Arterial dissections, which involve an abrupt tear in the wall of a major artery resulting in the intramural accumulation of blood, are a family of catastrophic disorders causing major, potentially fatal sequelae. Involving diverse vascular beds, including the aorta or coronary, cervical, pulmonary, and visceral arteries, each type of dissection is devastating in its own way. Traditionally they have been studied in isolation, rather than collectively, owing largely to the distinct clinical consequences of dissections in different anatomical locations – such as stroke, myocardial infarction, and renal failure. Here, we review the shared and unique features of these arteriopathies to provide a better understanding of this family of disorders. Arterial dissections occur commonly in the young to middle-aged, and often in conjunction with hypertension and/or migraine; the latter suggesting they are part of a generalized vasculopathy. Genetic studies as well as cellular and molecular investigations of arterial dissections reveal striking similarities between dissection types, particularly their pathophysiology, which includes the presence or absence of an intimal tear and vasa vasorum dysfunction as a cause of intramural hemorrhage. Pathway perturbations common to all types of dissections include disruption of TGF-β signaling, the extracellular matrix, the cytoskeleton or metabolism, as evidenced by the finding of mutations in critical genes regulating these processes, including LRP1, collagen genes, fibrillin and TGF-β receptors, or their coupled pathways. Perturbances in these connected signaling pathways contribute to phenotype switching in endothelial and vascular smooth muscle cells of the affected artery, in which their physiological quiescent state is lost and replaced by a proliferative activated phenotype. Of interest, dissections in various anatomical locations are associated with distinct sex and age predilections, suggesting involvement of gene and environment interactions in disease pathogenesis. Importantly, these cellular mechanisms are potentially therapeutically targetable. Consideration of arterial dissections as a collective pathology allows insight from the better characterized dissection types, such as that involving the thoracic aorta, to be leveraged to inform the less common forms of dissections, including the potential to apply known therapeutic interventions already clinically available for the former.
Subanalysis of the prevalence and detection of carbohydrate disorders among the cohort of respondents with overweight and obesity, depending on the degree and type of obesity in a large population within the definition of risk factors in our research of Ukraine on urban population in 2009-2013. Methods: The study protocol included the definition and evaluation of the 20 factors of cardiovascular risk of 1000 respondents (468 men and 532 women) at the age 30-69 years living in 5 regions of Dnipropetrovsk and subanalysis contained in this publication concerned the prevalence
Familial hypercholesterolemia (FH) is one of the most common, inherited autosomal dominant diseases. Most often, FH is caused by dominant mutation of the gene, responsible for the synthesis of low density lipoprotein (LDL) membrane receptors that remove LDL from the blood plasma. As a result, individuals with a mutation of this gene from birth have a significantly increased level of cholesterol LDL in the blood. FH mediates the accelerated development of cardiovascular disease of atherosclerotic genesis, especially coronary heart disease (CHD), so the level of cardiovascular mortality in the population of such patients is extremely high. The article focuses on the fact that the main threat of these lipid disorders is the early and rapid initiation of atherosclerotic lesions of coronary vessels: in patients with heterozygous FH with a total cholesterol level of 8–15 mmol/l, CHD usually manifests up to 55 and 60 years, whereas in homozygous patients with a total cholesterol level of 12–30 mmol/l, CHD manifests at the start of their life and if left untreated, death occurs by the age of 20 years. The major genetic disorders in familial hypercholesterolemia and the frequency of their detection in the population are characterized. There are definitions of clinical screening options for FH: targeted, opportunistic, universal, cascadic. A comprehensive view of the diagnosis of FH according to the Dutch Lipid Clinic Network (DLCN) is provided. The basic principles of non-medication and three-step medication treatment of FH are presented. The article presents a clinical case of the homozygous FH taking into account the peculiarities of the disease course, the results of laboratory and instrumental studies and step-by-step treatment in the department of dyslipidemia of M.D. Strazhesko Institute of Cardiology of NAMS of Ukraine. The epidemiological data of the Ukrainian population survey on the possible prevalence of FH in Ukraine are presented. The preliminary analysis of the Ukrainian registry of patients with FH as a national fragment of the international ScreenProFH Registry and the European Register EAS-FHSC is provided.
Purpose: Subanalysis of the prevalence and detection of hypertension among the cohort of respondents with overweight and obesity, depending on the degree and type of obesity in a large population within the definition of risk factors in our research of Ukraine on urban population in 2009-2013.
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