STRUCTURAL AND FUNCTIONAL STATE OF THE LIVER IN PATIENTS WITH CHRONIC HEART FAILURE

Аннотация

INTRODUCTION depending on the role of each organ, which is the Heart and liver diseases are considered a major primary source of damage. [1,2]: - liver diseases burden on the healthcare system and a leading resulting from heart disease; - heart disease problem. cause a deterioration in the quality of life resulting from liver disease (for example, cirrhotic and a reduction in life expectancy. In this review, cardiomyopathy); -systemic diseases affecting we discuss the complex cardiohepatic interactions both the heart and liver (for example, systemic in major heart and liver diseases. This review aims amyloidosis). The first group has generally been to highlight how acute and chronic heart failure can called “cardiac hepatopathy,” although there is still lead to cardiogenic disorders. In each section, we no consensus on terminology [3,4]. The two main briefly discuss the likely mechanisms underlying forms of cardiac hepatopathy are acute cardiogenic this association, clinical manifestations, and liver injury (also called hypoxic hepatosis) and diagnostic approaches. congestive hepatopathy (CH). Both conditions Congestive hepopathy. often coexist and enhance each other's harmful The interaction between the heart and liver has effects on the liver [3–5]. Any cause of right-sided been known for a long time. However, in recent heart failure due to diseases such as constrictive years, these cardiohepatic interactions have gained pericarditis, mitral stenosis, severe tricuspid greater interest, prompting the study of these regurgitation, congenital heart disease or end- interactions and a rethinking of their stage cardiomyopathy can lead to congestive pathophysiology. The relationship between the hepatopathy [7,8]. In summary, the incidence of liver and the heart is divided into three groups liver cirrhosis caused by noncongenital heart https://www.theamericanjournals.com/index.php/tajmspr 11 THE USA JOURNALS THE AMERICAN JOURNAL OF MEDICAL SCIENCES AND PHARMACEUTICAL RESEARCH (ISSN – 2689-1026) VOLUME 06 ISSUE09 failure is decreasing, and ischemic cardiomyopathy demonstrated sinusoidal thrombi confined to areas is now the leading cause of right heart failure, of fibrosis, suggesting that intrahepatic thrombosis surpassing rheumatic heart disease and post- is involved in the progression of liver fibrosis [18]. Fontan heart failure, which creates non-pulsatile This is now defined as an area with focal loss of high-pressure flow in the inferior vena cava and adjacent hepatocytes and adjacent microvascular this condition leads to chronic hepatic venous structures. This microvascular injury causes congestion. [1,2,4,9]. venous obstruction to spread to larger vessels, resulting in persistence of venous obstruction and Pathophysiology. The liver is a highly vascular worsening congestion [19]. Clinical picture and organ that receives up to 25% of total cardiac diagnosis. Chronic hepatosis can be asymptomatic output. The hepatic artery delivers well- for a long time, and in these patients this is the only oxygenated blood and contains approximately sign that allows one to suspect its presence if there 25% of the total hepatic blood flow, while the are changes in the tests[8]. Hepatic symptoms are remaining 75% is blood coming from the portal usually masked by disorders associated with right- vein. The liver has robust vascular mechanisms sided HF [6]. Stretching of the liver capsule due to that protect the liver from ischemic injury [1]. The liver congestion is the cause of some symptoms, hepatic artery buffer response is a local regulatory such as heaviness or dull pain in the right upper mechanism leading to an increase in the quadrant, nausea. Other symptoms include concentration of the vasodilator adenosine with a anorexia, general weakness, absence of ascites or decrease in portal blood flow. [12]. In contrast, the edema of the lower extremities [1]. Classic portal vein does not have the ability to self-regulate complications of liver cirrhosis, such as hepatic its own blood flow and depends on cardiac output encephalopathy or hepatocarcinoma, occur in late and the pressure gradient in the portal and hepatic stages of cardiac cirrhosis and may eventually veins [5,8]. The high permeability of the liver become as clinically important as cardiac disease sinusoids allows oxygen extraction up to 90%, and and further complicate the course [10]. When during hypoxia, oxygen consumption by the liver addressing a patient with new-onset ascites, it is decreases, despite normal hepatic blood flow difficult to differentiate the cardiac etiology of [5,13,14]. This unique resistance to ischemic injury ascites since in both cases the serum-ascitic contrasts with the paucity of protective albumin gradient is ≥1.1 g/dL [25]. However, with mechanisms. The resulting liver congestion leads cardiac ascites, the protein level is higher than >2.5 to liver damage through several pathogenic g/dl, which is due to the preservation of the mechan