Platelets were traditionally considered to purely have a role in the maintenance of haemostasis. Recently their role in vasomotor function, inflammation and atherosclerosis has been very well-recognized. Endothelium which was originally considered as a simple passive barrier, it is now viewed as an organ whose normal functioning is crucial for maintaining vascular health. When endothelial balance is disturbed, vascular disease initiates. Platelet interactions with endothelium have an important contribution in this process. Lowgrade inflammation, endothelial dysfunction, and platelet hyper-reactivity are all independently associated with an increased risk of cardiovascular events. Older antiplatelet agents like aspirin and clopidogrel and newer more potent agents like prasugrel and ticagrelor have been proven effective in all the clinical spectrum of coronary artery disease patients. Current antiplatelet medications and especially newer generation P2Y12 inhibitor ticagrelor, offer clinical benefits not only due to their well-recognized antithrombotic effect, but also via the attenuation of platelet inflammatory action, impediment of P2Y12 activation effects in other cells and through other complex and sometimes undefined pathways. Future research is expected to better define platelet-endothelium interactions and the multiple impact of current antiplatelet therapy on them.

No abstract

No abstract

Aims Endothelial progenitor cells (EPCs) are bone marrow‐derived cells that are mobilized into the circulation to migrate and differentiate into mature endothelial cells contributing to post‐natal physiological and pathological neovascularization. In this study, we evaluated circulating EPCs in patients with hypertrophic cardiomyopathy (HCM) and examined a potential association with clinical parameters of the disease. Methods and results We included 40 HCM patients and 23 healthy individuals. Using flow cytometry we measured EPCs in peripheral blood as two subpopulations of CD45–/CD34+/VEGFR2+ and CD45–/CD34+/CD133+ cells. Circulating CD45–/CD34+/VEGFR2+ cells were significantly increased in HCM patients in comparison with the controls (0.000238 ± 0.0003136 vs. 0.000057 ± 0.0001316, respectively, P = 0.002). However, there was no significant difference in the number of circulating CD45–/CD34+/CD133+ cells (0.003079 ± 0.0033288 vs. 0.002065 ± 0.0022173, respectively, P = 0.153). The CD45–/CD34+/VEGFR2+ subpopulation revealed a moderate correlation with LV mass index (r = 0.35, P = 0.026), while both EPC subpopulation levels showed strong positive correlations with th E/e' ratio (r = 0.423, P = 0.007 for CD45–/CD34+/VEGFR2+ and r = 0.572, P < 0.001 for CD45–/CD34+/CD133+). Conclusion HCM patients showed an increased mobilization of EPCs compared with healthy individuals that correlated with diastolic dysfunction. Our findings may open up new dimensions in the pathophysiology, prognostication, and treatment of HCM.

In 'real-life' ACS undergoing PCI, diabetic patients have higher - although not significantly - MACE rate and no difference in bleeding events. This difference in MACE was significant among clopidogrel-treated patients, whereas when newer antiplatelet agents were used the negative impact of DM on ischemic events was eliminated.