Abstract
Despite the fact that cardiac troponins (cTnI and cTnT) are cardiospecific, they can be elevated in many systemic and non-cardiac physiological and pathological conditions. The diagnostic value of cTnI and cTnT significantly depends on the method of their determination. Thus, previously used low- and moderate-sensitivity immunoassays detected only serious myocardial damage and did not determine troponins in patients suffering from certain chronic pathologies. High-sensitivity troponin assays can detect minor damage to cardiac muscle cells in many pathological conditions, and troponin levels have a high predictive value. Among the early pathological conditions requiring the attention of clinicians is arterial hypertension (AH), which is also accompanied by an increase in the levels of hsTn in serum and urine. Currently, mechanisms responsible for increased levels of cardiac troponins in the blood serum and urine in hypertension are not well covered in the scientific literature. This article discusses in detail the presumptive mechanisms that cause increased levels of cTnI and cTnT in AH.
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