarkers of any myocardial damage, but cannot be considered specific for any particular type of damage or pathological condition affecting myocardial tissue.…”

“…As an exception to this rule, a group of causes of false-positive increases in cTnI and cTnT can be noted, which includes cross-reactions of diagnostic anti-cTnI and anti-cTnT antibodies with skeletal troponins, the influence of heterophilic antibodies, alkaline phosphatase, biotin, hemolysis, ictericity and lipemia. 33 , 36 In general, the main reasons for the increase in cTnI and cTnT, which are not directly related to AMI, can be divided into three groups ( Figure 1 ).

Figure 1 Main groups of causes of increased cTnI and cTnT that are not associated with AMI, according to 33 , 36 as amended.

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“… 33 , 36 In general, the main reasons for the increase in cTnI and cTnT, which are not directly related to AMI, can be divided into three groups ( Figure 1 ).

Figure 1 Main groups of causes of increased cTnI and cTnT that are not associated with AMI, according to 33 , 36 as amended.

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“… Main groups of causes of increased cTnI and cTnT that are not associated with AMI, according to 33 , 36 as amended. …”

“…Another mechanism responsible for the growth of troponins in CRF may be the adverse effect of accumulated toxic metabolic products that have a direct cytotoxic effect on the myocardium. 33 , 49 , 50 In addition, in conditions of chronic renal failure, the volume of circulating blood may increase, leading to a proportional increase in blood pressure and myocardial load. The latter circumstance will trigger a number of intracellular signaling pathways, leading to activation of enzymes (caspases, matrix metalloproteinases, calpain), causing splitting of molecules into small fragments inside the cell and their release outside.…”