The long existence of arterial hypertension in combination with insulin resistance inevitably impairs the functioning of all elements of hemostasis. In these circumstances, there is a weakening of the vascular control of platelet aggregation, hemocoagulation and fibrinolysis. This is based on the decreased production in the blood vessels of substances with thromboresistant properties, increasing the permeability of the endothelium to macromolecules, accumulation in the vascular wall lipoproteins, adhesion of platelets and leukocytes. For patients with hypertension and insulin resistance characteristic of platelet activation, leading to increased circulating blood platelets with a modified surface structure and their aggregates. It caused such patients, high content in platelets of biologically active substances and the increase in the number of different receptors on their surface, including fibrinogen. The combination of hypertension with insulin resistance inevitably impairs the functioning and coagulation component of hemostasis in the blood increases the content of fibrinogen, VII, VIII, IX coagulation factors, von Willebrand factor by lowering the activity of antithrombin III, protein C and protein S.
Hemostasis; Hypertension; Insulin resistance; Hyperinsulinaemic; Impaired glucose tolerance
In recent years, cardiologists have shown a strong interest in studying the combination of arterial hypertension (AH) with various elements of the metabolic syndrome. This is due to the increasing frequency of their occurrence in developed countries [1-3] with the prevalence of hyperinsulinemia and impaired glucose tolerance are particularly high and tend to gradually increase . The main link of their link is insulin resistance, which has been repeatedly confirmed in a large number of multicenter studies . As a rule, the development of a violation of glucose tolerance in patients with AH is preceded by hyperinsulinemia . The reasons for the onset of insulin resistance are not fully understood. It is assumed that there is a common genetic defect that promotes development and insulin resistance and AH [7-9].
The prolonged existence of AH in combination with insulin resistance ultimately leads to the development of a complex of metabolic, hormonal and clinical disorders that are risk factors for the development of cardiovascular diseases, which are based on insulin resistance and compensatory hyperinsulinemia, which are the basis of MS formation [10,11].
The combination of hypertension and impaired glucose tolerance has been known for a long time. As early as 1922, Georgii Fyodorovich Lang pointed out the relationship between hypertension and metabolic disturbances, while still young at that time his students Grotelle et al.  noted in hypertensive patients a sufficiently high frequency of the pathology of carbohydrate metabolism.
Subsequently, it was found that the basis for lowering the sensitivity to insulin may be a violation of its ability to suppress the production of glucose in the liver and/or stimulate the capture of glucose by peripheral tissues. Since 75-80% of glucose is consumed in skeletal muscles in healthy people, it became clear that the main cause of insulin resistance is the disturbance of insulin-stimulated glucose utilization in skeletal muscles . It has been found that disorders leading to insulin resistance can occur at several levels: pre-receptor (abnormal insulin), receptor (decrease in the number or affinity of receptors), glucose transport level (decrease in the number of GLUT4 molecules) and postreceptor (signal transduction and phosphorylation) [14,15]. Anomalies of the insulin molecule are rare and have no clinical significance. The density of insulin receptors can only sometimes be reduced in patients with insulin resistance by the mechanism of negative feedback against hyperinsulinemia . There are serious reasons to believe that the main defects that determine insulin resistance are localized at the postreceptor level. They are not the same for different patients, but the acquired disorders in the body, in particular, in the hemostatic system, are important for the manifestation of existing genetic defects . The presence of these disorders can greatly increase the risk of thrombosis, which shortens the duration of the life of patients. In this connection, the goal is to summarize the available information on haemostasis disorders in hypertension and insulin resistance.
Long-existing hyperinsulinemia negatively affects the state of the vessels largely due to stimulation of the development of various growth factors in them, which leads to intensive proliferation and migration to the intima of arterial smooth muscle cells. This is accompanied by excessive production of an inhibitor of plasminogen activator-1. All this contributes to vascular remodeling and accelerates the development of atherosclerosis [18,19]. A definite value in the acceleration of these processes in the vascular wall with hypertension with insulin resistance is the stimulating effect of excess insulin on the synthesis of collagen in fibroblasts . It has also been established that the thickness of the intima-media complex of arteries and the number of circulating blood in the blood desquamated endotheliocytes in patients with AH with insulin resistance are closely correlated with an increase in insulin levels [21,22].
The presence of persons with arterial hypertension and insulin resistance inevitably reduces the response of the vessels to vasodilator and strengthens it on vasoconstrictor effects. These effects can be caused not only by changes in the metabolism and architectonics of the vascular wall, but also by negative effects on the vascular endothelium and platelets, accompanied by increased production of endothelin, thromboxane A2, prostaglandin F2α, and a decrease in prostacyclin synthesis [23,24]. In this connection, the effect of excess insulin on the synthesis of lipids, not only in the liver, but also directly in the vascular wall, is very pathogenetically important .
The influence of insulin resistance and hyperinsulinemia on the vascular tone and level of arterial pressure was studied in sufficient detail. Insulin has a normally protective effect on blood vessels due to the activation of phosphatidyl-3-kinase in endothelial cells and micro vessels, induces endothelial NO synthase gene expression, enhances NO release by endothelial cells and insulin-induced vasodilation. At the same time, with chronic hyperinsulinemia, pathological vasospastic mechanisms are triggered, leading to AH progression [26,27].
Normally, the vascular endothelium has a leading role in the clear modulation of the entire haemostatic potential. With hyperinsulinemia in the vascular endothelium, persistent metabolic disorders occur leading to the development of severe hemostasiopathy . So, with insulin resistance, there is often a decrease in the blood of substances of vascular origin with antiaggregatory activity, compounds limiting vasospasm and coagulation and enhancing fibrinolysis. The leading factors contributing to the disruption of vascular hemostasis in these patients are elevated blood pressure, hyperinsulinemia, as well as the onset of hypercholesterolemia and hypertriglyceridemia. Their combination promotes the acceleration of the development of atherosclerotic plaques, the death of endotheliocytes and an increase in the production in the vascular wall of von Willebrand factor. The effect of over-listed factors is realized through activation of lipid peroxidation in the bloodstream , which in itself is able to weaken the antithrombotic abilities of the vascular wall in normal and pathological conditions [29,30]. First of all, this is manifested by a decrease in the formation in the vascular endothelium of substances that provide vasodilation, inhibiting the adhesion and aggregation of platelets that inhibit the proliferation of smooth muscle cells . In addition, under conditions of AH with insulin resistance, the endothelium itself begins to produce free radicals that cause a deepening of its dysfunction. This was confirmed by morphological studies that found degenerative changes in endothelial cells .
It becomes clear that endothelial dysfunction is an important factor that significantly worsens the prognosis and aggravates the course of hypertension due to thickening of the middle shell of the vessels, a decrease in their lumen, an increase in the degree of vasoconstriction due to the growth of total peripheral vascular resistance [33,34]. The vicious circle closes: violations of hemodynamics in hypertension are very active in changing the structure and function of the endothelium, which further increases hypertension . The emerging imbalance between substances produced in the endothelium with thrombogenic and thrombotic resistance promotes an increase in its permeability for macromolecules, accumulation of lipoproteins, adherence to it of platelets and leukocytes [36-38]. The most likely cause of this is the weakening of the vascular enzymatic system of arachidonic acid metabolism and the production of prostacyclin in endotheliocytes under the influence of free radical oxidation, which is activated as the body ages, develops hypertension and metabolic disorders [39,40]. Also, with AH with insulin resistance, the ability of endothelial cells to release NO decreases, leading not only to weakening of vasodilation but also to the process of remodeling the vascular wall, but also to weakening the inhibition of adherence and aggregation of platelets and monocytes, atherogenesis and thrombosis [41,42]. This aggravates unfavorable changes in the microcirculation system, which, with hypertension with insulin resistance, is often associated with a decrease in the diameter of the micro vessels and the violation of blood outflow. At the same time micro vessels are transformed into passive conductors of blood flow, which leads to its redistribution according to the principle of least resistance. The emerging situation causes a shunting of blood flow, as a result of which a lack of blood flow to the metabolic tissue structures is formed . Negative changes in the diameter and structure of the arterial wall, as well as the rate of blood flow, lead to a violation of laminar flow and increased pressure on the vascular wall, which directly activates platelets, which occupy an important place in the cell-humoral interaction of the hemostatic system [44,45].
Data from the literature indicate an increase in the functional activity of platelets already in the early stages of hypertension, manifested by an increase in sensitivity to aggregation inducers, an increase in their adhesive, aggregation, and secretory properties [32,37]. In patients with AH and insulin resistance, these platelet changes closely correlate with the magnitude of systolic and diastolic arterial pressure and the severity of hyperinsulinemia. Electron microscopic study of platelets of AH patients with insulin resistance revealed the presence among them of various morphological forms, caused by their increased activation. At the same time, the most characteristic for them is the echinocyte change in shape. Also in hypertensive patients with insulin resistance, there is an increase in circulating blood of various sizes of platelet aggregates, the number of which closely correlates with the frequency of thrombotic complications .
With AH with insulin resistance in circulating platelets, the levels of chemokines, cytokines, growth factor, proteins, fibrinogen, von Willebrand factor, the 4th platelet factor and thromboglobulin are very often increased. Moreover, in the platelets, the content of dense granules accumulating small molecules-Ca2+, ADP, ATP, biogenic amines (serotonin, catecholamines, etc.) can also increase . In addition, under these conditions, the functioning of platelet-localized receptors for collagen, thrombin, ADP, catecholamines, serotonin, thromboxane A2, platelet activating factor, immunoglobulin Fc fragment, complement components, insulin, endothelin, adrenoreceptors can significantly increase from the initial stimulus, to the strengthening of their universal response - aggregation . At the same time, the number of glycoproteins IIb/IIIa, which play an important role in aggregation for any stimuli, is significantly increased on platelets of hypertensive patients with insulin resistance. The practical significance of these changes was confirmed by the prospective study PROCAM, conducted among men aged 40-60 years, who showed that the increased risk of cardiovascular disease in hypertension with insulin resistance largely depends on the imbalance in the system of platelet hemostasis [48,49].
The hyper function of thrombocytes, which comes with AH with insulin resistance, is also associated with the activation of enzyme systems in them, which strengthens aggregation, which ultimately increases the risk of thrombotic complications. This is also caused by an increase in the content of magnesium platelets in the cytoplasm, an increase in its pH and an increase in the sensitivity of platelets to arachidonic acid .
In patients with hypertension with insulin resistance, in contrast to healthy individuals, there is a high degree of correlation between the increase in calcium level in platelets under the influence of aggregation inducers (ADP and platelet activating factor), the thickness of the wall of the left ventricle and the level of arterial pressure. This is due to the development of abnormalities in the structure of the plasma membrane of platelets, changes in the work of sodium, potassium, and calcium pumps that develop with hypertension and deeper as the duration of its duration increases .
In view of the fact that Ca2+ ions directly participate in the realization of phosphoinositol, prostaglandin-thromboxane, tyrosine kinase, and phospholipase pathways of platelet activation, its excessive intracellular content inevitably leads to AH with insulin resistance to enhance their aggregation. The rise in these conditions of Ca2+level in platelets, stimulated by various inducers, correlate with the severity of their aggregation activity and the degree of the release reaction. Disruption of the trans-membrane exchange of Na+ in the blood plates helps to reduce the normal capture of serotonin from the peripheral blood by platelets, since this process is highly Na+-dependent, which can lead to an increase in the concentration of aggregation inducers in the blood plasma of AH patients with insulin resistance and additional platelet stimulation [51,52].
The combination of hypertension with insulin resistance inevitably disturbs function and coagulation component of hemostasis system. So, in hypertension with insulin resistance detected elevated levels of fibrinogen in plasma, which is strongly positively correlated with blood pressure. The degree of this dependence varies somewhat for men and women .
The level of synthesis of VII,VIII, IX coagulation factors is normally clearly genetically determined  closely correlates with hypertension with insulin resistance with an increase in arterial pressure and the duration of the violation of glucose tolerance . Even with a high normal arterial pressure with hyperinsulinemia, a significant increase in the activity of VIII and XII coagulation factors and a decrease in activated partial thromboplastin time are found . With the formation of hypertension with insulin resistance, an even more pronounced increase in the amount of fibrin monomers in the blood, the activity of VIII and VII clotting factors, closely correlated with the systolic blood pressure . In addition, with AH with insulin resistance, there is often an increase in WF, which, however, may not be recorded in all cases because of the varying degree of endothelial damage. Also, with a long-term high blood pressure level under conditions of insulin resistance, a decrease in the activity of antithrombin III , protein C and protein S [55,58] can be noted.
A certain role in the formation of changes in the functioning of the anticoagulant and fibrinolytic blood systems in AH patients with insulin resistance is apparently played by sex hormones. Thus, in women with pre-menopausal hypertension, a significant increase in the activity of the level of the inhibitor of the tissue activator plasminogen-1, which closely correlates with a decreased level of estradiol, is recorded. In this case, the increase of this inhibitor in men with AH and insulin resistance occurs, as a rule, with a low content of testosterone in their serum .
Morning rise in blood pressure in patients with AH and insulin resistance, which is an independent prognostically important factor in the development of cerebral stroke in the morning hours , is associated with pronounced activation of coagulation, increased viscosity, reduced fibrinolytic blood properties and platelet hyperactivation. Also at the heart of the danger of a vascular catastrophe in this contingent lies the onset of instability of atherosclerotic plaques and the multifocality of endothelial alteration , the increased susceptibility to which is largely genetically determined .
A systematic study of hemostasis dysfunctions in patients with arterial hypertension with elements of the metabolic syndrome is a very promising and practically sought-after direction, which is rightly given great attention. In connection with the important role of hemostasis in the regulation of vital body functions, it can be assumed that further elucidation of the state of its mechanisms in arterial hypertension with insulin resistance can lead to the development of new methods for the prevention and treatment of cardiovascular disorders.
- Gerieva IS, Volkova NI (2010) Arterial hypertension and metabolic syndrome. Clinical Medicine 88: 4-8.
- Mancia G (2008) Metabolic syndrome. Hypertension 50: 32-40.
- Ceska R (2008) The clinical significance of the metabolic syndrome. DiabetVasc Dis Res 5-8.
- Skoryatina IA, Zavalishina SY, Makurina ON, Mal GS, Gamolina OV (2017) Some aspects of Treatment of Patients having Dislipidemia on the Background of Hypertension. Prensa Med Argent 103.
- Cuspidi C, Sala C, Zanchetti A (2008) Metabolic syndrome and target organ damage: role of blood pressure. Expert Rev CardiovascTher 6: 731-743.
- Sizov AA, Zavalishina SJ (2015) Russian Criminal Legislation in Prevention of Sexually Transmitted Diseases in the Territory of the Russian Federation. Biol Med 7.
- Kotseva K, Wood D, Backer GD, Bacquer DD, Pyorala K, et al. (2009) Cardiovascular prevention guidelines in daily practice: a comparison of Euroaspire I, II, and III surveys in eight European countries. Lancet 373: 929-940.
- Skoryatina IA, Zavalishina SY (2017) A Study of the Early Disturbances in Vascular Hemostasis in Experimentally Induced Metabolic Syndrome. Annu Res Rev Biol 15: 1-9.
- Robinson TG, Dawson SL, Ahmed U, Manktelow B, Fotherby MD et al. (2001) Twenty-four hour systolic blood pressure predicts long-term mortality following acute stroke. J Hypertens 35: 103-107.
- Yakovlev VM, Yagoda AV (2008) Metabolic syndrome and vascular endothelium. Stavropol.
- Shmeleva SV, Yunusov FA, Morozov YUS, Seselkin AI, ZavalishinaSYu (2018) Modern Approaches to Prevention and Correction of the Attorney Syndrome at Sportsmen. Prensa Med Argent 104: 2.
- Lang GF (1922) About hypertension: Archive of the State Clinical Institute for the improvement of doctors. Leningrad 1: 16-66.
- Moura RF, Ribeiro C, Oliveira JA, Stevanato E, de Mello MA (2009) Metabolic syndrome signs in Wistar rats submitted to different high-fructose ingestion protocols. Br J Nutr 8: 1178-1184.
- Morozova EV, Shmeleva SV, Rysakova OG, Bakulina ED, Zavalishina SY (2018) Psychological Rehabilitation of Disabled People Due to Diseases of the Musculoskeletal System and Connective Tissue. Prensa Med Argent 104.
- Zavalishina SYu (2017) Physiological Dynamics of Spontaneous Erythrocytes’ Aggregation of Rats at Last Ontogenesis. Annu Res Rev Biol 13: 1-7.
- Izmozherova OI (2005) Arterial hypertension, disorders of carbohydrate and lipid metabolism in women with obesity. Therapeutic archive 77: 67-69.
- Kutafina NV (2017) Platelet Parameters of Holstein Newborn Calves. Annu Res Rev Biol 15: 1-8.
- Chazova IE, Mychka VB (2008) Metabolic syndrome. Media Medica 324.
- Bikbulatova AA, Andreeva EG (2017) Dynamics of Platelet Activity in 5-6-Year Old Children with Scoliosis Against the Background of Daily Medicinal-Prophylactic Clothes’ Wearing for Half A Year. Biomed Pharmacol J 10.
- Bikbulatova AA (2017) Dynamics of Locomotor Apparatus’ Indices of Preschoolers with Scoliosis of I-II Degree Against the Background of Medicinal Physical Training. Biomed Pharmacol J 10.
- Butrova SA (2007) Modern possibilities and prospects of therapy of metabolic syndrome. Difficult patient 5: 31-34.
- Veselovskaya NG, Chumakova GA, Ott AV (2013) Noninvasive insulin resistance marker in obese patients. Russ J Cardiol 3: 28-32.
- Zavalishina SY (2017) Restoration of Physiological Activity of Platelets in New-Born Calves with Iron Deficiency. Biomed Pharmacol J 10: 711-716.
- Vorobyeva NV (2017) Physiological Reaction of Erythrocytes’ Microrheological Properties on Hypodynamia in Persons of the Second Mature Age. Annu Res Rev Biol 20: 1-9.
- Sanchez-Lozada LG, Tapia E, Jimenez A, Bautista P, Cristobal M et al. (2007) Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats. Am J Physiol Renal Physiol 292: 423-429.
- Skoryatina IA, Zavalishina SYu (2017) Impact of Experimental Development of Arterial Hypertension and Dyslipidemia on Intravascular Activity of Rats’ Platelets. Annu Res Rev Biol 14: 1-9.
- Glagoleva TI, Zavalishina SY (2017) Aggregation of Basic Regular Blood Elements in Calves during the Milk-feeding Phase. Annu Res Rev Biol 17: 1-7.
- Glagoleva TI, Zavalishina SY (2017) Physiological Peculiarities of Vessels’ Disaggregating Control over New-Born Calves’ Erythrocytes. Annu Res Rev Biol 19(1) : 1-9.
- Maksimov VI, Parakhnevich AV, Parakhnevich A?, Glagoleva TI, Kutafina NV (2017) Physiological Reaction of Erythrocytes’ Micro Rheological Features in Newborn Piglets on Unfavourable Environmental Factors. . Annu Res Rev Biol 16: 1-8.
- Bikbulatova AA (2014) Determining the thickness of materials in therapeutic and preventive heat-saving garments. Proceedings of higher education institutes. Textile industry technology 1: 119-123.
- Belozerova TB, Agronina NI (2017) The Development of the Social Service System in Russia. Prensa Med Argent 103: 4.
- Kutafina NV, Zavalishina SY (2012) Mechanisms of Vascular-Thrombocytic Hemostasis. Bulletin of the Peoples’ Friendship University of Russia, series “Ecology and Life Safety” 1: 30-37.
- Apanasyuk LA, Soldatov AA (2017) Socio-Psychological Conditions for Optimizing Intercultural Interaction in the Educational Space of the University. Scientific Notes of Russian State Social University 16: 143-150.
- Maloletko AN, Yudina TN (2017) (Un) Making Europe: Capitalism, Solidarities, Subjectivities. Contemporary problems of social work 3: 4-5.
- Roberson LL, Aneni EC, Maziak W (2014) Beyond BMI: The Metabolically healthy obese» phenotype; its association with clinical/subclinical cardiovascular disease and all-cause mortality – a systematic review. BMC Public Health 8: 14.
- Pozdnyakova ML, Soldatov AA (2017) The Essential and Forms of the Approaches to Control the Documents Execution 3: 39-46.
- Navarro J, Redon J, Cea-Calvo L, Lozano JV, Bonet C, et al. (2007) Metabolic syndrome, organ damage and cardiovascular disease in treated hypertensive patients. The ERICHTA study. Blood Press 16: 20-27.
- Weber M, Bakris G, Dahlöf B, Pitt B, Hester A et al. (2007) Baseline characteristics in the Avoiding Cardiovascular events through Combination therapy in Patients Living with Systolic Hypertension (ACCOMPLISH) trial: a hypertensive population at high cardiovascular risk. Blood Press 16: 13-19.
- Tikhonoff V, Casiglia E (2007) Metabolic syndrome: nothing more than constellation. Eur Heart J 28: 780-781.
- Aijaz B, Ammar KA, Jimenez FL, Redfield MM, Jacobsen SJ et al. (2008) Abnormal Cardiac Structure and Function in the Metabolic Syndrome: A Population-Based Study. Mayo Clin Proc 83: 1350-1357.
- Okauchi Y, Nishizawa H, Funahashi T, Ogawa T, Noguchi M et al. (2007) Reduction of visceral fat is associated with decrease in the number of metabolic risk factors in Japanese men. Diabetes Care 30: 2392-2394.
- Mensah GA (2002) The global burden of hypertension: good news and bad news. CardiolClin 20: 181-185.
- Anton FH, Ballantyne M, Stalenhoef AF, Sarti C, Murin J (2005) A comparative study with rosuvastatin in subjects with METabolic Syndrome: results of the COMETS study. European Heart Journal 26: 2664-2672.
- Belyakov NA, Chubrieva SY (2007) Metabolic syndrome and atherosclerosis. Med Academ J 7: 45-59.
- Palomo I, Alarcon M, Moore-Carrasco R, Argiles JM (2006) Hemostasis alterations in metabolic syndrome (review). Int J Mol Med 18: 969-974.
- Plochaya AA (2007) Metabolic syndrome. Med Herald 19: 25-29.
- Podrez EA, Byzova TV, Febraio ? (2007) Platelet CD36 links hyperlipidemia, oxidant stress and a prothromotic phenotype. Nat. Med 13: 1086-1095.
- Rendu F, Brohard-Bohn B (2001) The platelet release reaction: granules constituents secretion and function. Platelets 12: 261-273.
- Yaron G, Brill A, Dashevsky O (2006) C-reactive protein promotes platelet adhesion to endothelial cells: a potential pathway in atherothrombosis. British Journal of Haematology 134: 426-431.
- Nesova TN, Kisileva ZM, Khlevchuk ?V (2001) Evaluation of the functional activity of glycoproteins IIb-IIIa and von Willebrand factor in patients with various variants of acute coronary syndrome, the effect of arterial hypertension on the degree of activity of glycoproteins IIb-IIIa, von Willebrand factor. Thrombosis, Hemostasiology 5: 115-116.
- Sushkevich GN (2010) Pathological systems of hemostasis and principles of their correction. Krasnodar: Soviet Kuban 240.
- Fogari R, Mugellini A, Destro M, Corradi L, Zoppi A, et al. (2006) Losartan and prevention of atrial fibrillation recurrence in hypertensive patients. J Cardiovasc Phatmacol 47: 46-50.
- Belozerova TB, Agronina NI (2017) Russian Practice of Independent Quality Assessment of Social Services for People with Health Disorders and In Difficult Life Situations. Prensa Med Argent 103: 5.
- Alifirov AI, Mikhaylova IV, Makhov AS (2017) Sport-specific diet contribution to mental hygiene of chess player. Teoriya i praktika fizicheskoy kultury 4: 17.
- Woodward M, Lowe GD, Rumley A, Tunstall-Pedoe H, Philippou H (1997) Epidemiology of coagulation factors, inhibitors and activation markers: The Third Glasgow Monica Survey II. Relationships to cardiovascular risk factors and prevalent cardiovascular disease. Brit. J. of Haemat 97: 785-797.
- Cleerup GVR (1995) Platelet function and fibrinolytic activity duringrest and exercise in borderline hypertensive patients. Eur. J. Clin. Invest 25: 266-270.
- Donders SH, Lustermans FA, Van Wersch JW (1993) Coagulation factors and lipid composition of the blood in treated and untreated hypertensive patients. Scand. J. Clin. Lab. Invest 53: 179-86.
- Oganov RG, Timofeeva TN, Koltunov IE (2011) Epidemiology of arterial hypertension in Russia. The results of the federal monitoring of 2003-2010. Cardiovascular therapy and prevention 10: 9-13.
- Evdokimova AG, Evdokimov VV (2013) Possibilities of using drugs and inhibitors of angiotensin-converting enzyme in patients with arterial hypertension and coronary heart disease. Cardiovascular therapy and prevention 1: 80-87.
- Mikhaylova IV, Makhov AS, Alifirov AI (2015) Chess as multi-component type of adaptive physical culture. Teoriya i praktikaf izicheskoy kultury 12: 56-58.