Do blood constituents in varicose veins differ from the systemic blood constituents?

OBJECTIVE: Varicose veins represent one of the most frequent vascular diseases and are in most cases benign. However, advanced disease is frequently associated with complications such as chronic venous insufficiency and superficial vein thrombosis. The pathogenic mechanisms are not well understood. Besides increased venous pressure, it is suggested that local blood constituents trigger various mechanisms responsible for the progression of the disease and its complications. DESIGN: The aim of this study was to investigate the changes in the blood in varicose veins and to compare them with the systemic markers of inflammation and endothelial damage. MATERIALS AND METHODS: Forty patients with primary varicose veins were included in the study. Most patients were class C2. Blood samples were taken from the leg from the tortuous and dilated varicose tributaries of the great saphenous vein and from the cubital vein. RESULTS: The values of basic hematologic tests were comparable between blood samples (varicose vs. systemic). In varicose veins, the following parameters were significantly increased in comparison with systemic blood: hsCRP (3.12 ± 2.18 mg/L vs. 2.04 ± 2.21 mg/L, p = .04), IL-6 (3.54 ± 2.59 pg/mL vs. 2.25 ± 1.27 pg/mL, p = .008), vWF (118.4  ±  27% vs. 83.2  ±  22%, p < .05). D-dimer, in samples taken from the leg varicose veins, was also significantly higher than in the systemic blood (104.3 ± 9.3 ng/mL vs. 89.5 ± 8.3 ng/mL, p = .039). CONCLUSIONS: Some inflammatory markers and indicators of endothelial dysfunction are increased in varicose vein blood. This is most probably the consequence of deteriorated blood flow in dilated and tortuous superficial veins, and increased venous pressure. Damage to the venous wall, which causes a chronic inflammatory response, together with the procoagulant properties of local blood may promote further progression of the disease and thrombotic complications.

Growth Hormone, Atherosclerosis and Peripheral Arterial Disease: Exploring the Spectrum from Acromegaly to Growth Hormone Deficiency.

Growth hormone (GH) and insulin-like growth factor 1 (IGF-1) are increasingly recognised for their role in cardiovascular (CV) physiology. The GH-IGF-1 axis plays an essential role in the development of the CV system as well as in the complex molecular network that regulates cardiac and endothelial structure and function. A considerable correlation between GH levels and CV mortality exists even among individuals in the general population without a notable deviation in the GHIGF- 1 axis functioning. In addition, over the last decades, evidence has demonstrated that pathologic conditions involving the GH-IGF-1 axis, as seen in GH excess to GH deficiency, are associated with an increased risk for CV morbidity and mortality. A significant part of that risk can be attributed to several accompanying comorbidities. In both conditions, disease control is associated with a consistent improvement of CV risk factors, reduction of CV mortality, and achievement of standardised mortality ratio similar to that of the general population. Data on the prevalence of peripheral arterial disease in patients with acromegaly or growth hormone deficiency and the effects of GH and IGF-1 levels on the disease progression is limited. In this review, we will consider the pivotal role of the GH-IGF-1 axis on CV system function, as well as the far-reaching consequences that arise when disorders within this axis occur, particularly in relation to the atherosclerosis process.

Endocrine Disorders and Peripheral Arterial Disease - A Series of Reviews Cushing Syndrome-Cortisol Excess.

Cushing syndrome (CS), characterised by endogenous or exogenous glucocorticoid hormone excess, is associated with several systemic complications, including impaired glucose metabolism, which often becomes clinically manifest as diabetes mellitus (DM). In addition, CS can harm the arterial wall because of hyperglycaemia, dyslipidaemia, hepatic steatosis, and central obesity. These metabolic disorders promote atherosclerosis by synthesising adipokines, leptin, and proinflammatory cytokines. Lower limb arterial complications in CS are common and significantly impact morbidity and mortality. Furthermore, CS, in combination with DM, is likely to cause more diffuse vascular disease that predominantly affects distal arterial beds. In conclusion, CS promotes atherosclerosis, including peripheral artery disease, by causing functional and morphological deterioration of the arterial vessel wall and increasing the presence of classical risk factors of atherosclerosis.

Enlargement of the diameter of the peripheral arteries in patients with idiopathic venous thrombosis.

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.

Endothelium-dependent and independent dilation capability of peripheral arteries in patients with systemic lupus erythematosus and antiphospholipid syndrome.

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.

The influence of atorvastatin on walking performance in peripheral arterial disease.

BACKGROUND: Recently it has been shown that statins can improve walking distance in patients with peripheral arterial disease. We examined whether statins used in moderate dosages with the aim of reaching the target levels for hypercholesterolemia could improve walking performance in patients with peripheral arterial disease. PATIENTS AND METHODS: 37 patients with hypercholesterolemia (LDL cholesterol = 3.46 +/- 0.13 mmol/l), who had previously not been treated by statins, were randomized in a double-blind study to a group receiving either atorvastatin at 20 mg/day (N = 20) or placebo (N = 17). All patients had stable intermittent claudication (Fontaine class IIa or IIb). At baseline, after one and three months the pain-free walking distance was measured in all patients. RESULTS: After 3 months patients in the treated group had reached target cholesterol values (LDL cholesterol = 2,34 +/- 0.9 mmol/l), whereas no significant change in lipids was observed in the control group. The ankle-brachial pressure index (ABPI) did not change significantly in either group. After 3 months the pain-free walking distance was increased significantly (p < 0.001), but similarly in both groups (at entry: 56 (53-108) m vs 53 (53-106) m; after 3 months: 79 (53-108) m vs 106 (66-159) m, for the treated and placebo group, respectively). Therefore this effect had to be attributed to regular exercise and not to statin use. CONCLUSIONS: Our results show that routine treatment with statin (atorvastatin 20 mg/day), which is effective in reducing the level of cholesterol, does not produce an improvement in walking performance in patients with peripheral arterial disease.

Does the preventive effect of different drugs depend on location of the atherosclerotic process?

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.

Endothelial dysfunction in post-myocardial infarction patients with various expressions of risk factors.

It has not been established yet whether patients who suffer myocardial infaction (MI) in the absence of classic risk factors also have endothelial dysfunction (ED), as has been shown for patients with risk factors, and if so, to what extent it is manifested. Young male patients in the stable phase after MI were included in the study. At the time of MI, 20 patients had high and 21 patients low expression of risk factors. The control group consisted of 35 healthy age-matched males. ED was estimated by ultrasound measurement of the endothelium-dependent dilation of the brachial artery, induced by the reactive hyperemia test. Compared to the control group, the level of endothelium-dependent vasodilation was significantly reduced in both groups of patients (controls: 9.1% +/- 5.6%; patients with high risk: 5.5% +/- 5.1%; patients with low risk: 5.6 +/- 3.5 %; ANOVA, p<.01). There was no difference between both groups of patients. These results showed that ED is not associated or due only to classic risk factors. It appears that ED may occur and precede development of atherosclerosis in the absence of classic risk factors. These novel findings can have important clinical implications.

The role of inflammation in venous thromboembolism and the link between arterial and venous thrombosis.

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.

Rivaroxaban versus warfarin in the prevention of post-thrombotic syndrome.

INTRODUCTION: Post-thrombotic syndrome (PTS) is a chronic complication of deep vein thrombosis (DVT) that affects 20% to 50% of DVT patients. Standard DVT treatment included vitamin K antagonists (usually warfarin) with low-molecular-weight heparin in the initial period. In recent years, direct oral anticoagulants (DOAC) were introduced. We aimed to investigate the influence of rivaroxaban and warfarin on PTS development. METHODS: Consecutive patients treated for DVT were included, 39 were treated with warfarin and 61 with rivaroxaban. We assessed symptoms and signs of PTS and calculated Villalta score 23months (median) after acute DVT diagnosis. Differences between patients treated with rivaroxaban and warfarin were investigated. RESULTS: Patients in the rivaroxaban group had a lower prevalence of PTS than those treated with warfarin (25% vs. 49%, p=0.013). Logistic regression showed odds ratio of 2.9 (1.2-6.8, p=0.014) for PTS development in warfarin group compared to rivaroxaban group. When adjusted for other variables, the odds ratio was 3.5 (1.1-11.0, p=0.035). CONCLUSIONS: Treatment of DVT with rivaroxaban might be associated with a lower risk for PTS development. A larger randomized trial would be needed for stronger evidence.

Endothelial dysfunction predictor of structural changes of arterial wall in type I diabetes.

AIM: We examined whether alteration in vascular endothelial function exists in non-insulin dependent diabetes mellitus (NIDDM) and whether impaired endothelium-dependent responses in those patients are associated with increased intima-media thickness (IMT), the time sequence of their appearance and the role of individual risk factors in development of structural deterioration of arterial wall. METHODS: Ultrasound technique was used to measure brachial artery flow mediated dilation (FMD) response and carotid IMT in 38 young adults with type I diabetes aged 22-34 years and 35 healthy controls aged 22-36 years. RESULTS: Patients had significantly lower FMD than controls (4.15/2.8/ vs 11.3/3.6/, P<0.0001) and was in all diabetic patients below the mean value of controls. Further, carotid intima-media was in insulin dependent diabetes mellitus (IDDM) patients significantly thicker than in healthy subjects (0.65/0.04 vs 0.56/0.04, P=0.0001) and was related to body mass and body mass index, to the age of patients, the duration of diabetes and several risk variables. In a multivariate model FMD was most significantly and independently associated to IMT. However, significant thickening of intima-media was observed only in patients with progressed deterioration of FMD and it appeared in those subjects with long-lasting disease. IMT was also influenced by urinary albumin excretion and low-density lipoprotein (LDL) cholesterol concentration. CONCLUSIONS: Endothelium dependent FMD response is impaired in IDDM and is associated with increased carotid artery IMT. Significant thickening of intima-media appears in patients with advanced deterioration of FMD that is related to the duration of the disease. These data suggest that advanced endothelial dysfunction in IDDM may predispose to development of morphologic atherosclerotic lesions of arterial wall.

Determination of amputation level in ischaemic limbs using tcPO2 measurement.

BACKGROUND: Determination of the optimal amputation level is essential for patients, morbidity and rehabilitation. Various non-invasive procedures have been proposed to determine the optimal level of amputation. There is no consensus on the minimal tcPO2 level that is required to predict the healing of the stump. Therefore we aimed to rank the probability of primary wound healing at the most distal level and to answer the question if there is a lower limit of tcPO2 below which healing cannot occur. PATIENTS AND METHODS: 56 consecutive patients undergoing amputation below the knee for ischaemic gangrene of limbs were prospectively enrolled in the study. 39 were men (18 of whom were diabetics) and 17 women (8 diabetics) whose ages ranged from 45 to 87 years (mean 73 years). The total of 71 amputations was performed on the 56 patients: 39 below-knee with primary healing and, in 16 patients the above-knee reamputation was performed, due to the non-healing wound on the below-knee stump. The level of the amputation (below or above the knee) was in all cases decided solely on clinical grounds. TcPO2 was measured on each patient prior to amputation, on the dorsum of the foot and 10 cm below the knee. RESULTS: The median tcPO2 value on the dorsum of the foot of diseased legs before amputation was 12 mm Hg (range from 0 to 22 mm Hg). At the anticipated level of the amputation of the shank, the median value of tcPO2 was 28 mm Hg (8-56 mm Hg). Patients with primary healing of postoperative wounds had significantly higher values of tcPO2 than patients with fialure to heal (37 mm Hg; range 15-56 mm Hg vs. 18 mm Hg; range 8-36 mm Hg, p < 0.01). The success rate increased with higher tcPO2 values at the level of amputation. The 15% prevalence of reamputations was obtained for tcPO2 values between 25 and 36 mm Hg (median value 33 mm Hg) and the threshold value of tcPO2 below which the stump failed to heal was 15 mm Hg. CONCLUSIONS: Our study showed that tcPO2 is a reliable indicator of local ischemia. The integration of this parameter with other personal clinical criteria may be a valuable help to the surgeon in decision making.

Medical management of patients with peripheral arterial disease.

Peripheral arterial disease (PAD) is one of the most frequent manifestations of atherosclerosis and is associated with atherosclerosis in the coronary and carotid arteries, leading to a highly increased incidence of cardiovascular events. Major risk factors of PAD are similar to those that lead to atherosclerosis in other vascular beds. However, there are differences in the power of individual risk factors in the different vascular territories. Cigarette smoking and diabetes mellitus represent the greatest risks of PAD. For prevention of the progression of PAD and accompanying cardiovascular events similar preventative measures are used as in coronary artery disease (CAD). However, recent data indicate that there are some differences in the efficacy of drugs used in the prevention of atherothrombotic events in PAD. Antiplatelet treatment is indicated in virtually all patients with PAD. In spite of the absence of hard evidence- based data on the long term efficacy of aspirin, it is still considered as a first line treatment and clopidogrel as an effective alternative. The new antiplatelet drugs ticagrelol and prasugrel also represent promising options for treatment of PAD. Statin therapy is indicated to achieve the target low density lipoprotein cholesterol level of ≤2.5 mmol/L (100 mg/dL) and there is emerging evidence that lower levels are more effective. Statins may also improve walking capacity. Antihypertensive treatment is indicated to achieve the goal blood pressure (<140/90 mmHg). All classes of antihypertensive drugs including beta-blockers are acceptable for treatment of hypertension in patients with PAD. Diabetic patients with PAD should reduce their glycosylated haemoglobin to ≤7%. As PAD patients represent the group with the highest risk of atherothrombotic events, these patients need the most intensive treatment and elimination of risk factors of atherosclerosis. These measures should be as comprehensive as those in patients with established coronary and cerebrovascular disease.

Growth hormone (GH) treatment reverses early atherosclerotic changes in GH-deficient adults.

Hypopituitary patients have increased mortality from vascular disease, and in these patients, early markers of atherosclerosis [increased carotid artery intima-media thickness (IMT) and reduced distensibility] are more prevalent. As GH replacement can reverse some risk factors of atherosclerosis, the present study examined the effect of GH treatment on morphological and functional changes in the carotid and brachial arteries of GH-deficient (GHD) adults. Eleven GHD hypopituitary men (24-49 yr old) were treated with recombinant human GH (0.018 U/kg BW x day) for 18 months. IMT of the common carotid artery (CCA) and the carotid bifurcation (CB), and flow-mediated endothelium-dependent dilation (EDD) of the brachial artery were measured by B mode ultrasound before and at 3, 6, 12, and 18 months of treatment, and values were compared with those in 12 age-matched control men. Serum concentrations of lipids, lipoprotein(a), insulin-like growth factor I (IGF-I), and IGF-binding protein-3 (IGFBP-3) were also measured. In GHD men before treatment the IMTs of the CCA [mean(SD), 0.67(0.05) mm] and CB [0.75(0.04) mm] were significantly greater (P < 0.001) than those in control men [0.52(0.07) and 0.65(0.07) mm, respectively]. GH treatment normalized the IMT of the CCA by 6 months [0.53(0.04) mm] and that of the CB by 3 months [0.68(0.05) mm]. The IMT of the carotid artery (CCA and CB) was negatively correlated with serum IGF-I (r = -0.53; P < 0.0001). There was a significant improvement in flow-mediated EDD of the brachial artery at 3 months, which was sustained at 6 and 18 months of GH treatment (P < 0.05). GH treatment increased high density lipoprotein cholesterol at 3 and 6 months, but did not reduce total or low density lipoprotein cholesterol and was without effect on lipoprotein(a). There was no correlation between plasma lipids and changes in IMT or EDD of the arteries examined. In conclusion, GH treatment of hypopituitary GHD men reverses early morphological and functional atherosclerotic changes in major arteries and, if maintained, may reduce vascular morbidity and mortality. GH seems to act via IGF-I, which is known to have important effects on endothelial cell function.

Relation of blunted dilation of the brachial artery in insulin-dependent diabetes mellitus to microalbuminuria.

Endothelium-dependent vasodilation in the conduit peripheral arteries of patients with insulin-dependent diabetes mellitus is impaired and is closely related to microalbuminuria. The diabetic state does not significantly influence the vascular smooth muscle functional capability.

Endothelial dysfunction in the pathogenesis of atherosclerosis.

Healthy endothelium plays a central role in cardiovascular control. Therefore, endothelial dysfunction (ED), which is characterized by an imbalance between relaxing and contracting factors, procoagulant and anticoagulant substances, and between proinflammatory and antiinflammatory mediators, may play a particularly significant role in the pathogenesis of atherosclerosis. Endothelial dysfunction is closely related to different risk factors of atherosclerosis, and to their intensity and duration. The involvement of risk factors in ED is also supported by results of interventions studies that showed regression of ED with treatment of risk factors. Because risk factors are commonly accompanied by decreased bioavailability of nitric oxide, the common denominator whereby different risk factors cause ED is most probably increased oxidative stress. Endothelial dysfunction may promote atherogenesis through different mechanisms such as increased adherence of monocytes, macrophages, and enhanced permeability of the endothelial layer. Further, ED probably plays an important role in the growth of atherosclerotic lesions and in the development of thrombotic complications in late stages of the disease. Because ED is a key underlying factor in the atherosclerotic process, markers of endothelial abnormalities have been sought. Detection of ED is based on tests of endothelium-dependent vasomotion (dilation capability of peripheral and coronary arteries) and on circulating markers of endothelial function (endothelin-1, von Willebrand factor, tissue plasminogen activator, plasminogen activator inhibitor, and adhesion molecules). Using these tests it is possible to follow the dose response of harmful effects of risk factors, and the effects of preventive procedures on vessel wall function.

Endothelial dysfunction in the pathogenesis of atherosclerosis.

A healthy endothelium plays a central role in cardiovascular control. Therefore, endothelial dysfunction (ED), which is characterized by an imbalance between relaxing and contracting factors, procoagulant and anticoagulant substances, and between pro-inflammatory and anti-inflammatory mediators, may play a particularly significant role in the pathogenesis of atherosclerosis. ED is closely related to different risk factors of atherosclerosis, to their intensity and their duration. The involvement of risk factors in ED is also supported by results of intervention studies that showed regression of ED with treatment of risk factors. The common denominator whereby different risk factors cause ED is most probably increased oxidative stress and/or inflammation. ED promotes atherosclerosis and probably plays an important role in the development of thrombotic complications in the late stages of the disease. As ED is a key underlying factor in the atherosclerotic process, markers of endothelial abnormalities have been sought. Detection of ED is based on tests of endothelium-dependent vasomotion (dilation capability of peripheral and coronary arteries) and on circulating markers of endothelial function (endothelin-1, von Willebrand factor, tissue plasminogen activator, plasminogen activator inhibitor, adhesion molecules). Using these tests it is possible to follow the dose-response of harmful effects or risk factors, and the effects of preventive procedures on vessel wall function.

Dependence of morphological changes of the carotid arteries on essential hypertension and accompanying risk factors.

AIMS: to evaluate morphological changes (intima-media thickness, IMT) of the carotid arteries in patients being treated for essential hypertension (EH), and to discover whether this abnormality can be detected in normotensive offspring of subjects with EH (familial trait, FT); and to investigate the interrelationship between IMT and accompanying risk factors. EXPERIMENTAL DESIGN: cross-sectional study. SETTING: angiology department, university teaching hospital. SUBJECTS: the study encompassed 172 subjects, of whom 46 were treated hypertonics aged 40-55 (49) years, and 44 age matched, normotensive volunteers as controls. We also investigated 41 normotensives with FT for essential hypertension aged 20-30 (25) years and 41 age- and sex-matched controls without FT. INTERVENTIONS: the hypertensive subjects were being treated either with long-acting calcium-channel antagonists or ACE-inhibitors. MEASURES: using high resolution ultrasound, IMT of the carotid bifurcation and of the common carotid artery was measured. RESULTS: In the hypertensives, the mean IMT was greater than that in the controls (0.92 (0.10) mm vs 0.72 (0.07) mm; p<0.00005). The IMT was independently related to accompanying risk factors: a positive family history of hypertension, age of the patient, duration of EH and the level of systolic/diastolic blood pressure (BP), body mass index and total/LDL-cholesterol. In subjects with FT, IMT was also greater compared to the control group (0.60 (0.05) mm vs 0.55 (0.04) mm; p<0.00005). IMT was not related to BP values. CONCLUSIONS: In treated essential patients with the EH, the IMT was increased. Individuals with FT also had greater IMT in the absence of elevated BP. The IMT in hypertensives was related to accompanying risk factors, which could be pathogenetic determinants of EH and/or its complications.

Interrelationship between peripheral arterial occlusive disease, carotid atherosclerosis and flow mediated dilation of the brachial artery.

AIM: Atherosclerosis is considered a systemic disease. Therefore, in patients with atherosclerotic disease effects on various sections of the arterial system are expected. The aim of our study was to determine whether patients with evident peripheral arterial occlusive disease (PAOD) of the lower limbs have any subclinical functional or structural arterial wall changes in other sections of the arterial system. METHODS: The study included 54 patients with PAOD, Fontaine stage II and a claudication distance from 50 to 500 m (average 250+/-170 m). Their mean age was 64. None of them had any symptoms or signs of coronary or cerebrovascular atherosclerosis (CVD). The control group consisted of 50 healthy volunteers with a mean age of 64 years without any risk factors of atherosclerosis. In all subjects the carotid intima-media thickness (IMT), was measured, the presence of atherosclerotic plaques in the carotid artery (CA) was registered and the endothelium-dependent dilation capability of the brachial artery (BA) during reactive hyperemia was measured using the B-mode ultrasound technique. RESULTS: The average IMT was significantly greater in PAOD patients than in controls (0.8+/-0.2 mm vs 0.6+/-0.1 mm, p<0.001). In patients atherosclerotic plaques in the CA were also more numerous than in controls (38 vs 4, p<0.001). The IMT of patients was related to body mass index (BMI), ankle-brachial pressure index (ABI), LDL cholesterol and to the number of atherosclerotic plaques. In PAOD patients flow-mediated dilation of the BA was significantly lower than in controls (7.2+/-4.9% vs 12.3+/-2.1%, p<0.001). The dilation capability of the BA was linearly related to the BMI, ABI and IMT. CONCLUSION: The results of our study show that PAOD patients without clinical evidence of CVD have morphological changes of the CA, increased IMT and numerous atherosclerotic plaques. Furthermore, in PAOD patients flow-mediated endothelium-dependent dilation of the peripheral arteries is decreased. These results support the hypothesis that atherosclerosis is a generalized disease, leading to functional and structural changes in several segments of the arterial system.