Importance of adhesion molecules for children with congenital heart disease

2012 ◽  
Vol 23 (1) ◽  
pp. 35-40
Author(s):  
Ayşe Yıldırım ◽  
Aysu T. Karaağaç ◽  
Fusun Güzelmeriç ◽  
Nihat Çine ◽  
Naci C. Öner
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Pulmonary Blood Flow ◽  
Congenital Heart ◽  
Heart Diseases ◽  
Cellular Adhesion ◽  
Mean Values ◽  
Cellular Adhesion Molecule

AbstractBackgroundThe aim of our study was to compare the blood levels of adhesion molecules in children with different heart diseases and pulmonary flow rates.MethodsIn this study, we evaluated the levels of soluble intercellular adhesion molecule-1 and soluble vascular cellular adhesion molecule-1 in blood samples of 65 children with different congenital heart diseases. The patients were divided into four groups according to their pulmonary blood flow. The first group had increased pulmonary blood flow with pulmonary hypertension and left-to-right shunt. The second group had increased pulmonary blood flow without pulmonary hypertension and left-to-right shunt. The third group had decreased pulmonary blood flow with cyanotic congenital heart disease and the fourth group had normal pulmonary blood flow with left ventricle outflow tract obstruction and aortic stenosis.ResultThe highest soluble intercellular and vascular cellular adhesion molecule-1 levels with the mean values of 420.2 nanograms per millilitre and 1382.1 nanograms per millilitre, respectively, were measured in the first group and the lowest levels with the mean values of 104.4 and 358.6 nanograms per millilitre, respectively, were measured in the fourth group. The highest pulmonary blood pressure levels were found in the first group.ConclusionEndothelial activity is influenced not only by left-to-right shunt with pulmonary hypertension, but also by decreased pulmonary blood flow in cyanotic heart diseases. Adhesion molecules are valuable markers of endothelial activity in congenital heart diseases, and they are influenced by pulmonary blood flow rate.

scholarly journals Pulmonary Hypertension in Children with Congenital Left to Right Cardiac Shunt Anomalies

2015 ◽  
Vol 14 (2) ◽  
pp. 31-37
Author(s):  
Chaity Barua ◽  
Sunam Kumar Barua ◽  
Md Zahid Hossain ◽  
Tahmina Karim
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Congenital Heart ◽  
Heart Diseases ◽  
Congenital Heart Diseases ◽  
Age Group ◽  
Cardiac Defects ◽  
Pulmonary Arterial

The Normal Pulmonary Artery (PA) systolic pressure of children and adults is < 30 mm Hg and the mean PA pressure is < 25 mm Hg at sea level. Pulmonary hypertension (PH) is defined as a mean pulmonary artery pressure > 25 mm Hg at rest or > 30 mm Hg during exercise. An increase in pulmonary flow, vascular resistance, or both can result in pulmonary hypertension. Pulmonary Arterial Hypertension (PAH) commonly arises in patients with Congenital Heart Diseases (CHD) are usually associated with increased pulmonary blood flow. Greater number of patients with Pulmonary Arterial Hypertension (PAH), associated with congenital heart disease, are now surviving into adulthood, many with increasingly complex cardiac defects. Patients with cardiac defects which result in left-to-right shunting tend to develop PAH, owing to the increased shear stress and circumferential stretch induced by pulmonary blood flow, which leads to endothelial dysfunction and progressive vascular remodeling followed by vascular resistance. Pulmonary hypertension in association with congenital heart diseases is seen in large systemicto- pulmonary communications such as Ventricular Septal Defect (VSD), Patent Ductus Arteriosus (PDA) atrioventricular septal defects, aorticopulmonary window defect etc. Pulmonary hypertension associated with large L-R shunt lesions (e.g. VSD, PDA) is called Hyperkinetic Pulmonary Hypertension (PH). It is the result of an increase in pulmonary blood flow, a direct transmission of the systemic pressure to the pulmonary artery, and compensatory pulmonary vasoconstriction. Hyperkinetic PH is usually reversible if the cause is eliminated before permanent changes occur in the pulmonary arterioles. If large L-R shunt lesions are left untreated, irreversible changes take place in the pulmonary vascular bed, with severe pulmonary hypertension and cyanosis due to a reversal of the L-R shunt. This stage is called Eisenmenger syndrome or Pulmonary Vascular Obstructive Disease (PVOD). Surgical correction is not possible at this stage. Due to lack of formal study which of the L-R congenital shunt is more commonly associated with the development of pulmonary hypertension is not known the cross-sectional study therefore intends to find the pattern of congenital L-R heart diseases commonly attributed to the development pulmonary hypertension. The diagnosis of the abovementioned congenital heart disease will be made by echocardiography. In this study, most of the participant [22 (44.0%)] were in the ‘< 1 years’ age group, female were proportionately higher, most patients presented with cough and difficulty in breathing, dyspnoea and tachycardia were the most common clinical findings, murmur mostly systolic were found, Eisenmenger syndrome was not found in any child, ASD was the most common congenital anomaly. About four-fifth of the participants had single congenital anomaly. Two-fifth of the participant was found having severe PAH. Significant correlation were revealed between age group and Pulmonary arterial pressure (R= 0.775), Status of PAH was found significantly different (p< 0.05) in age groups and presence of number of anomalies.Chatt Maa Shi Hosp Med Coll J; Vol.14 (2); Jul 2015; Page 31-37

Endothelin-1 vasoactive responses in lambs with pulmonary hypertension and increased pulmonary blood flow

1995 ◽  
Vol 269 (6) ◽  
pp. H1965-H1972 ◽  
Author(s):  
J. Wong ◽  
V. M. Reddy ◽  
K. Hendricks-Munoz ◽  
J. R. Liddicoat ◽  
R. Gerrets ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Blood Flow ◽  
Heart Diseases ◽  
Main Pulmonary Artery ◽  
Similar Degree ◽  
Fetal Sheep ◽  
Endothelin 1

Increased concentrations of endothelin-1 (ET-1) are found in children with congenital heart diseases that produce increased pulmonary blood flow and pulmonary hypertension, but the role of ET-1 in the pathophysiology of pulmonary hypertension is unclear. Therefore, we investigated ET-1-induced vasoactive responses and ET-1 concentrations in an animal model of pulmonary hypertension and increased pulmonary blood flow. Vascular shunts were placed between the ascending aorta and main pulmonary artery in seven late-gestation fetal sheep. Four weeks after spontaneous delivery, ET-1 increased pulmonary vascular resistance by 29.7 +/- 34.4% (P < 0.05), the ETb-receptor agonist [Ala1,3,11,15]ET-1 (4AlaET-1) had no effect, and the ETa-receptor antagonist cyclo(D-Asp-L-Pro-D-Val-L-Leu-D-Trp) (BQ-123) decreased pulmonary vascular resistance by -16.0 +/- 5.6% (P < 0.05). In contrast, in six control lambs with a similar degree of pulmonary hypertension induced by U-46619, ET-1 and 4AlaET-1 decreased pulmonary vascular resistance by 24.8 +/- 17.6, and 20.0 +/- 13.8%, respectively (P < 0.05). In addition, systemic arterial concentrations of immunoreactive ET-1 were elevated in lambs with pulmonary hypertension (29.2 +/- 9.6 vs. 15.2 +/- 10.7 pg/ml, P < 0.05). Pulmonary hypertension and increased pulmonary blood flow alters the response of ET-1 from pulmonary vasodilation to vasoconstriction. These altered responses suggest a role for ET-1 and its receptors in the pathogenesis of pulmonary hypertension secondary to increased pulmonary blood flow.

Increased levels of Vascular Cell Adhesion Molecule-1 (VCAM-1) and Inter-Cellular Adhesion Molecule-1 (ICAM-1) Correlate with Advanced Disease Features and Poor Survival in Newly Diagnosed Patients with Multiple Myeloma. Reduction Post-Bortezomib- and Lenalidomide-Based Regimens.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1824-1824
Author(s):  
Magdalini Migkou ◽  
Evangelos Terpos ◽  
Dimitrios Christoulas ◽  
Maria Gavriatopoulou ◽  
Georgios Boutsikas ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Advanced Disease ◽  
Serum Levels ◽  
Cellular Adhesion ◽  
Newly Diagnosed ◽  
Poor Survival ◽  
Β2 Microglobulin ◽  
Cellular Adhesion Molecule ◽  
First Relapse

Abstract Abstract 1824 Poster Board I-850 Interactions between myeloma (MM) cells and bone marrow stromal cells (BMSCs) are strongly implicated in the biology of MM. The aim of this study was to evaluate the serum levels of adhesion molecules, such as VCAM-1 (CD106), ICAM-1 (CD54), P-, L- and E-selectin in patients with MM and explore possible correlations with clinical and laboratory data. The study population included 87 newly diagnosed patients (42M/45F; median age 68 years): 59 with symptomatic MM, 21 with asymptomatic MM (AMM) and 7 with MGUS, as well as 21 MM patients at first relapse (11M/10F, median age 69 years) who received the combination of bortezomib/dexamethasone (VD) and 20 MM patients at first relapse (11M/9F, median age 68.5 years) who were treated with the combination of lenalidomide plus low-dose dexamethasone (Rd). The aforementioned adhesion molecules were measured in the serum of newly-diagnosed patients before the administration of any kind of therapy, in relapsed patients on Day 1 of cycle 1 and on the last day of cycle 4 and in 43 healthy controls using ELISA method (R&D Systems, Minneapolis, MN, USA). Patients with newly-diagnosed or relapsed MM had increased levels of all studied molecules compared to controls (p<0.01), while in MGUS only serum VCAM-1 and ICAM-1 levels were elevated compared to controls (p<0.01). Newly-diagnosed patients with symptomatic MM had increased levels of VCAM-1 (mean±SD: 1168.5±810.4 ng/ml) and ICAM-1 (371.0±162.7 ng/mL) when compared to AMM patients (642.6±340.9 ng/ml, p<0.0001; and 274.4±65.5 ng/ml, p=0.002, for VCAM-1 and ICAM-1, respectively) and to MGUS patients (629.8±228.5 ng/ml, p=0.012; and 247.9±53.9, p=0.009, for VCAM-1 and ICAM-1, respectively). Furthermore, newly-diagnosed symptomatic MM had increased levels of E-selectin (43.2±20.0 ng/ml) compared to AMM (33.6±16.6 ng/ml, p=0.047). VCAM-1 was lower in patients with ISS-1 (768.2±225.1 ng/ml) compared to patients with ISS-2 (1121.7±991.2 ng/ml) and ISS-3 (1456.8±785.7 ng/ml; ANOVA p=0.04), while P-selectin was higher in ISS-1 (172.7±76.6 ng/ml) compared to ISS-2 (118.7±75.5 ng/ml) and ISS-3 MM (108.3±76.4; ANOVA p=0.042). For all newly-diagnosed patients, there was a strong correlation between VCAM-1 and ICAM-1 (r=0.598, p<0.0001). Serum VCAM-1 showed strong positive correlations with β2-microglobulin (r=0.564, p<0.0001), urea (r=0.384, p=0.001) and creatinine (r=0.376, p=0.001) and negative correlation with Hb (r=-0.346, p=0.002). Similarly, ICAM-1 positively correlated with β2-microglobulin (r=0.340, p=0.003), creatinine (r=0.290, p=0.01) and urea (r=0.254, p=0.025), and negatively correlated with Hb (r=-0.237, p=0.037). Serum P-selectin positively correlated with platelet counts (r=0.555, p<0.0001), Hb (r=0.416, p<0.0001) and albumin (r=0.270, p=0.017), but negatively correlated with β2-microglobulin (r=-0.383; p=0.001) and creatinine (r=-0.294, p=0.009). For L-selectin there was a positive correlation with albumin (r=0.370; p=0.001). The median follow-up of patients with newly-diagnosed symptomatic MM was 22 months (range: 4-54 months) and the median OS was 42 months. Increased levels of VCAM-1, ICAM-1 and L-selectin predicted for inferior survival. In particular, patients with VCAM-1 >1358.5 ng/ml had a median OS of 20 months in comparison to 42 months of all others (p=0.006), while patients with elevated ICAM-1 (>400.6 ng/ml) had a median OS of 13 months compared to 42 months of all others (p<0.0001) and patients with L-selectin >928.2 ng/ml had a median OS of 23 months compared to 42 months of all others (p=0.024). MM patients at first relapse had increased levels of VCAM-1 and ICAM-1 even compared to newly-diagnosed symptomatic MM patients (p<0.01). Both BD and Rd administration reduced dramatically serum VCAM-1 and ICAM-1 after 4 cycles of therapy (p<0.01 for all comparisons) but had no effect on the levels of selectins. The reduction of VCAM-1 and ICAM-1 was more pronounced in responders than in non-responders (p=0.032). In conclusion, patients with newly diagnosed MM have increased serum levels of VCAM-1 and ICAM-1 that correlate with advanced disease features and poor survival suggesting an important role in the biology of the disease. Selectins seem also to participate in MM pathogenesis. The administration of novel agents such as bortezomib and lenalidomide resulted in the reduction of VCAM-1 and ICAM-1 and supports a direct effect on the adhesion of MM cells to BMSCs. Disclosures No relevant conflicts of interest to declare.

scholarly journals Pulmonary hypertension in infants with congenital heart defects: are leukotrienes involved?

1997 ◽  
Vol 6 (5-6) ◽  
pp. 323-326 ◽  
Author(s):  
A. Serraf ◽  
J-P. Gascard ◽  
J. Bruniaux ◽  
C. Labat ◽  
C. Planche ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Congenital Heart Defects ◽  
Pulmonary Blood Flow ◽  
Congenital Heart ◽  
Heart Defects ◽  
Blood Levels ◽  
Blood Samples ◽  
Number Of Patients ◽  
Pulmonary Arterial

The circulating levels of leukotriene E4in infants with congenital heart defects, increased pulmonary blood flow and pulmonary arterial hypertension, were determined and compared with infants with decreased pulmonary blood flow (Tetralogy of Fallot). There was no correlation (r=0.38) between the pulmonary arterial pressure (56 ± 4 mmHg) and the leukotriene E4levels (1.37 ± 0.67 ng/ml blood) measured in peripheral blood samples from the hypertensive group prior to surgery. There was considerable variation in the detectable leukotriene E4levels in blood samples from different patients. The levels detected in the blood samples between the two groups of patients was similar. These data suggest that neither the surgical repair during cardiopulmonary bypass nor the pulmonary hypertension appeared to modify the leukotriene E4blood levels in the small number of patients studied.

Increased endothelial NOS in lambs with increased pulmonary blood flow and pulmonary hypertension

1998 ◽  
Vol 275 (5) ◽  
pp. H1643-H1651 ◽  
Author(s):  
Stephen M. Black ◽  
Jeffrey R. Fineman ◽  
Robin H. Steinhorn ◽  
James Bristow ◽  
Scott J. Soifer
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Vascular Graft ◽  
Pulmonary Blood Flow ◽  
Congenital Heart ◽  
Vascular Reactivity ◽  
Heart Defects ◽  
Pulmonary Arteries ◽  
Enos Gene ◽  
Rnase Protection

Altered pulmonary vascular reactivity is a source of morbidity and mortality for children with congenital heart defects and increased pulmonary blood flow. Nitric oxide (NO) is an important mediator of pulmonary vascular reactivity. The objective of this study was to characterize potential early alterations in expression, localization, and activity of endothelial NO synthase (eNOS) induced by increased pulmonary blood flow and pulmonary hypertension. Utilizing aortopulmonary vascular graft placement in the fetal lamb, we have established a unique animal model of pulmonary hypertension that mimics congenital heart disease with increased pulmonary blood flow. Ten fetal lambs underwent in utero placement of an aortopulmonary vascular graft (shunt). RNase protection assays and Western blotting were performed on lung tissue prepared from 4-wk-old shunt lambs and age-matched controls. eNOS mRNA (2.4:1, P < 0.05) and protein (2.08:1, P < 0.05) were increased in lungs of shunt lambs. In situ hybridization and immunohistochemistry revealed that the increase was confined to the endothelium of pulmonary arteries. eNOS protein (1.55:1, P < 0.05) and tissue cGMP concentrations (2.1:1, P < 0.05) were also increased in isolated fifth-generation pulmonary arteries of shunt lambs. In addition, total lung eNOS activity was increased (2.9:1, P < 0.05). Thus we report a previously undescribed, early upregulation of eNOS gene expression and activity in lambs with increased pulmonary blood flow and pulmonary hypertension.

Decreased surfactant proteins in lambs with pulmonary hypertension secondary to increased blood flow

2001 ◽  
Vol 281 (5) ◽  
pp. L1264-L1270 ◽  
Author(s):  
Jorge A. Gutierrez ◽  
Andrew J. Parry ◽  
D. Michael McMullan ◽  
Cheryl J. Chapin ◽  
Jeffrey R. Fineman
Keyword(s):  
Congenital Heart Disease ◽  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Pulmonary Blood Flow ◽  
Congenital Heart ◽  
Surfactant Proteins ◽  
Control Value ◽  
Mrna Content ◽  
Increased Blood Flow

Infants with increased pulmonary blood flow secondary to congenital heart disease suffer from tachypnea, dyspnea, and recurrent pulmonary infections. We have recently established a model of pulmonary hypertension secondary to increased pulmonary blood flow in lambs after in utero placement of an aortopulmonary vascular graft. The purpose of the present study was to utilize our animal model to determine the effects on the expression of surfactant proteins A (SP-A), B (SP-B), and C (SP-C). At age 4 wk, SP-A mRNA content in lambs decreased to 61.4 ± 8% of age-matched control value ( n = 5; P < 0.05). In addition, SP-A protein content was decreased to 50 ± 12% of control value ( n = 6; P < 0.0001). Although we did not observe statistically significant changes in SP-B mRNA content, SP-B protein was decreased to 74 ± 25% of control value ( n = 4; P < 0.02). There was no difference in SP-C mRNA. These data show that in a model of congenital heart disease with pulmonary hypertension secondary to increased pulmonary blood flow, there is a decrease in SP-A gene expression as well as a decrease in SP-A and SP-B protein contents.

scholarly journals Cellular Adhesion Molecules in Healthy Subjects: Short Term Variations and Relations to Flow Mediated Dilation

2008 ◽  
Vol 3 ◽  
pp. 117727190800300 ◽  
Author(s):  
Ole Eschen ◽  
Jeppe Hagstrup Christensen ◽  
Claus Dethlefsen ◽  
Erik Berg Schmidt
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Individual Variation ◽  
Healthy Subjects ◽  
Preliminary Finding ◽  
Cellular Adhesion ◽  
Negative Association ◽  
Intercellular Adhesion Molecule ◽  
Short Term ◽  
Cellular Adhesion Molecule

The objective was primarily to describe short term intra-individual variation in serum levels of soluble adhesion molecules (sCAMs: E-selectin, P-selectin, intercellular adhesion molecule-1(sICAM-1) and vascular cellular adhesion molecule-1(sVCAM-1)) in healthy subjects. Secondly, sCAMs were correlated to brachial artery flow mediated vasodilation (FMD). Forty healthy subjects aged 24–66 years had sCAMs measured twice with 4 week intervals and short-term intra-individual variation was estimated as variation in the paired measurements after correcting for the analytical precision of the used method. At baseline, brachial FMD was measured. No difference was observed in mean sCAMs in the whole study group. Estimated intra-subject variations in sCAMs were 7.6–11.3%. In a regression analysis, significant negative association was found between sE-selectin and FMD after controlling for possible confounders (p < 0.04) while no significant correlation could be demonstrated between the other sCAMs and FMD. In conclusion, short term intra-individual variations in sCAMs were 7.6–11.3% in healthy subjects. We also found a significant negative association between sE-selectin and FMD, indicating an possible association between inflammation and dysfunction of the vascular endothelium; however further studies are required to confirm this preliminary finding.

Abstract 61: Anti-inflammatory Effect Of Resveratrol In Human Coronary Arterial Endothelial Cells Via Autophagy: Implication For The Treatment Of Kawasaki Disease

Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Fu-Chen Huang Huang ◽  
Ho-Chang Kuo ◽  
Hong-Ren Yu
Keyword(s):  
Endothelial Cells ◽  
Kawasaki Disease ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Cellular Adhesion ◽  
Tnf Alpha ◽  
Coronary Aneurysms ◽  
Cellular Adhesion Molecule ◽  
Increased Risk ◽  
Anti Inflammatory

Kawasaki disease (KD) is an acute febrile vasculitis of childhood and is the leading cause of acquired heart disease in children in the developed world. If untreated, KD can result in coronary aneurysms in 25% of patients, who are at risk of myocardial infarction, sudden death, and congestive heart failure. Despite the success, 10-20% of children will have persistent or recrudescent fever after their first infusion of IVIG. These patients are at increased risk of developing coronary artery abnormalities. Additional therapies should be explored to decrease the incidence of coronary arteritis complication and improve the prognosis in Kawasaki disease. Induced autophagy with resveratrol confers cardioprotection during ischemia and reperfusion in rats. KD is associated with elevated production of inflammatory cytokines, causing damage to the coronary arteries. Serum TNF-alpha levels are elevated in KD, which was supposed to activate the endothelial cells. As a result, adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1(VCAM-1) are expressed in the endothelial cells, and leucocytes adhere firmly to endothelial cells. The leucocytes then damage the endothelial cells and smooth muscle cells and cause vasculitis. In this study, we examined the anti-inflammatory effects of resveratrol on TNF-alpha-induced adhesion molecule expression (VCAM-1 and ICAM-1) and cytokine production (interleukin (IL)-1beta, IL-6 and IL-8) in HCAECs. Pretreatment with resveratrol significantly inhibited TNF-alpha-induced adhesion molecules and cytokines production in HCAECs via the activation of autophagy. Our results suggest that adjunctive resveratrol therapy may modulate the inflammatory response during KD vasculitis and explore the role of autophagy in the pathogenesis of the complication and the promising therapy.

High Levels of Adhesion Molecules Are Associated with Impaired Endothelium-dependent Vasodilation in Patients with Peripheral Arterial Disease

2001 ◽  
Vol 85 (01) ◽  
pp. 63-66 ◽  
Author(s):  
Vincenzo Martone ◽  
Tiziana de Cristofaro ◽  
Salvatore Corrado ◽  
Antonio Silvestro ◽  
Anna Maria Di Donato ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Close Association ◽  
Plasma Concentrations ◽  
Arterial Disease ◽  
Cellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Cellular Adhesion Molecule

SummarySoluble intercellular adhesion molecule-1 (sICAM-1) and vascular cellular adhesion molecule-1 (sVCAM-1) were measured alongside flow-mediated vasodilation (FMD) in 34 patients with intermittent claudication and 14 control subjects. Patients with plasma sICAM-1 >253 ng/mL (median value) showed lower FMD than those with sICAM-1 <253 ng/mL (5.6 ± 1.8% vs 9.6 ± 4.2%, p <0.01). Similarly, in the 17 patients with plasma sVCAM-1 >414 ng/mL, FMD was lower than in the remaining 17 patients (6.1 ± 1.9% vs 9.2 ± 4.5%, p <0.05). Additionally, when endothelial dysfunction was defined as FMD ≤5.5%, patients with FMD below this value had higher plasma concentrations of sICAM-1 and sVCAM-1 than those with FMD >5.5%. Therefore, our findings indicate a close association between elevated plasma levels of adhesion molecules and endothelial dysfunction. As impaired endothelial function is one of the first steps in atherogenesis, our findings have clinical relevance since they serve as the basis for further evaluation of sICAM-1 and sVCAM-1 as potential plasma markers for progression of atherosclerosis in a population at high risk.

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