Predictors of late complications in pregnant women with arterial hypertension

Abstract

Arterial hypertension occurs in 829% of pregnant women and is a common form of endothelial dysfunction during gestation. In recent decades, the prevalence of arterial hypertension has increased several times largely due to the increasing maternal age of primiparous women and the increased incidence of obesity, diabetes mellitus, and carbohydrate metabolism disorders.
 The aim of this study was to formulate the management tactics for pregnant patients with high blood pressure, based on the current understanding of the causes and mechanisms of the disease and the ability to influence the molecular links of pathogenesis, and to identify possible markers for predicting the progression of endothelial dysfunction in pregnant women with arterial hypertension. This review, based on the literature, raises the problem of modern diagnosis of arterial hypertension in pregnancy. We discuss the consequences of late initiation of the therapy and evaluate possible complications.
 The severity of arterial hypertension is assessed differently in pregnant and non-pregnant women, according to current clinical guidelines. Thus, chronic arterial hypertension in pregnant women corresponds to grade II arterial hypertension in non-pregnant women, according to the American Heart Association and American College of Cardiology classification. Both untimely diagnosis and delayed or inadequate treatment result in adverse obstetric outcomes. Recent studies indicate the ability of earlier antihypertensive therapy (already at stage I according to the American Heart Association and American College of Cardiology classification) to reduce maternal and fetal adverse effects and prolong pregnancy. The CHAP 2022 study showed that using a blood pressure treatment threshold of 140/90 mmHg for pregnant women with chronic arterial hypertension provides better outcomes compared to treatment at higher numbers. Despite early initiation of therapy, some patients with elevated blood pressure subsequently develop thrombotic and gestational complications associated with endothelial dysfunction. There is an obvious need to introduce early preclinical diagnostic methods that would narrow the risk group and prevent late complications. The authors consensus on personalization of acetylsalicylic acid intake has emerged. The review analyzes the potential mechanisms of aspirin resistance, as well as the influence of genetic (the PTGS1, PTGS2, ITGB3, ITGA2, GP6, GP1BA, P2RY1, P2RY12 genes, other genes, and associated microRNA) and biochemical markers (11-dehydrotromboxane B2), which presumably may have prognostic value and applicability in clinical practice.
 Our current understanding of the problem of diagnosis and early treatment of arterial hypertension in pregnancy can reduce the number of complications. The problem of predicting the development of endothelial dysfunction remains unresolved to the end. Active implementation of the studied markers into practice requires a further more detailed study of this area and the optimization of research design.