• R. Trofimjak Lviv national university of veterinary medicine and biotechnologies named after S. Gzhytskyj
  • L. Slivinska Lviv national university of veterinary medicine and biotechnologies named after S. Gzhytskyj
Keywords: chronic heart failure, dog, cardiac biomarkers, myocardium, cardiac troponin C, I and T


The article analyzes the current scientific work related to the study of processes of chronic heart failure (CHF), and the use of biomarkers in the diagnosis of heart disease in dogs. Thoracic radiography, electrocardiography, and echocardiography are used to diagnose heart disease in dogs but despite the use of non–invasive methods, there is uncertainty about the severity of the disease and prognosis for each patient individually. In veterinary practice for the diagnosis of myocardial lesions in animals are clinically valuable, highly sensitive and simple to use cardiac biomarkers. A biomarker is typically a substance in the blood that can be objectively measured and indicates a biologic or pathologic process or response to therapy.1 There are scores of cardiac biomarkers,but this article will focus on the 2 most clinically useful ones in the dog and cat:cardiac troponin I (cTnI) and N–terminal pro–B–type natriuretic peptide (NT–proBNP). The cardiac troponins I, T, and C (cTnI, cTnT, and cTnC) are thin filament–associated regulatory proteins of the heart muscle. Cardiac troponin I («I» for inhibition) is uniquely expressed in the myocardium and is a potent inhibitor of the process of actin–myosin cross–bridge formation. The molecular weight is 24.000 D. Cardiac troponin T («T» for tropomyosin binding) has a molecular weight of 37.000 D and binds the troponin complex to tropomyosin. Cardiac troponin C («C» for calcium) binds to calcium and starts, therefore, the crossbridge cycle. As with cTnI, approximately 95% of cTnT in man and dogs is myofibril bound and about 5% is cytosolically dissolved. Mechanisms for an elevation in circulating cardiac troponins include an increase of myocyte membrane permeability (initial release of the cytosolic troponin pool) or cell necrosis (release of myofibrilbound troponins). Four to six hours after acute myocardial cell injury, the cardiac troponin concentration in blood increases in a biphasic pattern. Plasma half–life of cardiac troponins is approximately two hours, and elimination mainly occurs via the reticuloendothelial system (cTnI and cTnT) and renal loss (cTnT). Cardiac troponins are phylogenetically highly preserved proteins with a more than 95% total structural agreement between mammals. Therefore, established human serologic tests for troponin analysis may be used reliably in pets as well. Myocardial cell injury, manifested anatomically as inflammation (endomyocarditis, myocarditis, perimyocarditis), acute degeneration, apoptosis, or necrosis or hemodynamically as transient or permanent cardiac contractile dysfunction, is a frequent consequence of physical myocardial trauma (cardiac contusion), cardiomyopathy, metabolic or toxic myocardial damage (anthracyclines, catecholamines, bacterial endotoxins, tumor necrosis factor), myocardial ischemia or infarction. However, early diagnosis of myocardial injury may be important from a therapeutic and prognostic perspective.



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How to Cite
Trofimjak, R., & Slivinska, L. (2016). DIAGNOSIS OF CHRONIC HEART FAILURE DOGS – EXISTING METHODS AND FUTURE PROSPECTS. Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies. Series: Veterinary Sciences, 18(3(71), 130-133. https://doi.org/10.15421/nvlvet7129