Reduction of Platelet Activity Markers in Type II Hypercholesterolemic Patients by a HMG-CoA-Reductase Inhibitor

Huhle, G.; Abletshauser, C.; Mayer, Nóra; Weidinger, Gottfried; Harenberg, Job; Heene, D. L.

doi:10.1016/s0049-3848(99)00037-7

Cited by 112 publications

(65 citation statements)

References 17 publications

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“…[1][2][3][4][5][6]22,23 Statins increase production of nitric oxide in the endothelium, which has local vasodilatory properties in addition to antithrombogenic, antiproliferative, and leukocyte-adhesion inhibiting effects. 22,23 Other mechanisms by which statins favorably influence atherosclerosis include enhancement of endothelium-dependent relaxation, 3 inhibition of platelet function, 5 and inhibition of endothelin-1, a potent vasoconstrictor and mitogen. 4 Therefore, it is biologically plausible that statins might improve lowerextremity functioning in PAD by retarding the deleterious effects of atherosclerosis on leg arteries.…”

Section: Discussionmentioning

confidence: 99%

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Statin Use and Leg Functioning in Patients With and Without Lower-Extremity Peripheral Arterial Disease

et al. 2003

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Background-We determined whether statin use (versus nonuse) is associated with superior lower-extremity functioning independently of cholesterol levels and other confounders in patients with and without peripheral arterial disease. Methods and Results-Participants included 392 men and women with an ankle brachial index (ABI) Ͻ0.90 and 249 with ABI 0.90 to 1.50. Functional outcomes included 6-minute walk distance and 4-meter walking velocity. A summary performance score combined performance in walking speed, standing balance, and time for 5 repeated chair rises into an ordinal score ranging from 0 to 12 (12ϭbest

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Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6] Statins stabilize atherosclerotic plaques, reduce oxidative stress, and decrease vascular inflammation. 1,2 In vascular endothelium, statins increase concentrations of nitric oxide, which has vasodilator, antithrombotic, and antiproliferative properties.…”

mentioning

confidence: 99%

Statin Use and Leg Functioning in Patients With and Without Lower-Extremity Peripheral Arterial Disease

et al. 2003

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“…Statins have also been shown to modify the function of ECs, smooth muscle cells, platelets, and monocytes/macrophages (22). Their effects include decreasing the expression of adhesion molecules in monocytes and leukocyte-endothelial interactions (23)(24)(25)(26), inhibiting platelet function (27), inhibiting tissue factor expression by mononuclear cells (28,29), down-regulating inflammatory cytokines in ECs (30), increasing fibrinolytic activity (31,32), and immunomodulation by decreasing the expression of class II major histocompatibility complex antigen (33).…”

Section: Conclusion These Findings Indicate That Fluvastatin Signifimentioning

confidence: 99%

Inhibition of the thrombogenic and inflammatory properties of antiphospholipid antibodies by fluvastatin in an in vivo animal model

Ferrara¹,

Liu²,

Espinola³

et al. 2003

Arthritis & Rheumatism

138

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Methods. Two groups of CD-1 male mice, each comprising ϳ18 mice, were fed either normal saline solution or 15 mg/kg fluvastatin for 15 days. Each of the 2 groups was further subdivided to receive either purified IgG from patients with the antiphospholipid syndrome (IgG-APS) or normal IgG from healthy subjects. Analysis of thrombus dynamics was performed in treated and control mice, using a standardized thrombogenic injury procedure, and the area (size) of the thrombus was measured. Adhesion of leukocytes to ECs was analyzed with a microcirculation model of exposed cremaster muscle. Baseline and posttreatment soluble intercellular adhesion molecule 1 (sICAM-1) levels were determined by enzyme-linked immunosorbent assay.Results. IgG-APS mice treated with fluvastatin showed significantly smaller thrombi, a reduced number of adherent leukocytes, and decreased levels of sICAM-1 compared with IgG-APS animals treated with placebo.Conclusion. These findings indicate that fluvastatin significantly diminishes aPL-mediated thrombosis and EC activation in vivo. These results may have important implications for the design of new treatment strategies aimed at preventing recurrent thrombosis in patients with APS.

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“…Statins increase the production of nitric oxide in the endothelium, which has local vasodilatory properties in addition to antithrombogenic, antiproliferative, and leukocyteadhesion inhibiting effects, as well as intense inflammatory activity. [24][25][26] Other mechanisms by which statins favorably influence atherosclerosis include enhancement of endothelium-dependent relaxation, inhibition of platelet function, 27) and inhibition of endothelin-1, a potent vasoconstrictor and mitogen. 28) Some studies have also shown that statins can improve the leg function of patients with PAD.…”

Section: Discussionmentioning

confidence: 99%

Effect of Statins and Calcium Channel Blockers on All-Cause Mortality and Cardiovascular and Cerebrovascular Disease Mortality in 958 Chinese Hospitalized Patients with Peripheral Arterial Disease after 13 Months of Follow-up

Nguyen³

et al. 2007

JOURNAL OF HEALTH SCIENCE

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Reduction of Platelet Activity Markers in Type II Hypercholesterolemic Patients by a HMG-CoA-Reductase Inhibitor

Cited by 112 publications

References 17 publications

Statin Use and Leg Functioning in Patients With and Without Lower-Extremity Peripheral Arterial Disease

Statin Use and Leg Functioning in Patients With and Without Lower-Extremity Peripheral Arterial Disease

Inhibition of the thrombogenic and inflammatory properties of antiphospholipid antibodies by fluvastatin in an in vivo animal model

Effect of Statins and Calcium Channel Blockers on All-Cause Mortality and Cardiovascular and Cerebrovascular Disease Mortality in 958 Chinese Hospitalized Patients with Peripheral Arterial Disease after 13 Months of Follow-up

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