Statin Use is Associated with a Significant Reduction in Cholesterol Content of Erythrocyte Membranes. A Novel Pleiotropic Effect?

Tziakas, Dimitrios; Chalikias, Georgios K.; Stakos, Dimitrios; Tentes, Ioannis; Thomaidi, Adina; Chatzikyriakou, Sofia; Mitrousi, Konstantina; Kortsaris, A.; Kaski, Juan Carlos; Boudoulas, Harisios; Konstantinides, Stavros

doi:10.1007/s10557-009-6202-7

Cited by 20 publications

(10 citation statements)

References 52 publications

(62 reference statements)

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“…Statin therapy has been posited to prevent neovascularization (29) and limit the cholesterol content of red blood cell membranes (30) segments ( Figure 5). Taken together with our previous study demonstrating that coronary lesions with Most importantly, HIP assessment may be more conveniently possible in Japanese subjects by virtue of the body habitus and its applicability elsewhere has yet to be determined.…”

Section: Discussionmentioning

confidence: 99%

Effect of Intensive Statin Therapy on Coronary High-Intensity Plaques Detected by Noncontrast T1-Weighted Imaging

Noguchi

Tanaka

Kawasaki

et al. 2015

Journal of the American College of Cardiology

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Section: Discussionmentioning

confidence: 99%

Effect of Intensive Statin Therapy on Coronary High-Intensity Plaques Detected by Noncontrast T1-Weighted Imaging

Noguchi

Tanaka

Kawasaki

et al. 2015

Journal of the American College of Cardiology

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“…114 Statins could also influence the consequences of microbleeding due to their ability to limit the cholesterol content of RBC membranes. 115 In particular, statins change the profile of cellular phospholipids by reducing the sphingomyelin content of cell membranes. 116 In parallel, statins are also able to limit neutrophil transendothelial migration.…”

Section: Therapeutic Consequencesmentioning

confidence: 99%

Intraplaque haemorrhages as the trigger of plaque vulnerability

Michel

Virmani

Arbustini

et al. 2011

European Heart Journal

315

218

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Atherothrombosis remains one of the main causes of morbidity and mortality in the western countries. Human atherothrombotic disease begins early in life in relation to circulating lipid retention in the inner vascular wall. Risk factors enhance the progression towards clinical expression: dyslipidaemia, diabetes, smoking, hypertension, ageing, etc. The evolution from the initial lipid retention in the arterial wall to clinical events is a continuum of increasingly complex biological processes. Current strategies to fight the consequences of atherothrombosis are orientated either towards the promotion of a healthy life style1 and preventive treatment of risk factors, or towards late interventional strategies.2 Despite this therapeutic arsenal, the incidence of clinical events remains dramatically high,3 dependent, at least in part, on the increasing frequency of type 2 diabetes and ageing. But some medical treatments, focusing only on prevention of the metabolic risk, have failed to reduce cardiovascular mortality, thus illustrating that our understanding of the pathophysiology of human atherothrombosis leading to clinical events remain incomplete. New paradigms are now emerging which may give rise to novel experimental strategies to improve therapeutic efficacy and prediction of disease progression. Recent studies strengthen the concept that the intraplaque neovascularization and bleeding (Figure 1, upper panel) are events that could play a major role in plaque progression and leucocyte infiltration, and may also serve as a measure of risk for the development of future events. The recent advances in our understanding of IntraPlaque Hemorrhage as a critical event in triggering acute clinical events have important implications for clinical research and possibly future clinical practice. Figure 1Macroscopic view and schematic representation of the detrimental consequences of intraplaque haemorrhages on plaque biology and stability.

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“…The release of pro-inflammatory free cholesterol of erythrocyte membrane (CEM) from red blood cells in atherosclerotic plaques during intraplaque haemorrhage or neoangiogenesis has also been identified as a risk factor for CAD, and a marker of plaque vulnerability, which is independent of serum LDL-C concentrations. A study of 212 patients with acute coronary syndromes undergoing assessment for angina pectoris showed a substantial reduction in CEM in patients receiving statin therapy, which was not associated with changes in serum concentrations of LDL-C, HDL-C or triglycerides [77]. A retrospective database analysis of 105 patients with type III dysbetalipoproteinaemia, a remnant removal disease, has also shown statin-induced regression of lipid deposits in the skin (palmar crease xanthoma) [78].…”

Section: Mechanisms Of Atherosclerosis: the Significance Of Pleiotropmentioning

confidence: 99%

Pleiotropic effects of pitavastatin

Davignon

2012

Brit J Clinical Pharma

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3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are established first line treatments for hypercholesterolaemia. In addition to the direct effects of statins in reducing concentrations of atherogenic low density lipoprotein cholesterol (LDL-C), several studies have indicated that the beneficial effects of statins may be due to some of their cholesterol-independent, multiple (pleiotropic) effects which may differ between different members of the class. Pitavastatin is a novel synthetic lipophilic statin that has a number of pharmacodynamic and pharmacokinetic properties distinct from those of other statins, which may underlie its potential pleiotropic benefits in reducing cardiovascular risk factors. This review examines the principal pleiotropic effects of pitavastatin on endothelial function, vascular inflammation, oxidative stress and thrombosis. The article is based on a systematic literature search carried out in December 2010, together with more recent relevant publications where appropriate. The available data from clinical trials and in vitro and animal studies suggest that pitavastatin is not only effective in reducing LDL-C and triglycerides, but also has a range of other effects. These include increasing high density lipoprotein cholesterol, decreasing markers of platelet activation, improving cardiac, renal and endothelial function, and reducing endothelial stress, lipoprotein oxidation and, ultimately, improving the signs and symptoms of atherosclerosis. It is concluded that the diverse pleiotropic actions of pitavastatin may contribute to reducing cardiovascular morbidity and mortality beyond that achieved through LDL-C reduction.

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Statin Use is Associated with a Significant Reduction in Cholesterol Content of Erythrocyte Membranes. A Novel Pleiotropic Effect?

Abstract: The present study showed, that use of statins is associated with a reduction in CEM, an emerging marker of clinical instability and plaque vulnerability in CAD patients. The pleiotropic effects of statins at the cell membrane level represent a promising novel direction for research in CAD.

Cited by 20 publications

References 52 publications

Effect of Intensive Statin Therapy on Coronary High-Intensity Plaques Detected by Noncontrast T1-Weighted Imaging

Effect of Intensive Statin Therapy on Coronary High-Intensity Plaques Detected by Noncontrast T1-Weighted Imaging

Intraplaque haemorrhages as the trigger of plaque vulnerability

Pleiotropic effects of pitavastatin

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