This clinical case report describes the simultaneous development of an acute myocardial infarction, stroke, and a massive pulmonary thromboembolism in a 44-year-old patienta carrier of the thrombophilia gene polymorphisms: MTHFR C677T, A1298C, PAI-1 4G/5G, ITGA2 C807T. Multifocal thrombosis was probably due to the initial congenital deficiency of anticoagulants, accompanied by a decrease in antithrombin III and protein C, against the background of their critical consumption in cascade thrombosis, in combination with the carrier of polymorphisms of moderate and low thrombogenic risk. This case is unique in that there is usually a tendency toward clinical thrombosis when the level of antithrombin III is less than 70%. Such patients develop thrombosis at a younger age, and by the age of 35-40 years usually have a verified diagnosis of extremely high-risk hereditary thrombophilia. In this case, multifocal thrombosis was accompanied by critically low values of anticoagulants: antithrombin III -3.4%, and protein C -36.8%. The patient had suffered from epilepsy since childhood and took anticonvulsant drugs that increase the deficit of active folic acid and can lead to hyperhomocysteinemia, which in this case, against the background of an innate decrease in the activity of methyltetrahydrofolate reductase, could have aggravated the situation.

Osteoporosis is a widespread metabolic disease of the skeleton among the elderly. Osteoporotic fractures are significant manifestation of the disease, which can substantially affect the quality of life. The purpose of this article is to review approaches to the management of patients with acute osteoporotic fracture. This article consists of two parts. The first part reviews general information about osteoporosis, clinical course of osteoporotic fracture, differential diagnosis of pain syndrome, methods of visualization of fractures, differential diagnosis of osteoporosis. In the second part, we discuss differential diagnosis of osteoporotic fracture according to the data of imaging methods, non-pharmacologic, pharmacologic and surgical methods of treatment.

Peripartum cardiomyopathy (PPCM) is a diagnosis of exclusion in women presenting with heart failure due to left ventricular (LV) systolic dysfunction. PPCM should be considered in case of unknown etiology of heart failure during pregnancy or after childbirth. Long QT syndrome is a primary electrical heart disease associated with a prolonged QT interval on the ECG, recurrent paroxysms of ventricular tachycardia, and a high risk of sudden death. Our aim was to demonstrate a case of cardiomyopathy in combination with long QT syndrome in a patient with a mutation in the FLNC gene. A 38-years-old woman was hospitalized 4,5 months after childbirth after sudden cardiac arrest and successful cardiopulmonary resuscitation. Long QT interval was revealed on the electrocardiogram. Echocardiography registered an akinesis of the apical and middle segments of the anterior wall of the left ventricle and interventricular septum, apex, left ventricular ejection fraction – 32%. Coronary angiography revealed no stenotic lesion of the coronary arteries. N-terminal precursor of brain natriuretic peptide (NTproBNP) was 33300 mg/l. Mass parallel sequencing of 17 genes revealed the nucleotide variant c.1609T>G (chr7:128480661T>G, NM_001488.4; rs760471547) in a heterozygous state in exon 10 of the FLNC gene (OMIM 102565), leading to the amino acid variant p.Y537D.The combination of peripartum cardiomyopathy and long QT syndrome may increase the likelihood of sudden cardiac death, especially in individuals with a genetic mutation of cardiomyopathy. Timely diagnosis of the described conditions is necessary to prevent complications and increase the life expectancy of patients.