Thromb Haemost 2013; 110(02): 366-377
DOI: 10.1160/TH13-03-0238
Cardiovascular Biology and Cell Signalling
Schattauer GmbH

Lipid-lowering therapy with statins reduces microparticle shedding from endothelium, platelets and inflammatory cells

Rosa Suades
1   Cardiovascular Research Center (CSIC-ICCC), IIB-Sant Pau, Barcelona, Spain
2   CIBERobn – Pathophysiology of Obesity and Nutrition, Barcelona, Spain
,
Teresa Padró
1   Cardiovascular Research Center (CSIC-ICCC), IIB-Sant Pau, Barcelona, Spain
2   CIBERobn – Pathophysiology of Obesity and Nutrition, Barcelona, Spain
,
Rodrigo Alonso
3   Jimenez Diaz Foundation, Madrid, Spain
,
Pedro Mata
3   Jimenez Diaz Foundation, Madrid, Spain
,
Lina Badimon
1   Cardiovascular Research Center (CSIC-ICCC), IIB-Sant Pau, Barcelona, Spain
2   CIBERobn – Pathophysiology of Obesity and Nutrition, Barcelona, Spain
4   Cardiovascular Research Chair, UAB, Barcelona, Spain
› Author Affiliations
Financial support: Funds were provided by PNS SAF2010–16549 (to LB) from the Spanish Ministry of Science and Innovation; and CNIC-082008 (to LB and PM), CIBEROBNCB06/03 (to LB), TERCEL (to LB), FIS PI1001115 (to TP) and Fundación Investigación Cardiovascular – Fundación Jesús Serra. RS is a recipient of a predoctoral fellowship from Spanish Ministry of Health (PFIS-FI09/00092, ISCIII).
Further Information

Publication History

Received: 18 March 2013

Accepted after minor revision: 17 May 2013

Publication Date:
04 December 2017 (online)

Summary

Hyperlipidaemia is a causal factor in the ethiopathogenesis of atherosclerosis. Statins are the cornerstone drug therapy for LDL-cholesterol (LDL-c) lowering, that exert beneficial effects beyond lipid lowering. Circulating microparticles (cMPs), microvesicles released by activated cells into the bloodstream, are markers of vascular and inflammatory cell activation with tentative role in disease progression. However, the role of statins on cMPs seems controversial. We aimed at the evaluation of the effects of lipid-lowering treatment (LLT) on cMP generation in patients in primary prevention of atherosclerosis. A case-control study was conducted in hypercholesterolaemic patients receiving LLT with statins and normocholesterolaemic controls (LLT+ and LLT, respectively, n=37/group), matched by age, gender and LDL-c levels. cMPs were characterised by flow cytometry using annexin-V and cellspecific antibodies. In LLT+-patients overall numbers of cMPs (p<0.005) were lower than in controls. Levels of cMPs carrying parental cell markers from vascular and circulating cell origin (platelet, endothelial cell, pan-leukocyte and specific-leukocyte subsets) were significantly lower in blood of LLT+ compared to LLT-patients. Moreover, MPs from LLT+-patients had reduced markers of activated platelets (αIIbβ3-integrin), activated inflammatory cells (αM-integrin) and tissue factor. The effect of LLT on cMP shedding was found to be accumulative in years. cMP shedding associated to cardiovascular risk in LLT+-patients. In summary, at similar plasma cholesterol levels patients on statin treatment had a significant lower number of cMPs carrying markers of activated cells. These findings indicate that statins protect against vascular cell activation.

 
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