Rationale for choosing antihypertensive therapy in a patient with NAFLD and arterial hypertension

The concept of metabolic syndrome (MS) has existed since the 1980s and in its classical version includes obesity, lipid and carbohydrate metabolism disorders, and arterial hypertension (AH). Later (since 2009), non-alcoholic fatty liver disease (NAFLD) was considered as the fifth component of MS, which is currently proposed to be renamed steatotic liver disease by the International Working Group “Multi-Society and Multi-Stakeholder Consensus Revision of the NAFLD Nomenclature”. NAFLD and AH are pathogenetically interconnected through insulin resistance, systemic inflammatory response and oxidative stress, progressive endothelial dysfunction, impaired vasoconstriction and vasodilation mechanisms that develop against the background of liver fibrogenesis, which is described in detail in this article. Patients with hypertension and NAFLD often have unstable hypertension with episodes of hypotension, and insufficient effectiveness of antihypertensive therapy. NAFLD itself is associated not only with an increased risk of cardiovascular events, but also with other cardiac complications, regardless of traditional cardiovascular risk factors. At the same time, hypertension increases the risk of liver cirrhosis and, in addition, hypertension is independently associated with the development of severe liver diseases. In other words, the combination of NAFLD and hypertension in a patient worsens the course of both pathologies and the patient’s prognosis, especially with progressive fibrosis in the liver. Pathogenetically substantiated drugs of choice in the treatment of hypertension in a patient with NAFLD are drugs that affect the renin-angiotensin system, which will also be discussed in this article.