**1. Introduction**

Cardiovascular diseases (CVD) are the most common causes of death worldwide. As already well known, the CVD has several risk factors such as blood pressure, glucose, lipids, blood pressure, glucose, lipids, blood pressure glucose, lipids etc. As arterial as venous thrombosis are major cause's morbidity and mortality.

There is an exponential increase in the risk of arterial and venous thrombotic events with age, gender, smoking habits, diet type, etc. [1].

The reason of arterial thrombosis (AT) is rupture of atherosclerotic plaque and formation of platelet-mediated thrombi, which can cause ischemic injuries. The clinical manifestations of atherothrombosis in most cases are cardiac ischemia and stroke. After the acute Myocardial Infarction (MI) and stroke, venous thrombosis (VT) is most common vascular disease. Venous thrombi are produced by fibrin and red blood cells. VT and AT are associated with variety of causes. For example, VT is associated with hypercoagulatin or reduced blood flow, while AT has been linked to atherosclerosis [1].

The thrombocyte activation, which is triggered by major endothelial injury, creates main background for thrombus formation in the heart and arterial circulation. However, the high rate of blood flow prevents thrombus and clot formation. Activation and adherence of platelets are major predisposing circumstance for thrombus formation beneath the high shear stress in arteries [2]. Arterial thrombi (defined as "white") have been traditionally proposed to be composed mainly of fibrin and platelet aggregates. The Venous thrombi (defined as "red") have been proposed as mostly being enriched in fibrin and erythrocytes [3].

The significant determinant for AT is the complex interaction of lipids, inflammation and immune system, which is less, but, important for venous thrombosis as well [1]. The major mechanisms triggers intravascular thrombosis, lies at cellular and molecular levels, is known as "Virchow's triad" and includes endothelial injury, stasis or turbulent blood flow and blood hypercoagulability. Endothelial injury leading to platelet activation almost inevitably underlies thrombus formation in the heart and the arterial circulation, where the high rates of blood flow impede clot formation. Platelet adherence and activation is a necessary prerequisite for thrombus formation under high shear stress, such as exists in arteries [4].

Abnormal blood flow contributes to AT by causing endothelial injury or dysfunction. Furthermore, chaotic blood flow forms countercurrents and local pockets of stasis. Stasis is major factor in the development of venous thrombi. Under conditions of normal laminar blood flow all blood cells are found mainly in the center of the vessel lumen, separated from the endothelium by a slower moving layer of plasma, but static blood flow contributes to thrombosis. Hypercoagulability is high tendency of the blood to clot. It is an important risk factor for venous thrombosis [5].

Some peripheral blood biomarkers are useful preventive markers for arterial and venous thrombosis. The association of venous thrombosis and the ABO histo-blood group is well established. Numerous studies have demonstrated the association between the ABO blood system and venous thrombosis. It has already been frequently revealed in various populations that venous thrombosis is less frequent in the O group than in individuals with other ABO blood groups. Individuals including A, B and AB (non-O) blood group have increased of venous thrombotic disease incidence compared to the O blood group individuals.

The non-OO blood group carriers are at more significant, two-fold risk of thrombosis rather than the individuals falling into the OO blood group carriers. Accordingly, the significant serious risk of thrombosis was higher in B alleles' carriers than in those carrying A alleles [6]. Many scientific data showed the blood group's possible protective effect with venous thrombosis [7].

Under an increased risk of venous thrombosis discussed, the ABO blood group influences plasma levels of the coagulation glycoprotein named von Willebrand factor (vWF). The vWF levels are 25% lower in the O group individuals compared to other blood groups. The mechanism of how the ABO group determines plasma vWF levels has not been clearly determined. It is already known that ABO (H)

**89**

*The Study of Some Possible Risk Factors for Arterial Thrombosis in the Example of Georgian…*

carbohydrate antigenic determinants are expressed on the N-linked glycan chains of

As it already mentioned vWF is a risk factor as AT as VT. It is the molecular player in pathogenesis of thrombosis. The high level of vWF is correlated with arterial thrombosis, and especially morphological changes of vWF is a risk factor of cardiovascular disease, through promoting the platelet binding to damaged endothelium and platelet aggregation [9]. In the case of venous thrombosis, vWF is essential for flow reduction-induced thrombus formation in deep veins (Deep vein thrombosis (DVT)). The vWF-mediated platelet recruitment in DVT in the setting of blood flow disturbance plays an important pathogenic role. The gene mutations and polymorphisms, aging, hormone status, ABO blood groups, and systemic inflammation, have been involved in the modulation of both VTE predisposition

Aging and ABO blood type influence in the bidirectional and combined way on vWF and FVIII levels. There are many studies shown that vWF significantly elevated in centenarians and type non-O individuals achieved much earlier in life

It has been investigated that the rate of venous thromboembolism is higher in black rather than white populations. Also, the non-O blood types have been associated with a notably high risk of venous thromboembolism. Since the majority of black population has an O blood and B blood type, thus may expect low cases of this disease. But it is paradoxical to find that VT prevalence has been observed to be higher in blacks than whites [14]. Due to the study to reveal suppose association between ABO and VT in blacks separately was, find out that the rate of VT was quite higher in non-O blood type individuals comparing to those with O blood groups, which also previously fixed in whites. Obtained data suggests that non-O blood type may consider as protective factor against VT in blacks too. The VT rate was higher in both, black and white non-O blood group individuals and was higher in males comparing to females and increasing with age. Further studies also confirmed above mentioned association with O group, that it may be a protective factor

Various studies have also been reported similar to AT [15], while in different studies, this similarity was not found [6]. The study done in Switzerland reported that 2.5 times higher prevalence of B allele among MI patients than controls [16]. Underlined mechanism where may B allele is involved in pathogenesis of MI is still uncertain, since the role of ABH antigen is still unclear. In this regards various pos-

The association between ABO histo-blood group, factor VIII and vWF have currently been revealed by O'Donnel and Laffan et al., [17] where BB homozygous had significantly high levels of vWF. The mechanism how B blood type affects vWF plasma levels is uncertain, but it is already defined that epitopes of N-linked oligosaccharide on the serum proteins modulate their half-lives. Hence it may be suggested that the ABH epitopes affect vWF plasma levels which cause elevation of

There are two major pathophysiological explanations tell that B antigen determines an aggregation of platelets, which may be a precursor of MI. The first mechanism is that removal of B antigen from multimeric glycoprotein by α-galactosidase decreases ristocetin cofactor activity [18] and the second is the fact which is claiming that increased platelet adhesiveness is shown in non O group individuals.

A study confirms the link between some vascular disorders and the non-O blood groups. The study has shown that there was a similar effect of ABO(H) on the level of vWF, but further research is required for obtaining more details on O(H) antigen expression levels in thrombosis. However, as A1A, A1B and BB composed of the

vWF plasma levels, which is highly associated with increased risk of MI.

*DOI: http://dx.doi.org/10.5772/intechopen.96121*

circulating plasma vWF [8].

and plasma levels of vWF [10].

the high vWF levels [11–13].

against VT, regardless of age and gender.

sibilities can be discussed.

#### *The Study of Some Possible Risk Factors for Arterial Thrombosis in the Example of Georgian… DOI: http://dx.doi.org/10.5772/intechopen.96121*

carbohydrate antigenic determinants are expressed on the N-linked glycan chains of circulating plasma vWF [8].

As it already mentioned vWF is a risk factor as AT as VT. It is the molecular player in pathogenesis of thrombosis. The high level of vWF is correlated with arterial thrombosis, and especially morphological changes of vWF is a risk factor of cardiovascular disease, through promoting the platelet binding to damaged endothelium and platelet aggregation [9]. In the case of venous thrombosis, vWF is essential for flow reduction-induced thrombus formation in deep veins (Deep vein thrombosis (DVT)). The vWF-mediated platelet recruitment in DVT in the setting of blood flow disturbance plays an important pathogenic role. The gene mutations and polymorphisms, aging, hormone status, ABO blood groups, and systemic inflammation, have been involved in the modulation of both VTE predisposition and plasma levels of vWF [10].

Aging and ABO blood type influence in the bidirectional and combined way on vWF and FVIII levels. There are many studies shown that vWF significantly elevated in centenarians and type non-O individuals achieved much earlier in life the high vWF levels [11–13].

It has been investigated that the rate of venous thromboembolism is higher in black rather than white populations. Also, the non-O blood types have been associated with a notably high risk of venous thromboembolism. Since the majority of black population has an O blood and B blood type, thus may expect low cases of this disease. But it is paradoxical to find that VT prevalence has been observed to be higher in blacks than whites [14]. Due to the study to reveal suppose association between ABO and VT in blacks separately was, find out that the rate of VT was quite higher in non-O blood type individuals comparing to those with O blood groups, which also previously fixed in whites. Obtained data suggests that non-O blood type may consider as protective factor against VT in blacks too. The VT rate was higher in both, black and white non-O blood group individuals and was higher in males comparing to females and increasing with age. Further studies also confirmed above mentioned association with O group, that it may be a protective factor against VT, regardless of age and gender.

Various studies have also been reported similar to AT [15], while in different studies, this similarity was not found [6]. The study done in Switzerland reported that 2.5 times higher prevalence of B allele among MI patients than controls [16]. Underlined mechanism where may B allele is involved in pathogenesis of MI is still uncertain, since the role of ABH antigen is still unclear. In this regards various possibilities can be discussed.

The association between ABO histo-blood group, factor VIII and vWF have currently been revealed by O'Donnel and Laffan et al., [17] where BB homozygous had significantly high levels of vWF. The mechanism how B blood type affects vWF plasma levels is uncertain, but it is already defined that epitopes of N-linked oligosaccharide on the serum proteins modulate their half-lives. Hence it may be suggested that the ABH epitopes affect vWF plasma levels which cause elevation of vWF plasma levels, which is highly associated with increased risk of MI.

There are two major pathophysiological explanations tell that B antigen determines an aggregation of platelets, which may be a precursor of MI. The first mechanism is that removal of B antigen from multimeric glycoprotein by α-galactosidase decreases ristocetin cofactor activity [18] and the second is the fact which is claiming that increased platelet adhesiveness is shown in non O group individuals.

A study confirms the link between some vascular disorders and the non-O blood groups. The study has shown that there was a similar effect of ABO(H) on the level of vWF, but further research is required for obtaining more details on O(H) antigen expression levels in thrombosis. However, as A1A, A1B and BB composed of the

*Erythrocyte - A Peripheral Biomarker for Infection and Inflammation*

with age, gender, smoking habits, diet type, etc. [1].

atherosclerosis [1].

thrombosis [5].

There is an exponential increase in the risk of arterial and venous thrombotic events

The reason of arterial thrombosis (AT) is rupture of atherosclerotic plaque and formation of platelet-mediated thrombi, which can cause ischemic injuries. The clinical manifestations of atherothrombosis in most cases are cardiac ischemia and stroke. After the acute Myocardial Infarction (MI) and stroke, venous thrombosis (VT) is most common vascular disease. Venous thrombi are produced by fibrin and red blood cells. VT and AT are associated with variety of causes. For example, VT is associated with hypercoagulatin or reduced blood flow, while AT has been linked to

The thrombocyte activation, which is triggered by major endothelial injury, creates main background for thrombus formation in the heart and arterial circulation. However, the high rate of blood flow prevents thrombus and clot formation. Activation and adherence of platelets are major predisposing circumstance for thrombus formation beneath the high shear stress in arteries [2]. Arterial thrombi (defined as "white") have been traditionally proposed to be composed mainly of fibrin and platelet aggregates. The Venous thrombi (defined as "red") have been

The significant determinant for AT is the complex interaction of lipids, inflammation and immune system, which is less, but, important for venous thrombosis as well [1]. The major mechanisms triggers intravascular thrombosis, lies at cellular and molecular levels, is known as "Virchow's triad" and includes endothelial injury, stasis or turbulent blood flow and blood hypercoagulability. Endothelial injury leading to platelet activation almost inevitably underlies thrombus formation in the heart and the arterial circulation, where the high rates of blood flow impede clot formation. Platelet adherence and activation is a necessary prerequisite for throm-

Abnormal blood flow contributes to AT by causing endothelial injury or dysfunction. Furthermore, chaotic blood flow forms countercurrents and local pockets of stasis. Stasis is major factor in the development of venous thrombi. Under conditions of normal laminar blood flow all blood cells are found mainly in the center of the vessel lumen, separated from the endothelium by a slower moving layer of plasma, but static blood flow contributes to thrombosis. Hypercoagulability is high tendency of the blood to clot. It is an important risk factor for venous

Some peripheral blood biomarkers are useful preventive markers for arterial and venous thrombosis. The association of venous thrombosis and the ABO histo-blood group is well established. Numerous studies have demonstrated the association between the ABO blood system and venous thrombosis. It has already been frequently revealed in various populations that venous thrombosis is less frequent in the O group than in individuals with other ABO blood groups. Individuals including A, B and AB (non-O) blood group have increased of venous thrombotic disease

The non-OO blood group carriers are at more significant, two-fold risk of thrombosis rather than the individuals falling into the OO blood group carriers. Accordingly, the significant serious risk of thrombosis was higher in B alleles' carriers than in those carrying A alleles [6]. Many scientific data showed the blood

Under an increased risk of venous thrombosis discussed, the ABO blood group influences plasma levels of the coagulation glycoprotein named von Willebrand factor (vWF). The vWF levels are 25% lower in the O group individuals compared to other blood groups. The mechanism of how the ABO group determines plasma vWF levels has not been clearly determined. It is already known that ABO (H)

proposed as mostly being enriched in fibrin and erythrocytes [3].

bus formation under high shear stress, such as exists in arteries [4].

incidence compared to the O blood group individuals.

group's possible protective effect with venous thrombosis [7].

**88**

meaningful proportion of the population attributable fraction of VT, there may be a role for more widespread adoption of ABO(H) typing in testing strategies [19]. The study of the Iranian population has not shown a significant association between ABO blood groups and coronary artery diseases. Similar results have been shown in the cases of different blood groups as well [20]. Similar results were revealed according to the study of the cardiovascular risk factors and MI in the Turkish cohort. The study showed no difference according to the cardiovascular risk factors and different blood groups within patients with MI and healthy population [21]. No association of the blood group B with MI in the sample population in Malaysia has been revealed [22].

Our research aimed to find a possible relationship between the blood groups, such as ABO, Rh, Kell, MN and AT, based on the cases of the Georgian population. The cardiovascular system diseases are also topical for Georgia, which is proved by "The European Heart Network" (EHN) (based in Brussels, EHN is an alliance of different countries together with non-governmental organizations and "Heart Foundations"). According to the research conducted by the alliance, in 2015, 29.007 deaths were reported in men and 33.509 in women ([European Cardiovascular Disease Statistics 2017 (http://www.ehnheart.org/cvd-statistics.html).
