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Declaration of interest: The GREACE study was conducted independently; no Company or Institution has supported it financially. Some of the authors have attended conferences and participated in other trials sponsored by various pharmaceutical companies.We assessed the possible ‘synergy’ of statins and aspirin (ASA) in reducing vascular events in patients with coronary heart disease, in a post hoc analysis of the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study. All patients (n?=?1600) were divided into four groups according to long-term treatment: Group A (n?=?787; statin?+?ASA), B (n?=?93; statin?-?no ASA), C (n?=?599; no statin?-?on ASA) and D (n?=?121; no statin?-?no ASA). From all patients 692 were either on a statin or ASA monotherapy (Groups B?+?C). Relative risk reductions (RRRs) in ‘all events’ (primary endpoint) between groups were assessed. During the 3-year follow-up there were 292 cardiovascular events; 92 (12% of patients) in Group A, 14 (15%) in group B, 144 in Group C (24%) and 42 events in Group D (35%). The total number of events in Group B?+?C was 158 (23%). The RRRs in the primary endpoint were: Group A versus B 24% (P?=?0.1912), A versus C 51% (P<0.0001), A versus B?+?C 49% (P<0.0001) and A versus D 71% (P<0.0001). The RRRs in Group B versus C was 36% (P?=?0.0431) and B versus D 57% (P?=?0.0012), while in C versus D 33% (P?=?0.0084). Our findings show that statins and ASA have an additive effect in reducing cardiovascular events. Aggressive statin use in the absence of ASA also substantially reduced cardiovascular events. Treatment with ASA in the absence of statin use reduced clinical events in comparison to patients not treated with either drug. [ABSTRACT FROM AUTHOR]

The relationship between lipids and the haemostatic mechanisms participating in the evolution of the atherosclerotic plaque have been undergoing extensive investigation for over a century. Circulating lipoproteins can enhance platelet activity. Among these lipid fractions, lipoprotein (a) (Lp(a)), a predictor of atherosclerotic disease, has been proposed as a link between lipids and haemostasis. In this review, we briefly consider lipid-platelet, and particularly Lp(a)-platelet, interactions which may be relevant to the pathogenesis of atherosclerotic disease and its complications. [ABSTRACT FROM AUTHOR]

Platelets play an important role in the process of atherothrombosis, and antiplatelet therapy is of proven efficacy in the prevention of vascular events in high-risk patients. In this review, we briefly consider the studies reporting that circulating atherogenic lipoproteins enhance platelet activity. We also evaluate the evidence showing that lipid-lowering interventions (including the use of statins) are associated with the normalisation of platelet activity. This beneficial effect should enhance the anti-atherogenic and anti-thrombotic potential of lipid-lowering interventions. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article ‘‘Clinical outcome prediction from mean platelet volume (MPV) in patients under-going percutaneous coronary intervention (PCI) in Korean cohort: Implications of more simple and useful test than platelet function testing'' by Choi et al.

The author discusses the disease type 2 diabetes mellitus (T2DM) and the effects that it has on blood platelet functions. A gist is given about the use of the agent sitagliptin for glycemic control and the use of platelet aggression inhibitors and antihypertensive agent in people suffering from diabetes. The author concludes by suggesting that there is a need for research to find the links between the disease, platelet functions, the medicines used for the treatment and the patient's lifestyle.

Explains the action of aspirin on increasing the sensitivity of blood platelets to adenosine diphosphate used for coronary artery disease patients. Factors attributed to the increased sensitivity.

Two types of ADP receptors, P2Y(1) and P2Y(12) are involved in platelet aggregation. The P2X(1) receptor is also present but its role, in terms of platelet function, is not yet defined. The aim of this study was to establish if the ADP receptors, P2Y(1,) P2Y(12) and P2X(1) play a role in controlling platelet shape change (PSC) in human platelets. PSC is an early phase of platelet activation that precedes aggregation. Using a high-resolution channelyzer, PSC was assessed by measuring the median platelet volume (MPV). The P2Y(1) receptor antagonist MRS 2179 (1.06 - 10.25 micro mol/l) blocked ADP-induced PSC (by 100%). The median IC(50) was 3.16 micro mol/l. MRS 2179 also significantly (P = 0.01) inhibited PSC induced by the combination of ADP + serotonin (5HT). The P2Y(12) receptor antagonist AR-C69931MX significantly inhibited (at 10s, P = 0.009; 15 s, P = 0.001 and 30 s, P = 0.015) ADP-induced PSC. The P2X(1) receptor antagonist TNP-ATP had no significant effect on ADP- or ADP + 5HT-induced PSC. We conclude that the IC(50) of a P2Y(1)-blocker can be derived because of the high-resolution and reproducibility of the channelyzer technique. In addition to the P2Y(1) purinoceptor, the P2Y(12)receptor appears to be involved in ADP-induced PSC since this process was significantly inhibited by AR-C69931MX. The channelyzer technique may be more reliable than optical aggregometry to assess PSC.