Abstract

Though heart failure can mainly be caused by systolic or diastolic dysfunction, the impairments of the neurohormonal, immune, and hemostatic systems are observed too. Therefore, it is not easy to determine etiology of the syndrome. Parameters that can be helpful to predict chronic heart failure, to evaluate its course and the risk of complications are still being searched. The aim of this article is to review the recent studies in order to find the links between the coagulation system and the development of chronic heart failure. Stress is a key factor for the development of most diseases including chronic heart failure too. Signals of emotional and physical stress via particular structures trigger an increase in concentrations of the following hormones: noradrenaline, renin, angiotensin II, aldosterone, vasopressin. It is proved that it causes the disorders of the coagulation system: an increase in the following factors of plasma coagulation (fibrinogen, VII, VIII, fibrinopeptide A, thrombin-antithrombin complex), fibrinolysis (D-dimer), endothelium (interleukin 1, endothelin 1, vascular cell adhesion molecules, endothelial growth factor), platelet activity (von Willebrand factor, intercellular adhesion molecules, platelet factor 4, P-selectin, thromboxane A(2), thromboglobulin, CD63P) and cytokines (tumor necrosis factor, interleukin 6) and decrease in E-selectin. The role of particular coagulation factors for the development of chronic heart failure has not been understood yet. Thus, it is necessary to carry out further studies.

Highlights

  • In the general European population, the prevalence of symptomatic heart failure ranges from 0.4% to 2%

  • It is proved that it causes the disorders of the coagulation system: an increase in the following factors of plasma coagulation, fibrinolysis (D-dimer), endothelium, platelet activity and cytokines and decrease in E-selectin

  • It was found that significantly higher levels of the following parameters were present in subjects with chronic HF (CHF): hemostatic markers, von Willebrand factor and fibrinogen; intercellular adhesion molecules (ICAM); platelet and endothelial adhesion molecules (PECAM); platelet factor 4 (PF4), P-selectin; tissue-type plasminogen activator (t-PA), D-dimer; fibrinopeptide A; selectin; vascular cell adhesion molecules (VCAM) (Table); cytokines, tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6); enzyme urokinase, thromboxane reductase, other compounds; and lysosome and platelet dense granule transmembrane protein [16]

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Summary

The coagulation system changes in patients with chronic heart failure

Aušra Mongirdienė , Lolita Kuršvietienė, Artūras Kašauskas2 1Institute of Cardiology, Medical Academy, Lithuanian University of Health Sciences, 2Department of Biochemistry, Medical Academy, Lithuanian University of Health Sciences, Lithuania. The aim of this article is to review the recent studies in order to find the links between the coagulation system and the development of chronic heart failure. Stress is a key factor for the development of most diseases including chronic heart failure too. Signals of emotional and physical stress via particular structures trigger an increase in concentrations of the following hormones: noradrenaline, renin, angiotensin II, aldosterone, vasopressin. It is proved that it causes the disorders of the coagulation system: an increase in the following factors of plasma coagulation (fibrinogen, VII, VIII, fibrinopeptide A, thrombinantithrombin complex), fibrinolysis (D-dimer), endothelium (interleukin 1, endothelin 1, vascular cell adhesion molecules, endothelial growth factor), platelet activity (von Willebrand factor, intercellular adhesion molecules, platelet factor 4, P-selectin, thromboxane A2, thromboglobulin, CD63P) and cytokines (tumor necrosis factor, interleukin 6) and decrease in E-selectin. The role of particular coagulation factors for the development of chronic heart failure has not been understood yet.

Introduction
Literature in parameter source
Noradrenaline activates plateles
Findings
Krešėjimo sistemos pokyčiai sergant lėtiniu širdies nepakankamumu
Full Text
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