The causes and mechanisms of increased cardiac troponin T and I (cTnT and cTnI) concentrations are numerous and are not limited to acute myocardial infarction (AMI) (ischemic necrosis of cardiac myocytes). Any type of reversible or irreversible cardiomyocyte injury can result in elevated serum cTnT and cTnI levels. Researchers and practitioners involved in the diagnosis and treatment of cardiovascular disease, including AMI, should know the key causes and mechanisms of elevated serum cTnT and cTnI levels. This will allow to reduce or completely avoid diagnostic errors and help to choose the most correct tactics for further patient management. The purpose of this article is to discuss the main causes and mechanisms of increase in cardiac troponins concentrations in frequently occurring physiological (physical exertion, psycho-emotional stress) and pathological conditions (inflammatory heart disease, pulmonary embolism, chronic renal failure and sepsis (systemic inflammatory response)) not related to myocardial infarction.

The article is devoted to problems of clinical-diagnostic value of determination of cardio-specific troponins in human biological fluids. Improvement of laboratory instrumentation and emergence of high sensitivity methods of analysis have allowed to identify troponins in urine, dialysate, and oral fluid. In the review we present actual information related to measurement of troponins in blood serum, data on testing of cardio-specific troponins in urine, dialysate, and oral fluid. Special attention is paid to determination of some cardiomarkers in oral fluid with thorough analysis of diagnostic value and effectiveness of the conducted studies.

Laboratory diagnosis plays one of the key roles in the diagnosis of many diseases, including cardiovascular diseases (CVD). The methods underlying the in vitro study of many CVD biomarkers, including cardiac troponins (cTnI and cTnT), are imperfect and are continually being improved to enhance their analytical performance, with sensitivity and specificity being the most important. Recently developed improved cTnI and cTnT detection methods, referred to as highly sensitive methods (hs-cTnI, hs-cTnT), have changed many of our ideas about the biology of cardiac troponins and opened up a number of additional diagnostic capabilities for practical healthcare. This article systematizes some relevant data on the biology of cardiac troponins as well as on methods for determining cTnI and cTnT with an analysis of the diagnostic value of their analytical characteristics (limit of blank, limit of detection, 99th percentile, coefficient of variation, and others). Data on extracardiac expression of cTnI and cTnT, mechanisms of formation and potential clinical significance of gender, age, and circadian characteristics of hs-cTnI and hs-cTnT content in serum are discussed. Considerable attention is paid to the discussion of new diagnostic capabilities of hs-cTnI, hs-cTnT, including consideration of promising possibilities for their study in biological fluids that can be obtained by non-invasive methods. Also, some possibilities of using hs-cTnI and hs-cTnT as prognostic laboratory biomarkers in healthy people (for example, to assess the risk of developing CVD) and in patients suffering from a number of pathological conditions that cause damage to cardiomyocytes are examined, and the potential mechanisms underlying the increase in hs-cTnI and hs-cTnT are discussed.

The metabolic processes of endo- and exogenous compounds play an important role in diagnosing and treating patients since many metabolites are laboratory biomarkers and/or targets for therapeutic agents. Cardiac troponins are one of the most critical biomarkers to diagnose cardiovascular diseases, including acute myocardial infarction. The study of troponin metabolism is of great interest as it opens up new possibilities for optimizing laboratory diagnostics. This article discusses in detail the key stages of the cardiac troponins metabolism, in particular the mechanisms of release from a healthy myocardium, mechanisms of circulation in the bloodstream, possible mechanisms of troponin penetration into other biological fluids (oral fluid, cerebrospinal fluid, pericardial and amniotic fluids), mechanisms of elimination of cardiac troponins from the blood, and daily changes in the levels of troponins in the blood. Considering these aspects of cardiac troponin metabolism, attention is focused on the potential value for clinical practice.

Natriuretic peptides (NPs) are key diagnostic and prognostic biomarkers for patients with heart failure (HF). The main mechanism for increasing serum NP levels, which is characteristic of heart failure, is secretion in response to myocardial wall distention. At the same time, according to Russian and foreign literature, an increase in NPs is reported in a number of many other conditions that are not associated with HF. The study of these causes and mechanisms is necessary to improve the differential diagnosis of HF.This article discusses the mechanisms of increasing NPs and their diagnostic value in heart failure, as well as a number of other conditions, such as acute coronary syndrome and coronary artery disease, atrial fibrillation, exercise, kidney failure, taking cardiotoxic drugs (chemotherapy) and sacubitril/valsartan. The article also provides data on identifying NPs in non-invasively obtained biological fluids (urine and oral fluid).

Certain success has been achieved in the treatment of cancer due to the development of various effective chemotherapeutic drugs. However, an increase in their effectiveness (aggressiveness) was associated with a growth of undesirable effects on the entire human body, in particular, on the cardiovascular system. The damage to the cardiovascular system from chemotherapy in many cases is more significant than from the underlying disease. In recent years, a new direction of medicine has been formed - cardio-oncology. The major groups of cardiotoxic chemotherapeutic agents are anthracyclines, inhibitors of epidermal growth factor receptor type 2 (anti-HER2), antimetabolites, microtubule inhibitors, proteasome inhibitors, platinum-based chemotherapeutic drugs, and angiogenesis inhibitors (inhibitors of vascular endothelial growth factor). This review discusses principal pathophysiological mechanisms of the cardiotoxicity of these chemotherapeutic drugs.