Readiness of clinical laboratory diagnostics and cardiologists to implement the recommendations of the fourth universal definition of myocardial infarction.

This study describes the problems of the implementation of the fourth universal definition of myocardial infarction in the medical institutions of four cities: Volgograd (with Volzhsky), Yekaterinburg, Perm, Ufa, and districts of the Volgograd region. The multicenter study was conducted in the form of a questionnaire of specialists in cardiology and laboratory services. After a survey of cardiac specialists, it was found that a third of them did not see the benefits of the hs-cTn test recommended for the diagnosis of myocardial infarction, and almost half of the specialists surveyed believed that myoglobin was a necessary test for detecting myocardial infarction. Probably, this is due to the fact that 16 clinical diagnostic laboratories from the 5 above regions still perform the determination of myoglobin in patients with suspected myocardial infarction. The material and technical support of medical and diagnostic institutions generally meets the requirements of the fourth universal definition of myocardial infarction. However, there is a problem of «qualitative¼ equipment of the regions of the Volgograd region, since only 3 out of 31 districts declared the possibility of carrying out a quantitative determination of hs-cTn , and qualitative analysis was carried out on platforms that are not monitored by the IFCC. It is worrying that almost half of the specialists of the clinical and diagnostic laboratories of the central district hospitals of the Volgograd region did not indicate the manufacturer of reagents for determining troponins. Thus, in the educational programs of advanced training of specialists in cardiology and laboratory services, it is necessary to include aspects related to the explanation of analytical characteristics, the characteristics of the technology for performing troponin tests and the related interpretation options for the results.

Features of endothelial dysfunction and morphofunctional changes of the uteroplacental complex in experimentally induced pre-eclampsia.

BACKGROUND: Pre-eclampsia is considered to be a severe complication of pregnancy. Theoretical investigation of its etiology and pathogenesis, development of strategies for its prevention and treatment are conditioned by the development of appropriate experimental models of this pathology. METHODS: The study involved Wistar rat lines weighing 220-240g. Experimental pre-eclampsia was modeled by replacing drinking water consumed by pregnant female rats with 1.8% NaCl solution throughout gestation. Arterial pressure, protein concentration in urine and tissue hydration extent were measured on the 1st and 21st days of gestation. Uteroplacental blood flow, vasodilating and antithrombotic endothelial functions were also assessed. For pathomorphological and immunohistochemical investigation murine monoclonal antibodies against vascular endothelial growth factor (VEGF), polyclonal rabbit antibodies against inducible and endothelial NO-synthases were used. RESULTS: Replacing drinking water with 1.8% NaCl solution in female rats throughout gestation elevates arterial pressure, causes proteinuria and edema, impairs vasodilating and antithrombotic endothelial properties, and suppresses uteroplacental blood circulation. A morphological examination of the animals revealed the signs of focal duodenitis, spasms of myometrium arteries with no invasion of syncytiotrophoblast into its walls which also involved a raised VEGF and reduced eNOS expression in the endothelium of myometrial vessels, as well as cytoplasmic expression of iNOS in the cells of inflammatory infiltrate. CONCLUSIONS: These findings make it possible to conclude that replacing drinking water with 1.8% NaCl solution causes a number of changes typical of pre-eclampsia and, therefore, can be regarded as an experimental model of this pathologic condition.

[The effect of sulodexide on placental mitochondria function in rats with experimental preeclampsia]. / Vliianie sulodeksida na funktsional'noe sostoianie mitokhondrii platsenty samok krys s éksperimental'noi preéklampsiei.

Substitution of drinking water for 1.8% NaCl in pregnant rats caused a pronounced increase in arterial pressure by 24,3% and urinary protein by 117% to day 21 of pregnancy. State 4 respiration of isolated placental mitochondria in the group of negative control was 3- and 1.5-fold higher with malate/glutamate and succinate as substrates than in placental mitochondria isolated from uncomplicated pregnant animals. This led to a decrease of the respiratory control ratio. These results suggest that development of experimental preeclampsia is accompanied by mitochondrial dysfunction through uncoupling of oxidative phosphorylation. Daily administration of sulodexide to females with experimental preeclampsia (EP) per os at a dose of 30 LE during the whole period of gestation decreased manifestations of the disease as evidenced by a slight increase in blood pressure (by 8,6%) and less pronounces increase in urinary protein (by 58,9%). Sulodexide decreased development of mitochondrial dysfunction in EP rats as shown a decrease of non-stimulated ADP respiration with malate/glutamate and succinate (4.5- and 2.5-fold, respectively) as compared with the negative control group and the corresponding increase in the respiratory control ratio (2.5- and 1.5-fold, respectively). Thus, sulodexide reduces uncoupling of oxidative phosphorylation and enhances the functional activity of mitochondria in EP animals, possibly due to its antioxidant and endotelioprotective effects.