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Objectives: Hypercholesterolaemia is associated with increased plasma levels of vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8). We studied the effect of rosuvastatin monotherapy or its combination at a lower dose with omega-3 polyunsaturated fatty acids (ω-3 PUFAs) in the VEGF and IL-8 plasma levels in patients with mixed dyslipidaemia., Methods: Fifty patients with mixed dyslipidaemia were recruited. Fifty-five normolipidaemic, apparently healthy, ageand sex- matched subjects acted as controls. Patients were randomized to 40 mg/day rosuvastatin (R group, n=26) or 10 mg/day rosuvastatin plus 2 g/day of ω-3 PUFAs (R+O group, n=24). The levels of VEGF and IL-8 in plasma, were assessed at baseline and 3 months post-treatment., Results: At baseline, both plasma VEGF and IL-8 levels were significantly higher in the R and R+O groups compared with controls (p<0.04, p<0.03 and p<0.02, p<0.03, respectively). Post-treatment levels of VEGF were decreased in the R group while a significant increase was observed in the R+O group, compared with baseline levels (p<0.02 and p<0.03, respectively). Post-treatment IL-8 levels were decreased in both R and R+O groups (p<0.03 and p<0.04, respectively)., Conclusions: We show for the first time that either rosuvastatin monotherapy or its combination at a lower dose with ω-3 PUFAs reduces IL-8 levels in mixed dyslipidaemic patients. High-dose rosuvastatin monotherapy reduces VEGF values, whereas a significant increase is observed in patients receiving lower dose rosuvastatin with ω-3 PUFAs. The clinical significance of the above findings regarding cardiovascular risk remains to be established.

Cardiovascular risk factors are associated with coronary artery disease (CAD) and with cognitive dysfunction. However, the precise pathogenic mechanisms responsible for this association remain elusive. In the present study, CAD patients with cognitive impairment showed significantly higher platelet activation compared with CAD patients without cognitive impairment. In addition, we identified platelet activity to be a significant independent predictor for the severity of cognitive impairment in these patients. We discuss the link between platelet hyperactivity and dementia (including Alzheimer`s disease) based on the literature and our findings. We also discuss the potential mechanisms involved. This link may become a therapeutic option.

Platelets are involved in vascular homeostasis and inflammation through interaction with circulating blood cells and vascular wall. MiRNAs are small, conserved and non-coding RNA molecules, which interact directly with specific mRNAs regions regulating gene expression. The purpose of this review is to gather all known platelet miRNAs and summarize their role in platelet biogenesis and function. Increasing evidence supports the role of miR-34a and miR-150 in megakaryocytopoiesis and platelet production. Although 284 miRNAs are described to be present in platelets, their role is mostly unknown. The most abundant miRNA in platelets is miR-223 followed by miR-126. The miR-96, miR-200b, miR- 495, miR-107 and miR-223 are critically involved in platelet reactivity, aggregation, secretion and adhesion. The presence of miRNAs known to regulate angiogenesis in platelets is also discussed. Furthermore, platelet-derived microvesicles and microparticles contain several miRNAs, which may facilitate the communication between platelets with other vascular cells, a mechanism that may play an important role in vascular homeostasis and inflammation. Further studies are needed to elucidate the exact roles of platelet miRNAs in platelet function and vascular biology.

Platelets are known to play a fundamental role in acute coronary syndromes. After atherosclerotic plaque rupture, platelets can form pathogenic, occlusive thrombi leading to acute ischemic events. Today there are promising results from recently developed antiplatelet agents. However, morbidity and mortality from acute coronary syndromes remain significant despite the administration of combination therapies (aspirin, thienopyridines). Sharing similar mechanisms, platelets may also form a thin monolayer in areas of damaged endothelium contributing to primary hemostasis. For this reason, administration of antiplatelet drugs is often associated with increased bleeding risk. As a result, currently available antiplatelet therapy cannot be characterized as optimal. The precise mechanisms of platelet activation in acute coronary syndromes are still under investigation. The study of basic mechanisms of platelet adhesion, activation and aggregation after atherosclerotic plaque rupture may help to define new targets for their inhibition. In the future, newer antiplatelet agents may offer more comprehensive platelet inhibition without interfering with primary hemostasis, thus offering greater protection with lower hemorrhagic risk.

Vascular risk factors and atherosclerosis are critically involved in dementia development of both vascular and Alzheimer's type. However, the exact mechanisms linking atherosclerosis and the development of Alzheimer's disease (AD) are still unknown. As platelet activation and adhesion on vascular wall is the first step of vascular inflammation and atherosclerosis, it appears tempting to hypothesize that platelets could be the link between vascular risk factors/ atherosclerosis and AD. In recent years, much work has been accomplished to elucidate the role of platelets in AD. The present review will summarize and highlight the latest findings of this research area and provide novel insight and understanding in the association between platelet activation and AD.

Platelet adhesion on vascular wall is the first step following vascular injury. Differential platelet secretion supports angiogenesis and vascular homeostasis. Progenitor cells are pluripotent cells responsible for tissue regeneration and wound healing. Upon ischemia bone marrow-derived progenitor cells are mobilized into peripheral circulation and domiciliate into peripheral organ vasculature and either give birth to a series of cardiovascular cells, including endothelial cells, macrophages, smooth muscle cells, or support in a paracrinic way the angiogenic capacity of local tissue cells. Mobilization, chemotaxis, adhesion, differentiation and interaction with vascular cells are essential steps of progenitor cell-mediated tissue repair. This review summarizes the recent advances in our understanding of platelet function with focus on interaction with progenitor cells and its role in cardiovascular homeostasis. Moreover, the role of platelet microparticles in progenitor cell function is separately addressed. Understanding the mechanisms of platelet interaction with progenitor cells provides us with new insights in the mechanisms of vascular homeostasis and possible new therapeutical targets supporting vascular repair.

Platelets and their activation have a pivotal role in the development of atherosclerotic diseases such as acute myocardial infarction (AMI), stroke and peripheral arterial occlusion. Biomarkers of platelet activation are making inroads into clinical studies and may serve as promising agents upstream to established downstream markers of myocardial necrosis such as troponin and creatin kinase. Targeting the degree of platelet activation assessed by the key collagen receptor of platelet activation, glycoprotein VI (GPVI), may have diagnostic and prognostic value for the assessement of high-risk groups of patients with symptomatic coronary artery disease and ischemic stroke and may be worthwhile to help to facilitate clinical decision-making and to rapidly initiate adequate therapy. The concert of platelet count, platelet activation, platelet aggregation and subsequent inflammation has had a significant impact on the clinical outcome in patients with atherosclerotic diseases. For a therapeutical approach to ameliorate prognosis, the use of antiplatelet treatment in particular in AMI patients with low response to clopidogrel has partly been overcome by novel second antiplatelet drugs on top of aspirin such as prasugrel and ticagrelor. Antiplatelet therapy may be adapted according to a GPVI-based platelet activity monitoring along with aggregometry of residual platelet aggregation. Other approaches using protease-activated receptor- 1 antagonists vorapaxar or atopaxar, which inhibit the platelet thrombin receptor, soluble GPVI called Revacept©, which blocks the collagen binding sites at the vascular lesion and anopheline saliva protein derived from the malaria vector mosquito, a platelet adhesion inhibitor independent of a GPVI mechanism, still wait for their breakthrough.