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Biomedical subjects

P Poredos

Publications and source records attributed to P Poredos.

At least 19 recordsLinked to original sources
PubMed2006

Endothelial dysfunction in Buerger's disease and its relation to markers of inflammation.

BACKGROUND: Buerger's disease (BD) is a segmental occlusive vascular disease. The aim of this study was to detect functional changes in brachial artery and asymptomatic morphological changes in extra-cranial carotid arteries not affected by the disease process and to assess markers of inflammation and endothelial damage. MATERIALS AND METHODS: Fourteen patients in the remission phase of BD and the same number of age- and sex-matched healthy controls were included in the study. The capability of endothelium-dependent (flow-mediated) and endothelium-independent dilation of the brachial artery and intima-media thickness of the carotid arteries were measured using high-resolution ultrasound. Laboratory parameters of endogenous fibrinolytic activity, inflammation and endothelial dysfunction were also measured. RESULTS: Patients with BD had a diminished capability of endothelium-dependent vasodilation and higher levels of some circulating markers of inflammation, such as leukocytes, C-reactive protein, intercellular adhesion molecule-1 and E-selectin. Intercellular adhesion molecule-1 levels were related to some of the inflammatory markers (sedimentation rate, C-reactive protein, alpha2-globulins and fibrinogen), while E-selectin was correlated with decreased endogenous blood fibrinolytic activity. Endothelium-dependent vasodilation was in negative correlation with the relative share of neutrophil granulocytes. There were no significant differences in intima-media thickness between patients with BD and controls. CONCLUSIONS: Our study has expressed generalized functional arterial disorder in patients with BD not accompanied by any measurable morphological changes of the carotid arterial wall. Functional deterioration of brachial artery could be related to increased levels of various inflammatory markers--the process which is most probably the basic pathogenetic mechanism of the disease.

Adult↗
PubMed2006

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.

Adult↗
PubMed2005

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.

Aged↗
PubMed2003

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.

Arterial Occlusive Diseases↗
PubMed2002

The usefulness of transcutaneous oximetry in assessing the success of percutaneous transluminal angioplasty.

OBJECTIVE: to identify whether monitoring transcutaneous oxygen pressure (TcpO(2)) can provide an objective method of assessing the results of PTA. MATERIALS AND METHODS: fifty-seven patients (39 Fontaine stage II, <18 stage III or IV) had ABI, TcpO(2) at rest (stages III and IV) or during exercise (stage II) and total work capacity of the leg (stage II) measured before, 24-48 h, 2 and 6 weeks after PTA. RESULTS: a significant increase of ABI in both groups of patients was detected immediately after successful PTA. TcpO(2) measured on the foot at rest increased in stages III and IV patients immediately after PTA (from 14 (IQR)18 to 25 (IQR)32 mmHg,p <0.05) and again after 6 weeks in comparison to follow up two (from 25 (IQR)32 to 35 (IQR)21 mmHg,p <0.05). In patients in stage II TcpO(2) decreased in a typical fashion during exercise. Total oxygen drop was most evident before treatment (352 (IQR)458 smmHg) and decreased significantly immediately after PTA (148 (IQR)175 smmHg, p<0.001). CONCLUSIONS: TcpO(2) measurement is an useful method for investigating the success of PTA. While the macrocirculation improves immediately after successful recanalisation, complete normalisation of the microcirculation may take some weeks, especially stages III and IV disease.

Aged↗
PubMed2002

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

BACKGROUND 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. METHODS 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.

Adult↗
PubMed2002

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.

Arteriosclerosis↗
PubMed2001

Insulin resistance adds to endothelial dysfunction in hypertensive patients and in normotensive offspring of subjects with essential hypertension.

OBJECTIVES: To evaluate whether endothelium-dependent (nitric oxide-mediated) dilation of the brachial artery (BA) is impaired in patients being treated for essential hypertension (EH), and whether this abnormality can be detected in normotensive offspring of subjects with EH (familial trait, FT); and to investigate the interrelationship between flow-mediated vasodilation (FMD) and hyperinsulinaemia/insulin resistance. DESIGN: Cross-sectional study. SETTING: Angiology department at a 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 normotonics with FT aged 20-30 (25) years and 41 age-and sex-matched controls without FT. MAIN OUTCOME MEASURES: Using high-resolution ultrasound, BA diameters at rest, during reactive hyperaemia (endothelium-dependent dilation) and after sublingual glyceryl trinitrate (GTN) application (endothelium-independent dilation) were measured. RESULTS: In hypertonics FMD was significantly lower than in controls [2.4 (2.9) vs. 7.4 (2.5)%; P < 0.00005], as was GTN-induced dilation [12.1 (4.3) vs. 16.1 (4.6)%; P=0.0007]. In subjects with FT, FMD was also decreased compared with the control group [5.8 (4.1) vs. 10.0 (3.0)%; P < 0.00005]. The response to GTN was comparable in both groups of young subjects. FMD was negatively related to insulin concentration in all subjects studied (P < 0.00005). CONCLUSIONS: In treated patients with EH, flow-mediated dilation of the BA as well as endothelium-independent dilation are decreased. In individuals with FT the endothelial function of the peripheral arteries is also altered in the absence of elevated blood pressure. Endothelial dysfunction is related to hyperinsulinaemia/insulin resistance, which could be one of the pathogenetic determinants of EH and its complications.

Adult↗
PubMed2001

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.

Animals↗
PubMed2000

Possibilities for clinical use of prostacyclin in vascular disease.

Currently available drug therapies for patients suffering severe ischaemia with rest pain and trophic lesions of the limbs remain unsatisfactory. Also vascular reopening procedures are suitable in only about half of the patients. In atherosclerotic disease when the vascular endothelium is damaged prostacyclin synthesis is decreased and thromboxane A2 production increases. Prompted by this knowledge of the importance of prostacyclin in pathogenesis of atherosclerotic disease an attempt was made to employ PGI2 clinically--for treatment of advanced forms of peripheral arterial atherosclerotic disease. Favourable effects of the stable analogue of prostacyclin (Iloprost), were reported in various studies, which included patients with peripheral atherosclerotic arterial disease, thromboangiitis obliterans and Raynaud's phenomenon. The use of Iloprost resulted in a significantly superior response than other drugs and placebo in terms of alleviation of rest pain, ulcer healing and decrease of amputation rate of ischaemic limbs. Therefore prostacyclin provides a therapeutic option in patients with advanced forms of arterial disease--including critical ischaemia.

Arteriosclerosis↗
PubMed1999

LYS-plasminogen shortens the duration of local thrombolytic treatment of peripheral arterial occlusions--a randomized controlled trial.

Local thrombolytic treatment of peripheral arterial occlusions, which has been accepted as a therapeutic alternative to surgical treatment, is not always successful. One of the reasons for unsuccessful thrombolytic treatment might be a low concentration of plasminogen in the thrombus or insufficient activation of the thrombolytic system. Therefore the purpose of this study was to determine whether the success of local treatment of peripheral arterial occlusions of lower extremities with streptokinase could be improved by enriching the thrombus with exogenous plasminogen and furthermore, if the therapeutic success depends on a systemic fibrinolytic effect. In a prospective randomized study two groups of patients with acute and subacute arterial occlusions of the lower limbs (Stage III, IV) were treated with a continuous infusion of local low dose of streptokinase (SK). The first group (45 patients, mean age 73 years) was treated with SK only (3750 IU/hour) (SK group). While the patients in the second group (43 patients, mean age 72 years) received exogenous lys-plasminogen (7.5 mg) before application of SK in thrombi (SK-Plg group). The treatment was successful in 69% (31 out of 45 patients) of the SK group and in 77% (33 out of 43 patients) of the SK-Plg group. Although lysis of thrombi was observed more frequently in the SK-Plg group than in the SK-group, the clinical outcome was comparable between groups. In successfully treated patients from the SK-Plg group the duration of treatment was significantly shorter than in the SK group (33 +/- 8 hr vs. 53 +/- 11 hr, p < 0.01). A significant decrease of fibrinogen concentration as an indicator of activation of fibrinolysis was not observed in the majority of treated patients. On the other hand, in successfully treated patients of both groups, the following was observed: 24 hour after the beginning of treatment, euglobulin clot lysis times were shortened to half of baselines values, and the plasminogen concentration was also significantly reduced (to 55% of the baseline value). In unsuccessfully treated patients no significant changes in fibrinolytic parameters were observed. The results of our study indicated that enrichment of the thrombus with exogenous plasminogen does not significantly improve the percentage of successful recanalization of peripheral arteries with a local low dose of SK, but significantly shortens the duration of treatment up to reperfusion. The study also showed that in local thrombolysis for the treatment of arterial occlusion a certain degree of systemic activation of the fibrinolytic system is essential for successful dissolution of the thrombi.

Aged↗
PubMed1999

Alteration of the fibrinolytic system in patients with peripheral arterial occlusive disease.

BACKGROUND: The fibrinolytic system may play an important role in the development and progression of peripheral arterial occlusive disease. PATIENTS AND METHODS: The fibrinolytic system of the whole blood and a diseased leg was investigated in twenty men with chronic peripheral atherosclerotic occlusive arterial disease (PAOD, clinical stage II according to Fontaine), aged from 46 to 66 years (x = 55.3) [symbol: see text]. The diagnosis of PAOD was established by clinical examination and segmental systolic blood pressure measurements using a Doppler ultrasound detector. Twenty age-matched (x = 53.4) male volunteers with normal arterial circulation of the lower limbs and without risk factors of atherosclerosis, served as controls. In both groups fibrinolytic system was investigated in basal conditions and during provocation. Release of tissue-type plasminogen activator (t-PA) was provoked by 20 min venous occlusion of the arm and the leg and by infusion of DDAVP (1-desamino-8-D-arginine-vasopressin, 0.4 ug/kg of body weight). Blood samples were obtained from the arm and the leg before and after each stimulus. The fibrinolytic parameters: euglobulin clot lysis time, t-PA activity (amidolytic assay) and antigen (ELISA) and t-PA inhibitor (PAI) activity (amidolytic assay) were determined. RESULTS: With the exception of a boderline increase in PAI activity in patients, no other differences between the two groups were observed in basal conditions. The most prominent deterioration of the fibrinolytic system detected in male PAOD patients was a significantly higher residual PAI activity registered during venous occlusion of the arm and two minutes after combined stimulation. Two minutes after combined stimulation (DDAVP and venous occlusion of the arm) significantly lower t-PA activity was observed in patients. In patients t-PA antigen response to venous occlusion and DDAVP was not significantly different from the response observed in healthy volunteers. The fibrinolytic response of the leg to venous occlusion was poor and after DDAVP application it was comparable to the arm. The fibrinolytic response of the diseased leg in men was not significantly different from the healthy leg. CONCLUSION: The results of our study indicate that alteration of the fibrinolytic system in atherosclerotic disease is predominantly a generalised phenomenon and is not directly related to a local atherosclerotic process.

Adult↗
PubMed1999

Smoking is associated with dose-related increase of intima-media thickness and endothelial dysfunction.

Cigarette smoking is firmly established as a risk factor for atherosclerosis. However, the exact mechanism causing smoking-related damage to the arterial wall and its relation to the atherosclerotic process is not known. Also unknown is the time delay between the start of smoking and the sequence of functional and morphologic changes occurring in the arterial wall caused by smoking and their interrelationship. Therefore, the aim of this study was to evaluate the acute and chronic effects of smoking on endothelium-dependent (flow-mediated) dilation (FMD) of the peripheral arteries, the effects of dose and duration of chronic smoking on intima-media thickness (IMT) of the carotid arteries, and their interrelationship. The study encompassed two groups of smokers. In group A there were 40 subjects of both sexes, who smoked on average 17.6 +/- 6.5 cigarettes per day, for 5 to 15 years (mean 8.95 +/- 4.0 years), mean age 28.1 years. Group B consisted of 42 smokers of both sexes who smoked 21.15 +/- 8.2 cigarettes/day for more than 15 years (mean 21.15 +/- 3.4 years), mean age 39.5 years. The control group consisted of 40 healthy subjects without major risk factors of atherosclerosis, mean age 29.1 years. By means of high-resolution ultrasound the brachial artery diameter was measured at rest and during reactive hyperemia (after release of a forearm tourniquet) and the flow-mediated, endothelium-dependent dilation was calculated. The IMT of the carotid arteries was determined in all subjects by use of B-mode ultrasonography. Resting blood flow in the brachial arteries was significantly less in the smokers' groups than in controls (78.8 +/- 31.9 vs 134.9 +/- 45.0 mL/min, p<0.0001). This decrease was much more evident in female than in male smokers. Female smokers also had significantly smaller brachial artery diameter at rest. In smokers the FMD of the brachial artery was reduced (11 +/- 4% vs 7 +/- 4%, p<0.004) and the mean IMT was significantly greater than in controls (0.68 +/- 0.13 vs 0.59 +/- 0.04 mm, p<0.001). Impairments of FMD and IMT increase were related to the duration and to the number of cigarettes smoked. In all subjects IMT was significantly correlated with total and LDL cholesterol, fibrinogen, lipoprotein(a) concentration, body mass index, and age of the subjects, but multivariate analysis showed that only total dose smoked and fibrinogen concentration were independently related to IMT. The results of this study show that smoking is associated with dose-related impairment of FMD and increased IMT of the carotid arteries. Impairment of FMD occurs in smokers very early and is the earliest detectable event, preceding morphologic changes of the vessel wall. Some harmful effects of smoking on the vessel wall are gender related.

Adult↗
PubMed1999

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.

Adult↗
PubMed1997

Morphological and functional changes of the arterial wall in subjects at risk of atherosclerosis and in patients with peripheral arterial occlusive disease.

BACKGROUND: The aim of this study was to determine the intima-media thickness (IMT) of the carotid arteries, which is regarded as the earliest morphological evidence of the atherosclerotic process in subjects with risk factors of atherosclerosis. Changes of blood flow in the branchial artery during reactive hyperemia were also investigated. PATIENTS AND METHODS: In 4 groups of subjects: smokers, diabetics, patients with peripheral arterial occlusive disease (PAOD) and controls, the above mentioned morphological and functional changes were studied by ultrasound. Each group comprised 18 subjects, aged 32 to 56 years. First, IMT was measured at three different sites of the carotid arteries. Then blood flow in the brachial artery was determined at rest and during reactive hyperemia (caused by handgrip test). RESULTS: In the control group the mean IMT (all segments) was 0.65 +/- 0.08 mm. IMT of smokers was similar (0.65 +/- 0.07 mm), while in diabetics a tendency to IMT increase was detected at all three measuring sites, and in the common carotid artery the IMT was statistically significantly thicker than in the controls (0.75 +/- 0.08 mm vs. 0.65 +/- 0.08, p < 0.05). PAOD patients showed a significant increase of IMT at all three carotid segments (mean 0.77 +/- 0.10 mm p < 0.05). In all groups IMT was related to the number of atherosclerotic plaques (r = 0.6, p < 0.001), and was also correlated with body mass index (BMI) (r = 0.32, p < 0.01) and fibrinogen level (r = 0.32, p < 0.05). All groups demonstrated a significant increase of blood flow in the branchial artery during hyperemia. In PAOD patients this increase was significantly smaller than in the controls and other groups (212 +/- 61% vs 275 +/- 60%, p < 0.05). CONCLUSIONS: The results of our study indicated that the most important factors determining increase of IMT are diabetes, fibrinogen level, BMI and the presence of clinically manifested atherosclerosis. Hyperemic blood flow, which is predominantly determinated by the vasodilation capacity of the resistance vessel, is reduced in patients with clinically manifested atherosclerosis and not in subjects with risk factors and without atherosclerotic manifestation.

Adult↗