Effects of two different HMG-CoA reductase inhibitors on thromboxane production in type IIA hypercholesterolemia

Milani, Massimo; Cimminiello, Claudio; Lorena, Marcelo dos Santos Voltani; Arpaia, Guido; Soncini, Marco; Bonfardeci, Giuseppe

doi:10.1016/0753-3322(96)84824-4

Cited by 6 publications

(2 citation statements)

References 28 publications

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“…Even though our results showing potency order as lovastatin N fluvastatin N atorvastatin, we predict that differences in lipid solubility, structure form, and metabolic factor might be the reasons for the issue of selectivity and potency. As such, previous in vivo studies observed different actions among statins on inhibition of thromboxane production [69].…”

Section: Discussionmentioning

confidence: 98%

HMG-CoA reductase inhibitors induce COX-2 gene expression in murine macrophages: role of MAPK cascades and promoter elements for CREB and C/EBPβ

Chen

Huang

Wingerd

et al. 2004

Experimental Cell Research

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Section: Discussionmentioning

confidence: 98%

HMG-CoA reductase inhibitors induce COX-2 gene expression in murine macrophages: role of MAPK cascades and promoter elements for CREB and C/EBPβ

Chen

Huang

Wingerd

et al. 2004

Experimental Cell Research

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“…Several authors have demonstrated a decreased platelet dependent thrombin generation and thrombus formation during treatment with statins in humans [56][57][58][59] So we can affirm that several studies suggest an antiplatelet effect of statins, as detected by methods exploring different activation pathways, during treatment in vivo in humans. On the contrary only few studies in small populations have shown no effect of statins on platelet function that could be related to the etnicity or employed methods (platelet aggregation or urinary TXB2 levels) [60,61]. Moreover it has been suggested that statin withdrawal induce increased platelet reactivity that is modulated by the replace of statin therapy [62].…”

Section: Studies Showing Antiplatelet Action During Statin Treatment mentioning

confidence: 98%

Mechanisms for Antiplatelet Action of Statins

Puccetti¹,

Pasqui²,

Auteri³

et al. 2005

CDTCHD

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Hydroxymethyl-glutaryl coenzyme A reductase inhibitors (statins) offer important benefits for the large populations of individuals at high risk for coronary heart and cerebrovascular disease. the overall clinical benefits observed with statin therapy appear to be greater than what might be expected from changes in lipid profile alone, suggesting that the beneficial effects of such drugs may extend beyond their effects on serum cholesterol. Platelet hyperactivity is a key step in atherothrombosis and experimental data suggest that statins could exert an antiplatelet effect which could be involved in their protective action. In the present review we report of the major studies in humans showing the effect of statins on platelets, especially by the more sensitive methods to explore platelet function such as cytofluorymetric detection of specific proteins. Moreover we describe the putative mechanisms involved in platelet deactivation with particular regard to the effects related to cholesterol reduction or beyond lipid-lowering. Indeed, data from several studies suggest some differences among compounds in terms of timing of action by modulation of several activating pathways which could take part either in the early, cholesterol-lowering independent, effects in the acute phase of vascular disease or during chronic treatment.

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Fluvastatin for lowering lipids

Adams

Sekhon

Tsang

et al. 2018

Cochrane Database of Systematic Reviews

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Fluvastatin lowers blood total cholesterol, LDL cholesterol and triglyceride in a dose-dependent linear fashion. Based on the effect on LDL cholesterol, fluvastatin is 12-fold less potent than atorvastatin and 46-fold less potent than rosuvastatin. This review did not provide a good estimate of the incidence of harms associated with fluvastatin because of the short duration of the trials and the lack of reporting of adverse effects in 56% of the placebo-controlled trials.

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Effects of two different HMG-CoA reductase inhibitors on thromboxane production in type IIA hypercholesterolemia

Cited by 6 publications

References 28 publications

HMG-CoA reductase inhibitors induce COX-2 gene expression in murine macrophages: role of MAPK cascades and promoter elements for CREB and C/EBPβ

HMG-CoA reductase inhibitors induce COX-2 gene expression in murine macrophages: role of MAPK cascades and promoter elements for CREB and C/EBPβ

Mechanisms for Antiplatelet Action of Statins

Fluvastatin for lowering lipids

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