scholarly journals ДІАГНОСТИКА ХРОНІЧНОЇ СЕРЦЕВОЇ НЕДОСТАТНОСТІ СОБАК – ІСНУЮЧІ МЕТОДИ ТА ПОДАЛЬШІ ПЕРСПЕКТИВИ

2016 ◽  
Vol 18 (3(71)) ◽  
pp. 130-133
Author(s):  
R. Trofimjak ◽  
L. Slivinska

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. 

The Analyst ◽  
2020 ◽  
Vol 145 (13) ◽  
pp. 4569-4575 ◽  
Author(s):  
Chunli Xia ◽  
Dong Zhou ◽  
Yueming Su ◽  
Guangkai Zhou ◽  
Lishuang Yao ◽  
...  

Cardiac troponin I (cTnI) is one of the most sensitive and specific markers of myocardial cell injury. In this study, a label-free biosensor that utilizes the birefringence property of liquid crystal (LC) for the detection of cTnI is demonstrated.


2012 ◽  
Vol 158 (1) ◽  
pp. 120-122 ◽  
Author(s):  
Mao Chen ◽  
Shao-Di Yan ◽  
Hua Chai ◽  
Xiao-Jing Liu ◽  
Yong Peng ◽  
...  

2000 ◽  
Vol 46 (5) ◽  
pp. 650-657 ◽  
Author(s):  
Kristien M ver Elst ◽  
Herbert D Spapen ◽  
Duc Nam Nguyen ◽  
Christian Garbar ◽  
Luc P Huyghens ◽  
...  

Abstract Background: Cardiac depression in severe sepsis and septic shock is characterized by left ventricular (LV) failure. To date, it is unclear whether clinically unrecognized myocardial cell injury accompanies, causes, or results from this decreased cardiac performance. We therefore studied the relationship between cardiac troponin I (cTnI) and T (cTnT) and LV dysfunction in early septic shock. Methods: Forty-six patients were consecutively enrolled, fluid-resuscitated, and treated with catecholamines. Cardiac markers were measured at study entry and after 24 and 48 h. LV function was assessed by two-dimensional transesophageal echocardiography. Results: Increased plasma concentrations of cTnI (≥0.4 μg/L) and cTnT (≥0.1 μg/L) were found in 50% and 36%, respectively, of the patients at one or more time points. cTnI and cTnT were significantly correlated (r = 0.847; P <0.0001). Compared with cTnI-negative patients, cTnI-positive subjects were older, presented higher Acute Physiology and Chronic Health Evaluation II scores at diagnosis, and tended to have a worse survival rate and a more frequent history of arterial hypertension or previous myocardial infarction. In contrast, the two groups did not differ in type of infection or pathogen, or in dose and type of catecholamine administered. Continuous electrocardiographic monitoring in all patients and autopsy in 12 nonsurvivors did not disclose the occurrence of acute ischemia during the first 48 h of observation. LV dysfunction was strongly associated with cTnI positivity (78% vs 9% in cTnI-negative patients; P <0.001). In multiple regression analysis, both cTnI and cTnT were exclusively associated with LV dysfunction (P <0.0001). Conclusions: These findings suggest that in septic shock, clinically unrecognized myocardial cell injury is a marker of LV dysfunction. The latter condition tends to occur more often in severely ill older patients with underlying cardiovascular disease. Further studies are needed to determine the extent to which myocardial damage is a cause or a consequence of LV dysfunction.


Author(s):  
Paul O Collinson ◽  
Frances G Boa ◽  
David C Gaze

The cardiac troponins form part of the regulatory mechanism for muscle contraction. Specific cardiac isoforms of cardiac troponin T and cardiac troponin I exist and commercially available immunoassay systems have been developed for their measurement. A large number of clinical and analytical studies have been performed and the measurement of cardiac troponins is now considered the ‘gold standard’ biochemical test for diagnosis of myocardial damage. There have been advances in understanding the development and structure of troponins and their degradation following myocardial cell necrosis. This has contributed to the understanding of the problems with current assays. Greater clinical use has also highlighted areas of analytical and clinical confusion. The assays are reviewed based on manufacturers' information, current published material as well as the authors' in-house experience.


1997 ◽  
Vol 78 (4) ◽  
pp. 386-390 ◽  
Author(s):  
H Metzler ◽  
M Gries ◽  
P Rehak ◽  
T Lang ◽  
S Fruhwald ◽  
...  

Author(s):  
E. Murphy ◽  
C. Steenbergen ◽  
A. LeFurgey ◽  
M. Lieberman ◽  
R. E. London

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