Львівський клінічний вісник (Dec 2017)
The content of some vasoactive humoral-metabolic factors in patients with cirrhosis and their participation in pathogenesis of comorbid syntropical damages of cardiovascular system
Abstract
Introduction. Liver cirrhosis is an inveterate polyetiological disease that regards to the 6 main reasons of patients’ mortality at the age of 35-60. The management of treatment and prediction for patients with cirrhosis particularly are defined by syntropic polymorbidal damages of other organs and systems among which are circulatory system diseases – cardiomyopathy and arterial hypotension – the most frequent ones. Firts of all, the improvement of diagnostics and treatment of those patients supposes the studying their pathogenesis. For the time being, the most probable pathogenetic chains are endothelial dysfunction, imbalance in renin-angiotensin-aldosterone system, and also overproduction of brain natriuretic peptide. Aim. To examine the content of vasoactive humoral-metabolic factors, i.e. endothelium-dependent (cyclic guanosine monophosphate, endothelin-1), indexes of renin-aldosterone system (renin, aldosterone) and brain natriuretic hormone in blood plasma in patients with cirrhosis and discover their participation in pathogenesis of comorbid syntropical damages of cardiovascular system. Materials and methods. Randomly with the previous stratification due to the presence of cirrhosis there were 603 patients (445 men (73.8 %) and 158 women (26.2 %) at the age of 19-80 (average age 49.2 ± 10.6) who were treated in the Lviv Regional Hepatological Centre, they had the complex clinical-laboratorial and instrumental research of all organs and systems before treatment due to the orders of the Ministry of Healthcare of Ukraine. Using these results we have seperate 490 (81.3 %) cirrhosis patients with extrahepatic damages of cardiovascular system (investigational group which is stratified into 3 subgroups, i.e. those who have only syntropic cardiomyopathy (103 patients) – group A, only syntropic hypotension (89 patients) – group B and others (306 patients)), and also those who don’t have the damages of cardiovascular system (113 patients; 18.7 %) – the comparison group). Randomly, to achieve the aim the part of the patients from every subgroup (30 patients from A-group, 27 – from B-group and 25 from group of comparison) were screened for the content of the vasoactive humoral-metabolic factorsm. There were 17 almost healthy volunteers of the same gender and age in the control group. Results and discussion. The patients of both investigational groups have reasonably higher number of vasoactive humoral-metabolic factors. In particular, patients with cirrhosis and syntopetic cardiomyopathy dominate the effects of endothelin-1, renin and brain natriuretic peptide, and in patients with cirrhosis and syntropic arterial hypotension – cyclic guanosine monophosphate and aldosterone are the main factors. Additionally we recorded the pathological interaction among vasoactive material. Unlike of the results in comparison group, in patients with liver cirrhosis and syntropic cardiomyopathy, the local vasoactive compounds are in such interactions with each other that result in hyperactivity of the renin-angiotensin-aldosterone system and endothelial dysfunction with a significant increase in both vasoconstrictor endothelin-1 and vasodilator NO, and in patients with liver cirrhosis and arterial hypotension – to severe endothelial dysfunction with overproduction of NO. Conclusions. Cyclic guanosine monophosphate, endothelin-1, renin, aldosterone, and brain natriuretic peptide, have a pathological effect on each other and are involved in the pathogenesis of syntropic damages of the circulatory system in patients with liver cirrhosis. In patients with cirrhosis and syntropic cardiomyopathy, heart damage occurs through toxic myocardial damage due to excessive effects of renin, endothelin-1, and brain natriuretic peptide with the onset of systolic and diastolic dysfunction and overload of the heart with blood volume. And in patients with cirrhosis and syntropic arterial hypotension, the damage occurs due to the endothelial dysfunction with excessive cyclic guanosine monophosphate and hyperaldosteronism, which leads to the expansion of peripheral vessels, the depositing of excess blood in the organs and, consequently, the decrease in the effective volume of circulation blood.
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