Haemostatic parameters related to lipids and adhesion molecules

Østerud, Bjarne; Elvevoll, Edel O.; Brox, Jan; Anderssen, T.; Eliassen, Liv Tone; Halvorsen, H.; Høgmo, P.; Kvernmo, H.; Lia, Karin; Lund, Thomas Kromann; Olsen, Jan Ole; Olsen, Randi; Engstad, Charlotte Sissener; Vognild, Eva

doi:10.1097/00001721-199912000-00003

Cited by 25 publications

(14 citation statements)

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“…A number of publications have unequivocally shown increased cAM levels in atherosclerosis [18,31], which may even predict outcome [31]. In contrast with atherosclerosis, the effect of hypercholesterolaemia on cAM levels has been a source of controversy [13,14,[17][18][19][20][21][22][23]32,33]. We therefore aimed to clarify whether hypercholesterolaemia directly induces AM release into the circulation.…”

Section: Discussionmentioning

confidence: 99%

“…As circulating (c)AMs have been used as markers of atherosclerosis [9][10][11][12], clinical trials have tried to reveal a potential association between hypercholesterolaemia and AM expression by measurement of these cAMs : elevated cAM levels have been found in hypercholesterolaemic patients in some smaller studies [13], but not in larger trials [14]. Likewise, cross-sectional studies indicate rather weak or no correlations between cAM levels and plasma cholesterol levels [15][16][17][18][19][20][21][22]. Finally, pharmacological reduction of LDL-cholesterol (LDL-C) by statins was associated with a decrease in plasma levels of cE-selectin in ten patients [23], but further confusion arises from divergent results of statin therapy on cICAM-1 levels [24][25][26].…”

Section: Introductionmentioning

confidence: 99%

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Levels of adhesion molecules do not decrease after 3 months of statin therapy in moderate hypercholesterolaemia

et al. 2003

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Studies in animals and humans indicate a pivotal role for adhesion molecules (AMs) in the pathogenesis of atherosclerosis. Whereas an association between hypercholesterolaemia and AM expression has been suggested, it is unclear whether lowering cholesterol decreases AM expression and release. We compared the effects of a 3-month treatment with standard doses of three different statins (atorvastatin, simvastatin and pravastatin) on plasma levels of circulating AM (cAM) in 75 hypercholesterolaemic patients in a randomized clinical trial. Plasma levels of circulating (c)E-selectin, circulating intercellular adhesion molecule-1 (cICAM-1) and circulating vascular cell adhesion molecule-1 (cVCAM-1) were measured before and after 3 months of therapy. None of the statins lowered plasma cAM levels and pooled analyses of all patients showed a 1.7% [95% confidence interval (CI), -1.4-4.9%] increase in cE-selectin, a 2.1% (95% CI, -0.2-4.4%) increase in cICAM-1, and a 2.7% (95% CI, -0.6-6.1%) increase in cVCAM-1 levels. cAM levels did not decrease, even in patients with a >50% decrease ( n =19) in low-density lipoprotein cholesterol levels. This study provides strong evidence that 3 months of therapy with three different statins does not decrease cAM levels, despite normalization of cholesterol levels, and a minor decrease in C-reactive protein levels in patients with moderate hypercholesterolaemia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Levels of adhesion molecules do not decrease after 3 months of statin therapy in moderate hypercholesterolaemia

et al. 2003

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“…Furthermore, plasma levels of these cell adhesion molecules are increased in metabolic syndromes such as diabetes, hypertension and atherosclerosis [16][17][18][19][20][21], and predict adverse outcomes in patients at cardiovascular risk [22,23].…”

Section: Introductionmentioning

confidence: 99%

Effects of enalapril and losartan on circulating adhesion molecules and monocyte chemotactic protein-1

et al. 2002

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At least four independent studies in different clinical settings showed that angiotensin-converting enzyme inhibitors (ACE-Is) such as enalapril effectively decrease plasma levels of circulating adhesion molecules (cAMs). To examine whether this effect may be mediated by the decreased action of angiotensin, we compared the effects of enalapril with the direct angiotensin-II antagonist, losartan, on plasma levels of cAMs, and monocyte chemotactic protein-1 (MCP-1). In a randomized trial, we recruited 32 untreated patients (19 male, aged 59+/-13 years) with hypertension, who received either enalapril (mean dose 17 mg/day) or losartan (mean dose 77 mg/day) at equipotent doses. Enalapril decreased plasma levels of all cAMs after 8 weeks of treatment: cE-selectin levels decreased by 13% (P=0.007), intercellular adhesion molecule-1 (cICAM-1) by 15% (P=0.002) and vascular cell adhesion molecule-1 (cVCAM-1) by 19% (P=0.003). Similarly, enalapril decreased plasma levels of MCP-1 by 13% (P<0.001). Losartan did not significantly change cAM or MCP-1 plasma concentrations after 8 weeks of treatment: cE-selectin levels decreased by 3%, cICAM-1 by 5%, cVCAM-1 by 8%, whereas MCP-1 increased by 2% (all P=NS; not significant). The enalapril effect on percentage changes of cVCAM-1 was significantly different from losartan (P=0.0429). Eight weeks of antihypertensive treatment with enalapril but not losartan, significantly decreased plasma levels of cAMs and MCP-1 in hypertensive patients. The beneficial effects of ACE-Is on cAMs may have implications for atherogenesis and the reduction of cardiovascular events, which cannot be fully explained by their antihypertensive effects alone.

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“…The levels of soluble adhesion molecules are associated with diabetes mellitus [9,10] and hyperlipoproteinemia [11,12]. Studies evaluating the eect of cholesterol lowering therapy on adhesion molecule levels demonstrated inconclusive results.…”

Section: Introductionmentioning

confidence: 99%

The effects of three different LDL‐apheresis methods on the plasma concentrations of E‐selectin, VCAM‐1, and ICAM‐1

Empen

Otto

Brodl

et al. 2002

J of Clinical Apheresis

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Plasma concentrations of cellular adhesion molecules are associated with atherosclerotic diseases and major cardiovascular risk factors. It was shown that LDL-apheresis with dextran sulfate lowers the levels of E-selectin and ICAM-1 in patients with familial hypercholesterolemia. The effects of different LDL-apheresis methods have not been studied yet. Cholesterol, triglycerides, LDL cholesterol, HDL cholesterol, fibrinogen, and the adhesion molecules E-selectin, VCAM-1, and ICAM-1 were measured in 20 patients with coronary heart disease and severe hyperlipoproteinemia immediately before and after regular LDL-apheresis. Treatment was performed by different apheresis methods (direct absorption, DA, n = 6; dextran sulfate adsorption, DS, n = 7; heparin precipitation, HP, n = 7). Rebound data of adhesion molecule levels were obtained from 2 patients of each group. Lipids were reduced similarly in all groups. The concentrations of all adhesion molecules were lowered during apheresis. The reduction of E-selectin (-31 +/- 7 vs. -6 +/- 5 and -6 +/- 5%, respectively, P < 0.001) was most prominent in the patients treated by heparin precipitation. Depending on the method of LDL-apheresis, the concentrations of VCAM-1 and E-selectin in the outlets of the LDL-apheresis columns were significantly lower compared to the concentration in the inlets. Plasma concentrations of adhesion molecules increased to their pre-apheresis values within 2 to 4 days following LDL-apheresis. The reductions of adhesion molecule levels observed during LDL-apheresis are at least partly due to adsorption to the LDL-apheresis column. The extent of absorption depends on the principle of extracorporeal LDL elimination.

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Haemostatic parameters related to lipids and adhesion molecules

Cited by 25 publications

References 0 publications

Levels of adhesion molecules do not decrease after 3 months of statin therapy in moderate hypercholesterolaemia

Levels of adhesion molecules do not decrease after 3 months of statin therapy in moderate hypercholesterolaemia

Effects of enalapril and losartan on circulating adhesion molecules and monocyte chemotactic protein-1

The effects of three different LDL‐apheresis methods on the plasma concentrations of E‐selectin, VCAM‐1, and ICAM‐1

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