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Inflammation plays a major pathogenetic role in the development of atherosclerotic plaques and related thromboembolic events. The identification of vulnerable plaques is of the utmost importance, as this may allow the implementation of more effective preventive and therapeutic interventions. Fluorodeoxyglucose positron emission tomography (FDG-PET) has been shown to be useful for tracing inflammation within plaques. However, its relationship to immunohistochemical findings in different territories of the peripheral circulation was not completely elucidated. We aimed to determine whether plaque inflammation could be measured by PET in combination with computer tomography (CT) using FDG and what is the relationship between FDG uptake and immunohistochemical findings in the removed atherosclerotic lesions of the femoral and carotid arteries. The study included 31 patients, 21 patients with high-grade stenosis of the internal carotid artery (ICA) and 10 patients with occlusion of the common femoral artery (CFA), all of whom underwent endarterectomy. Before endarterectomy in all patients, FDG-PET/CT imaging was performed. FDG uptake was measured as the maximum blood--normalized standardized uptake value, known as the target to background ratio (TBR max). TBR max amounted to 1.72 ± 0.8, and in patients with ICA, stenosis was not significantly different from patients with CFA occlusion. Immunohistochemical and morphometric analyses of the plaques obtained at endarterectomy showed that the density of T lymphocytes and macrophages (number of cells per square millimeter) was significantly higher in subjects with stenosis of the ICA than in subjects with occlusion of the femoral arteries: lymphocytes, 1.26 ± 0.21 vs. 0.77 ± 0.29; p = 0.02 and macrophages, 1.01 ± 0.18 vs. 0.69 ± 0.23; p = 0.003. In the whole group of patients, the density of inflammatory cells significantly correlated with FDG uptake represented by PET-TBR max: T lymphocytes, r = 0.60; p < 0.01 and macrophages, r = 0.65; p < 0.01. The results of our study show that FDG uptake is related to the accumulation of inflammatory cells in atherosclerotic lesions. This finding suggests that FDG uptake reflects the severity of atherosclerotic vessel wall inflammation, and in stenotic lesions, it could be an indicator of their vulnerability. However, data from large outcome studies is needed to estimate the usefulness of this technique in identifying the most dangerous atherosclerotic lesions and vulnerable patients.

Antiplatelet drugs represent one of the basic options for management of patients with different atherosclerotic diseases. Aspirin is the oldest and most often prescribed antiplatelet drug. The efficacy of aspirin depends on the clinical characteristics of the treated population and probably also on the type or location of atherosclerotic disease. It seems that it is most effective in coronary patients with clinically unstable disease, less effective in prevention of cerebrovascular incidents, and its efficacy is uncertain in peripheral artery disease (PAD) patients. One of the first meta-analyses (Antithrombotic Trialists' Collaboration - ATC) indicated that antiplatelet drugs also significantly reduce cardiovascular events in patients with PAD. However, only one third of the PAD patients included were treated with aspirin, while the rest received other anti-platelet drugs. The latest ATC meta-analysis of randomized control trials of aspirin therapy involving patients with diabetes and PAD demonstrated no benefit of aspirin in reducing cardiovascular events. Also in patients with preclinical PAD (pathological ankle brachial index) aspirin did not result in a significant reduction of vascular events. The new anti-platelet drugs prasugrel, ticagrelor and picotamide seem to be more effective than aspirin in PAD patients, particularly in diabetic patients with PAD. In conclusion, antiplatelet drugs are effective in prevention of cardiovascular events in different atherosclerotic diseases, including PAD. However, recent studies indicated that in PAD patients aspirin is less effective than in coronary artery disease. New anti-platelet drugs showed marginal superiority over aspirin without definite advantages. Aspirin thus remains the first line of antiplatelet drug for secondary prevention of cardiovascular events in PAD patients and clopidogrel as its effective alternative. Further, new studies on PAD patients are necessary to better define the role of anti-platelet agents in these patients and one of the promising ways of access to anti-platelet treatment would be personalized anti-platelet therapy.

Endothelial dysfunction as an integrating index of the risk factor burden and genetic susceptibility is an early marker of atherothrombotic disease. Therefore, tremendous interest exists in its measurement and determination of the clinical utility of the evaluation of endothelial function.Different invasive and non-invasive techniques exist for exploring various aspects of the pathobiology of the endothelium. As endothelial dysfunction is a diffuse-systemic disorder, the peripheral arteries, because of their accessibility, represent the basis for assessment of endothelial dysfunction. Flow-mediated dilation (FMD) of the peripheral conduit arteries is one of the most widely used tests of endothelial function. FMD measures the endothelial vasomotor response during reactive hyperemia, but it does not provide information concerning the control of arterial tone at rest. A new technique, low-flow-mediated constriction (L-FMC), provides complementary information to that by FMD, quantifying the decrease in the forearm conduit artery diameter that occurs in response to the decrease in blood flow during occlusion. This indicated that the L-FMC response is not based on nitric oxide availability but it might be mediated by other substances, providing a coordinated effect of vasodilation and its inhibition; therefore, simultaneous determination of FMD and L-FMC may provide comprehensive information on vascular homeostasis.Peripheral arterial tonometry (PAT) evaluates pulse wave amplitude, which is linked to endothelial function. Like FMD, PAT has also been shown to be reduced in the presence of risk factors, as well as in patients with atherosclerosis; however, FMD of the brachial artery and PAT are very different methods for identification of the vascular reactivity of different arterial territories. FMD directly registers the dilation capability of the large-conduit artery, whereas PAT measures flow response hyperemia, which is related to the endothelial function of small arteries and to the endothelial function of the microcirculation. Therefore, this technique is mostly used for investigation of the functional capability of the microcirculation.Determination of venous endothelial dysfunction is more complicated and invasive and is less reproducible. Micro-invasive techniques such as the dorsal hand vein technique and radionuclide assessment of changes in volume of the legs provide limited information about venous endothelial health; however, as endothelial dysfunction is expected to be a systemic disorder affecting the complete circulatory system, determination of the endothelial function of peripheral arteries also gives insight into venous functional status.

Purpose: Recent findings indicate that enlargement of the diameter of the peripheral arteries represents a risk of atherosclerotic cardiovascular events. As the data indicate a relationship between atherosclerosis and venous thrombosis (VT), we investigated whether the diameter of the peripheral arteries is larger in patients with idiopathic VT than in healthy subjects., Materials and Methods: The study included 49 patients with idiopathic VT and 48 age-matched healthy controls. Diameters of the brachial, common carotid and common femoral arteries as well as the intima media thickness (IMT) of the carotid and femoral arteries were measured with the high frequency ultrasound method., Results: Patients had significantly higher values for the diameter of the common carotid artery than the controls: 7.9 mm (7.4 - 8.4 mm) vs. 7.4 mm (7.0 - 7.9 mm), p < 0.001, and for the common femoral artery: 10.3 mm (9.2 - 11.1 mm) vs. 9.5 mm (8.9 - 10.4 mm), p = 0.025. Both the carotid and femoral diameters showed significant correlations with gender, age, body mass index and IMT. Linear regression analysis confirmed that the presence of VT significantly and independently influenced the diameter of the carotid and femoral artery but not the brachial artery., Conclusion: The results of our study showed that carotid and femoral artery diameters are enlarged in patients with idiopathic VT in comparison to healthy subjects. Since enlargement of the investigated arterial diameters is an indicator of atherosclerosis, our findings are consistent with the presumption that there is some interrelationship between VT and arterial atherosclerotic disease., (© Georg Thieme Verlag KG Stuttgart · New York.)

Aim: After an acute episode of deep venous thrombosis (DVT) resolution of venous thrombi is followed. However, the complete recanalisation occurs only in about a half of the patients. Therefore, the disease is accompanied by different sequellae like post-thrombotic syndrome. Factors that contribute to lysis of thrombi remain poorly understood. Therefore, the aim of our study was to investigate whether levels of the circulating inflammatory markers and other factors like fibrinolytic parameters, sex, and extent of the thrombotic occlusion are related to the recanalisation rate., Methods: The study included 49 patients with idiopathic DVT in the stable phase of the disease (4-6 months after the diagnosis). All patients were evaluated for the presence of risk factors of atherosclerosis. Using Duplex ultrasound patients were examined in acute phase of the disease (before start of treatment), and at the end of the observation period (after 4 to 6 months). Each affected venous segment was classified as completely recanalised, partially obstructed, or completely occluded. Blood was collected for laboratory analysis of the fibrinolytic activity and circulating inflammatory markers., Results: Complete recanalisation occurred more frequently in distal (popliteal) than in proximal venous thrombosis (57% vs. 43%, P≤0.01), and the recanalisation rate was lower in patients with more extended thrombosis (increased thrombus load). The recanalisation rate (partial and total) was higher in females than in males: 87% vs. 73%, P=<0.05. Risk factors of atherosclerosis had no influence on the recanalisation rate of the occluded deep veins. Out of the endogenic fibrinolytic markers, t-PA activity only was significantly related to the recanalisation rate. The recanalisation was shown to be related to some circulating cytokines. The multivariate analysis, including inflammatory markers and the recanalisation of deep veins as dependent variables showed that IL-6 and P-selectin were the only statistically significant independent predictors of the recanalisation rate., Conclusion: The results of our study show that 4 - 6 months after an acute episode of DVT complete recanalisation of the occluded veins occurred in about 50%. The recanalisation rate is related to the extent of venous thrombosis, is lower in proximal occlusions and is higher in females than in males. In patients with increased cytokine levels and decreased t-PA activity recanalisation is less likely.

The aim of this study was to evaluate the levels of anti-inflammatory interleukin-10 and pro-inflammatory cytokines and their relationship to endothelial function in patients with idiopathic venous thrombosis. Forty-nine eligible patients of both sexes with idiopathic venous thrombosis and 48 matched control subjects were studied. Levels of inflammatory markers were determined. Endothelial function was evaluated by ultrasound measurement of the flow mediated dilatation (FMD) of the brachial artery. Compared to the control group, patients with idiopathic venous thrombosis had significantly lower levels of interleukin-10 1.81 pg/ml (1.53-2.21) versus 2.71 pg/ml (1.84-3.65), p < 0.001. Patients also had increased levels of pro-inflammatory cytokines: interleukin-6 2.37 pg/ml (1.59-4.09) versus 2.03 pg/ml (1.49-2.59), p = 0.025, interleukin-8 3.53 pg/ml (2.94-5.30) versus 2.25 pg/ml (1.77-2.90), p < 0.001. Furthermore, decreased FMD was observed in patients: 5.0% (3.9-6.9) versus 12.7% (10.8-15.6), p < 0.001. FMD was related to levels of interleukin-10 (r = 0.33, p = 0.001) and was inversely related to pro-inflammatory cytokines interleukin-6 (r = -0.34, p = 0.001) and interleukin-8 (r = -0.43, p < 0.001). Patients with idiopathic venous thrombosis have decreased levels of IL-10 and increased levels of pro-inflammatory cytokines. This imbalance indicates that in the stable phase of the disease, patients have an increased systemic inflammatory response. This inflammatory response could be the consequence of the disease, but most probably is involved in the pathogenesis of venous thrombosis.

Venous thromboembolism (VTE) is one of the most frequent and serious vascular diseases. Although the major risk factors of VTE are well recognized, the pathology often develops in subjects without any obvious precipitating factor. Recent evidence suggests a link between arterial and venous thrombosis, particularly in patients with idiopathic venous thrombosis. Therefore, similar or identical risk factors may play a role in the development of both diseases. A positive association between classical risk factors of atherosclerosis, including dyslipidemia, and VTE has been reported. Recent studies demonstrated an association between hypercholesterolemia and objectively verified VTE. Circulating lipids have been shown to have both prothrombotic- and endothelium-deteriorating properties. Studies suggested a greater generation of thrombin, endothelial dysfunction, and higher platelet activity in hyperlipidemic blood. By impeding these mechanisms, statins may protect against VTE. Observational, controlled studies and two meta-analyses showed that statins significantly reduced VTE risk, most likely in a process independent from cholesterol lowering, through mechanisms related to the pleiotropic effects of these drugs. Currently, it is unknown whether VTE prevention is a class-effect of statins, or if statins differ in their antithrombotic efficacy, and it is also unknown if statin benefit is dose-dependent. However, there are also opposite findings about the efficacy of statins in prevention of VTE. Therefore, the use of statins for prophylaxis of VTE cannot be generally recommended at this stage. Further studies are needed to identify those patients who could eventually benefit maximally from treatment with statins for prevention of VTE., (© Thieme Medical Publishers.)

Objectives: The study evaluated the systemic inflammatory response and endothelium-dependent and independent function of the brachial artery (BA) in systemic lupus erythematosus (SLE) patients with and without antiphospholipid syndrome (APS)., Methods: The study group consisted of 42 women with SLE (21 without APS; mean age 36.1 ± 9.1, and 21 with APS; mean age 43.9 ± 13.1) and 22 healthy controls (mean age 43.5 ± 10.3). Endothelium-dependent functional response was evacuate using the flow-mediated vasodilatation (FMD) of brachial artery and endothelium-independent vasodilatation by application of glyceryl trinitrate (GTN). Using biochemical methods, circulating inflammatory markers were determined., Results: In comparison to controls, in both groups of patients endothelium-dependent dilation of BA was significantly reduced, and there were no differences in FMD between patients with or without APS: SLE - 7.7% (11.9-12.1), SLE+APS 7.8% (2.4-12.8), controls - 14.6% (11.2-21.1), p<0.001. However, endothelium-independent dilation of the brachial artery was significantly lower in SLE-APS patients than in controls and also lower than in the SLE group: SLE - 24.3% (15.0-28.6), SLE+APS-17.4% (13.1-22.6), controls - 23.0% (17.8-30.1), p=0.015 vs. p=0.027. Patients with SLE had significantly higher values of VCAM-1, hs-CRP, and fibrinogen than controls. In patients with SLE+APS, an additional significant increase of inflammatory markers was registered., Conclusions: The results of our study indicate that patients with SLE have deteriorated endothelium-dependent and those with APS also independent vascular function which could be, together with increased inflammatory response, involved in vascular complications in these patients. The presence of APS aggravates systemic inflammatory response.

Aim: Determination of the functional capability of the peripheral arteries is increasingly used as an early marker of vessel disease. The aim of this study was to evaluate flow-mediated (FMD) and glyceryl trinitrate-mediated (NMD) dilation of the brachial artery in patients with idiopathic venous thrombosis (VT)., Methods: Flow-mediated brachial artery dilatation and the dilatation response to glyceryl trinitrate were measured using high-resolution ultrasound in 97 subjects (49 eligible patients of both sexes, mean age 51.5 ± 14.6 years, with idiopathic venous thrombosis, and 48 age-matched healthy controls)., Results: Compared to the control group, FMD was significantly reduced in the group of patients with idiopathic venous thrombosis -4.9% (95% CI 1.1-8.7%) vs. 12.7% (95% CI 7.8-17.6%), p<0.001. Patients also had diminished NMD of the brachial artery -12.5% (95% CI 6.6-18.4%) vs. 18.5% (95% CI 10.1-26.9%), p<0.001. In patients, significantly higher levels of circulatory markers (P-selectin, von Willebrand factor) of endothelial dysfunction were registered., Conclusions: Idiopathic venous thrombosis is associated with impaired flow- and GTN-mediated vasodilatory response of the brachial artery. This may suggest involvement of the functional deterioration of the vessel wall in the pathogenesis of idiopathic VT and indicate a relationship between VT and atherothrombosis.

Aim: During the past decade, the role of inflammation in the pathophysiology of arterial thrombosis has been elucidated. However, little is known about the relationship between inflammation and venous thrombosis. Recently, inflammation has been accepted as a possible mechanism through which different risk factors trigger thrombus formation in veins. The aim of the present study was to investigate the inflammatory markers and their relationship to idiopathic venous thrombosis., Methods: Fourty-nine patients with first idiopathic venous thrombosis and 48 age matched control subjects were included in the study. Patients were studied 2-4 months after the acute event. Patients and control subjects did not differ in the classical risk factors of atherosclerosis, except in body mass index. In both groups, blood markers of inflammation, namely high sensitive C-reactive protein (hs CRP), interleukins (IL-6, IL-8) and tumour necrosis factor alpha (TNF-a), and circulating markers of endothelial dysfunction/damage namely von Willebrand factor (vWF), P-selectin and the vascular adhesion molecule (VCAM-1) were measured., Results: In comparison to healthy subjects patients had significantly higher levels of inflammatory markers: hs CRP: 2.58 mg/L (1.37-6.61), vs. 1.67 mg/L (0.97-3.24) P=0.044, IL-6: 2.37 pg/mL (1.59-4.10), vs. 2.03 pg/mL (1.45-2.59), P=0.025, IL-8: 3.53 pg/mL (2.94-5.3), vs. 2.25 pg/mL (1.77-2.90) P < or = 0.0001. However, concentrations of TNF-a did not differ significantly between the groups. Also in patients higher levels of circulating markers of endothelial dysfunction: vWF 150.0 g/L (121.0-195.0) vs. 91.5 g/L (70.5-104.0), P < or = 0.0001, P-selectin 39.5 pg/L (34.0-40.6) vs. 34.8 pg/L (32.5-38.6) P=0.009. In contrast, levels of VCAM-1 were comparable between the groups. The levels of some inflammatory markers were related to the concentration of von Willebrand factor and P-selectin - IL-6: vWF (r=0.36, P=0.08), hs CRP: P-selectin (r=0.44, P=0.018), IL-6: P-selectin (r=0.51, P=0.0002), IL-8: P-selectin (r=0.38, P=0.043)., Conclusion: Patients with idiopathic venous thrombosis have increased levels of circulating markers of inflammation and blood markers of endothelial dysfunction. Higher levels of both groups of markers indicate that patients in the stable phase of the disease have an increased systemic inflammatory response. The interrelationship between inflammatory markers and markers of endothelial dysfunction favour the hypothesis that inflammation could be involved in the etiopathogenesis of idiopathic venous thrombosis.

Background: The outcome of percutaneous transluminal angioplasty (PTA) of peripheral arterial lesions is influenced by several factors, including the haemodynamic conditions. Our study tested: (a) whether infrapopliteal run-off after completed PTA influenced the time course of restenosis/reocclusion of the femoropopliteal arterial segment, and (b) whether worsening of infrapopliteal run-off influenced the long-term femoropopliteal patency after PTA., Patients and Methods: Among 245 patients treated by femoropopliteal PTA we enrolled 176 patients who consented to regular follow-up. Concomitant infrapopliteal PTA was performed whenever feasible. The technical success of PTA and the patency of calf arteries were assessed by angiography. Infrapopliteal run-off was scored by a modification of the Society for Vascular Surgery criteria. The treated patients' limbs were divided into a group with good infrapopliteal run-off and a group with compromised run-off. Follow-up examination of the femoropopliteal arterial segment was performed by vascular ultrasonography (US) 1, 6 and 12 months after PTA, and an adverse outcome was defined by a > or = 50 % stenosis, i.e., at least doubling of the maximal systolic velocity, or occlusion - evidenced by the absence of flow. The patency of calf arteries was re-assessed by US 12 months after PTA., Results: One month after femoropopliteal PTA 19 / 83 (23 %) of patients with compromised run-off developed the combined end-point of restenosis or reocclusion in comparison to 10 / 93 (11 %) with good run-off (p = 0.03). After 6 months the incidence of restenosis/reocclusion had increased in both groups at an approximately equal rate, but the differences were no longer significant: 39 / 80 (49 %) in the compromised run-off group vs. 36 / 83 (43 %) in the good run-off group after 6 months, p = 0.49, and 42 / 73 (57 %) vs. 38 / 73 (52 %) after 12 months, p = 0.51. However, in patients' limbs with good periprocedural run-off that deteriorated into compromised run-off in the year after PTA, femoropopliteal restenosis/reocclusion occurred more often than in limbs which retained good run-off: 10 / 14 (71 %) vs. 18 / 51 (35 %), p = 0.02., Conclusions: Compromised postprocedural infrapopliteal run-off predisposes to early restenosis/reocclusion after femoropopliteal PTA. Deterioration of infrapopliteal run-off in the year after femoropopliteal PTA is accompanied by worsening of long-term femoropopliteal patency.

Aim: There is growing evidence that venous thrombotic and arterial atherosclerotic diseases are interrelated. This presumption is supported by the similar ethiopathogenesis, risk factors and clinical appearance of the two diseases. We investigated whether the prevalence of preclinical indicators of atherosclerosis is higher in patients with spontaneous venous thrombosis than in healthy subjects. Further, we studied the extent of preclinical deterioration of the arterial wall in different beds of the arterial system., Methods: Forty seven patients of both sexes (mean age, 52.3+/-14.3 years) with idiopathic venous thrombosis and 44-age matched controls were studied. Using ultrasound, bifurcations of the carotid and femoral arteries were investigated and intima-media thickness plus the presence and thickness of atherosclerotic plaques were determined., Results: The intima-media was on average, and in all beds investigated, significantly thicker in patients than in controls (0.94 mm +/-0.29 vs. 0.71 mm +/-0.15, p<0.001). The prevalence of atherosclerotic plaques was higher in patients (33/47 vs. 15/44, p<0.001). Furthermore, the number of plaques per individual, the number of arterial segments involved, and total plaque thickness were significantly longer in patients than in controls., Conclusion: The findings showed a close interrelationship between idiopathic venous thrombosis and preclinical atherosclerotic changes in different arterial territories. This could mean that in patients with primary arterial or venous disease, the arterial and venous vessel walls deteriorate simultaneously, and that common local or systemic factors influence the clinical appearance of either or both diseases.

Platelets and coagulation system play a pivotal part in the progression of peripheral arterial disease (PAD) and the genesis of complications. Therefore, antiplatelet and antithrombotic drugs represent one of the basic options for prevention and the treatment in such patients. As the data on the efficacy of these drugs in PAD patients are limited and contradictory, authors prepared an overview of the literature and recommendations for the use of these drugs. Antiplatelet therapy significantly reduces the incidence of death and cardiovascular events and prevents progression of local disease in PAD patients. Aspirin represents the first-line of antiplatelet drugs. Low-dose aspirin (75-325 mg) is as effective as higher doses. However, higher doses of aspirin result in increased risk of gastrointestinal (GI) bleeding and very low-doses (<75 mg) are less effective. Clopidogrel is used in place of low-dose aspirin in patients who have aspirin-related intolerance or allergy. Combined antiplatelet therapy is slightly more effective than aspirin alone only in patients with a history of established vascular disease. Oral anticoagulant therapy alone or in combination with aspirin was in PAD patients not shown to be more effective than aspirin alone in prevention of cardiovascular events, but is probably more effective in prevention of graft occlusion. However the combination is related to an increased risk of bleeding. Moderate intensity of warfarin treatment would be acceptable in the presence of coexisting indications such as atrial fibrillation or recent venous thrombosis.

Atherosclerosis can affect nearly any part of the arterial system. Therefore, it is considered as a generalized disease. As most probably similar or identical etiopathogenetic mechanisms are involved in different atherosclerotic diseases, a different effect of treatment of risk factors on atherosclerotic lesions in different parts of the vascular system is expected. Until now, great emphasis has been placed on the aggressive pharmacological management of coronary artery disease, less attention has been devoted to the management of cerebrovascular and much less to peripheral arterial disease, despite their significant morbidity and mortality. The data from recent trials have indicated that treatment of patients with antiplatelet drugs, statins, antihypertensive and antidiabetic drugs prevents the progression of coronary atherosclerosis, reduces cardiovascular events and improves prognosis of coronary patients. Subgroup analyses from large studies have also shown that treatment of risk factors for atherosclerosis with drugs reduces cardiovascular events and improves prognosis of cerebrovascular and peripheral arterial occlusive disease. Although some studies indicate that the effects of distinct preventive procedures are to some extent dependent on the locations of atherosclerotic disease, it seems that the success of preventive measures is mostly related to the progression of the disease or the risk of treated population and not on the treated vascular bed.

During the last decade, the role of inflammation in the etiopathogenesis of arterial thrombosis has been elucidated. However, little is known about the relationship between inflammation and venous thrombosis. Recently, inflammation has been accepted as a possible mechanism through which different risk factors trigger thrombus formation in veins. The data indicate that inflammation of the vessel wall initiates thrombus formation in an intact vein and that inflammation and coagulation systems are coupled by a common activation pathway. The first event in thrombus formation is most probably activation of endothelial cells, platelets and leucocytes, with initiation of inflammation and formation of microparticles that trigger the coagulation system through the induction of a tissue factor. Therefore, the key event in the initiation of venous thrombus formation is most probably vein wall inflammation. However, expected relationship between inflammatory markers as indicators of inflammatory process and clinical venous thromboembolism (VTE) has not yet been elucidated. C-reactive protein does not appear to be useful in predicting future venous thrombosis or to be useful in the diagnosis of VTE. Recently, it was demonstrated that probable association between VTE and several other markers of inflammation such as: interleukin (IL)-6, IL-8 and tumor necrosis factor-a exists. While these markers of inflammation were studied during or after acute venous thrombosis, further prospective studies are needed to determine the predictive value of inflammatory markers for VTE. The identification and elucidation of inflammatory markers relevant to venous thrombosis could provide targets for future therapy. That inflammation is the basic etiopathogenetic process of VTE is also supported by the relation of some risk factors to both arterial and venous thrombosis: age, increased body mass index, hypercholesterolemia, hypertension, lupus anticoagulant and hyperhomocysteinemia. A relation was also found between preclinical and clinical atherosclerotic disease and VTE. Also in line with these arguments are the preventive effects of aspirin and statins in both arterial and venous disease.