Levels of soluble adhesion molecules in various clinical presentations of coronary atherosclerosis

Department of Cardiology, Yüksek Ihtisas Hospital, Ankara, Turkey.
International Journal of Cardiology (Impact Factor: 4.04). 09/2004; 96(2):235-40. DOI: 10.1016/j.ijcard.2003.07.014
Source: PubMed


Adhesion molecules play an important role in the development and course of coronary atherosclerosis. In this study, soluble forms of vascular cell adhesion molecule (VCAM-1) intercellular adhesion molecule-1 (ICAM-1), E-selectin and P-selectin were evaluated in patients with various clinical presentations of coronary atherosclerosis and compared them to those with angiographically documented normal coronary arteries. Venous plasma samples were collected from 43 patients with acute myocardial infarction (AMI), 45 with unstable angina pectoris (UAP), 34 with stable angina pectoris (SAP) and 29 subjects with normal coronary arteries (control). The VCAM-1 level was significantly higher in patients with AMI (mean +/- SEM; 799.8 +/- 26.3 ng/ml) than those with UAP (644.2 +/- 26.7 ng/ml) and SAP (526 +/- 32.5 ng/ml) and controls (270 +/- 26.8 ng/ml). In patients with UAP, VCAM-1 was found to be significantly elevated as compared to the SAP group and controls. VCAM-1 level was also higher in SAP group than the controls. Serum levels ICAM-1 were similar among patients with AMI (424.1 +/- 15.2 ng/ml), UAP (403 +/- 12.3 ng/ml) and SAP (381.2 +/- 16.2 ng/ml); however, levels of ICAM-1 was significantly elevated in these groups as compared to the controls (244.3 +/- 11). The mean level of E-selectin was not different in AMI and UAP groups (47.2 +/- 2.2 vs. 42.6 +/- 2.1 ng/ml; respectively). However, it was significantly higher in acute coronary syndrome groups as compared to SAP (33.4 +/- 2.3 ng/ml) and control subjects (30.7 +/- 1.9 ng/ml). Serum levels of E-selectin were similar in SAP group and controls. For P-selectin, no significant difference was observed between AMI and UAP groups (187.5 +/- 7.2 vs. 181.7 +/- 4.7 ng/ml; respectively), however, it was significantly higher in both groups as compared to SAP group (146.1 +/- 7.4 ng/ml) and controls (108 +/- 6.6 ng/ml). Serum level of P-selectin was significantly higher in patients with SAP than the control group. In conclusion, determination of serum VCAM-1, E-selectin and P-selectin levels seems more useful for detecting coronary plaque destabilization.

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    • "The sensitivity and specificity for IL-6 as a CAD prediction marker were 46% and 86%, respectively, which led the investigators to conclude that the use of IL-6 levels alone could be useful in ruling out CAD [23]. In other studies, higher IL-6 levels were found in patients who had already experienced UA when compared with patients with SA [24–26]. In the PRIME study [27], IL-6 levels showed their value for predicting SA or ACS over a 5-year followup. "
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    ABSTRACT: Inflammatory mediators appear to be the most intriguing yet confusing subject, regarding the management of patients with acute coronary syndromes (ACS). The current inflammatory concept of atherosclerotic coronary artery disease (CAD) led many investigators to concentrate on systemic markers of inflammation, as well as imaging techniques, which may be helpful in risk stratification and prognosis assessment for cardiovascular events. In this review, we try to depict many of the recently studied markers regarding stable angina (SA), their clinical usefulness, and possible future applications in the field.
    Disease markers 06/2014; 2014:831364. DOI:10.1155/2014/831364 · 1.56 Impact Factor
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    • "Adhesion molecules VCAM-1 and ICAM-1 have different expression patterns on endothelial membrane and probably play different roles in atherogenesis [51]. While sVCAM-1 is a predictive marker of increased risk for future coronary events only in patients with the presence of atherosclerosis [52], sICAM-1 is predictive – like hsCRP – also in initially healthy people [53]. "
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    ABSTRACT: Objectives: Both decreased and increased risk of cardiovascular events/mortality have been reported with high adiponectin levels. Only a few studies have reported an association of adiponectin with markers of hemostasis/endothelial dysfunction which might explain the reported discrepancies. Design and methods: We evaluated the association of total adiponectin with von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (t-PA), soluble thrombomodulin (sTM), adhesion molecules sICAM-1 and sVCAM-1, lipids and markers of insulin resistance (IR) in 308 asymptomatic dyslipidemic subjects and healthy controls. Subjects were divided into 4 dyslipidemic phenotypes (DLP): DLP1 (TG < 1.5 mmol/L + ApoB < 1.2 g/L), DLP2 (TG ≥ 1.5 + ApoB < 1.2), DLP3 (TG < 1.5 + ApoB ≥ 1.2) and DLP4 (TG ≥ 1.5 + ApoB ≥ 1.2). The results were evaluated also according to the presence (+) and absence (-) of metabolic syndrome (MS). Results: In hyperlipidemic subjects (DLP2-4), PAI-1, t-PA and sICAM-1 correlated with markers of IR but only t-PA correlated inversely with adiponectin. In contrast positive association of adiponectin with vWF, sTM and sVCAM-1 was found but none of these parameters correlated with markers of insulin resistance. In multiple regression analysis, adiponectin remained independently associated with vWF [in DLP3, DLP4, DLP2-4, MS(-)], with sTM [in DLP2, DLP4, DLP2-4, MS(+)] and with sVCAM-1 [in DLP2, DLP3, DLP4, DLP2-4, MS(+)]. In healthy controls (DLP1), no association between adiponectin and markers of hemostasis/endothelial dysfunction was found. Conclusion: The independent positive association of adiponectin with vWF, sTM and sVCAM-1 deserves further evaluation in connection with the risk of atherothrombotic cardiovascular events.
    Clinical biochemistry 03/2013; 46(9). DOI:10.1016/j.clinbiochem.2013.02.014 · 2.28 Impact Factor
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    • "Serum cellular adhesion molecule levels increase in association with cardiovascular risk factors and are associated with structural functional measures of atherosclerotic disease, as well as with adverse cardiovascular prognosis [9,11,15,43,44]. Serum VCAM-1, ICAM-1 and E-selectin concentrations are elevated in obesity [45-47], chronic renal failure [48], in lean and obese subjects genetically predisposed to T2DM [39,49] and in T2DM [16,50]. "
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    ABSTRACT: CVD in obesity and T2DM are associated with endothelial activation, elevated plasma vascular inflammation markers and a prothrombotic state. We examined the contribution of FFA to these abnormalities following a 48-hour physiological increase in plasma FFA to levels of obesity and diabetes in a group of healthy subjects. 40 non-diabetic subjects (age = 38 +/- 3 yr, BMI = 28 +/- 1 kg/m2, FPG = 95 +/- 1 mg/dl, HbA1c = 5.3 +/- 0.1%) were admitted twice and received a 48-hour infusion of normal saline or low-dose lipid. Plasma was drawn for intracellular (ICAM-1) and vascular (VCAM-1) adhesion molecules-1, E-selectin (sE-S), myeloperoxidase (MPO) and total plasminogen inhibitor-1 (tPAI-1). Insulin sensitivity was measured by a hyperglycemic clamp (M/I). Lipid infusion increased plasma FFA to levels observed in obesity and T2DM and reduced insulin sensitivity by 27% (p = 0.01). Elevated plasma FFA increased plasma markers of endothelial activation ICAM-1 (138 +/- 10 vs. 186 +/- 25 ng/ml), VCAM-1 (1066 +/- 67 vs. 1204 +/- 65 ng/ml) and sE-S (20 +/- 1 vs. 24 +/- 1 ng/ml) between 13-35% and by > or = 2-fold plasma levels of myeloperoxidase (7.5 +/- 0.9 to 15 +/- 25 ng/ml), an inflammatory marker of future CVD, and tPAI-1 (9.7 +/- 0.6 to 22.5 +/- 1.5 ng/ml), an indicator of a prothrombotic state (all p < or = 0.01). The FFA-induced increase was independent from the degree of adiposity, being of similar magnitude in lean, overweight and obese subjects. An increase in plasma FFA within the physiological range observed in obesity and T2DM induces markers of endothelial activation, vascular inflammation and thrombosis in healthy subjects. This suggests that even transient (48-hour) and modest increases in plasma FFA may initiate early vascular abnormalities that promote atherosclerosis and CVD.
    Cardiovascular Diabetology 02/2010; 9(1):9. DOI:10.1186/1475-2840-9-9 · 4.02 Impact Factor
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