The content of some vasoactive humoral-metabolic factors in patients with cirrhosis and their participation in pathogenesis of comorbid syntropical damages of cardiovascular system

Introduction. The management of treatment and prediction for patients with cirrhosis particularly are defined by syntropic polymorbid damages of other organs and systems among which are circulatory system diseases – cardiomyopathy and arterial hypotension - the most frequent ones. 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 Health of Ukraine. Using these results we have separated 490 (81.3 %) cirrhotic patients with extrahepatic damages of cardiovascular system. Results and discussion. The patients of both investigational groups have reasonably higher number of vasoactive humoral-metabolic factors. In particular, patients with cirrhosis and syntropic 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. 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.