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      Differences in thrombus structure and kinetics in patients with type 2 diabetes mellitus after non ST elevation acute coronary syndrome

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          Abstract

          Introduction

          Despite optimal secondary prevention therapy following non-ST elevation acute coronary syndrome (NSTE-ACS), recurrent thrombotic events are more frequent in patients with type 2 diabetes mellitus (T2DM).

          Materials and Methods

          This exploratory study was aimed to evaluate quantitative and qualitative aspects of thrombus. In 28 patients with and without T2DM treated with aspirin and clopidogrel we assessed thrombus quantity using an ex-vivo chamber, platelet reactivity, thrombus ultrastructure and thrombus kinetics one week after NSTE-ACS.

          Results

          T2DM was associated with increased thrombus [14861 (8003 to 30161) vs 8908 (6812 to 11996), μ 2/mm, median (IQR), p = 0.045] and platelet reactivity. In addition, diabetic thrombus showed lower visco-elastic tensile strength [(− 0.2(− 1.7 to 0.7) vs 1.0(− 0.9 to 3.3), p = 0.044)] and was more resistant to autolysis [(27.8(11.7 to 70.7) vs 78.8(68.5 to109.6) mm/min, p = 0.002)]. On SEM, fibrin fibres in diabetes were thinner, with higher lateral interlinkage and mesh-like organisation. Thrombus quantity correlated inversely with thrombus retraction (r = − 0.450 p = 0.016) but not with platelet reactivity (r = 0.153, p = 0.544).

          Conclusions

          Despite optimal antiplatelet therapy, T2DM patients after NSTE-ACS developed increased thrombus of lower tensile strength and slower retraction. SEM revealed loosely arranged fibrin fibres. Our data showed significant differences in the magnitude as well as structural and mechanistic characteristics of thrombus in patients with T2DM.

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          Most cited references29

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          ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine.

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            Bedside monitoring to adjust antiplatelet therapy for coronary stenting.

            Patients' responses to oral antiplatelet therapy are subject to variation. Bedside monitoring offers the opportunity to improve outcomes after coronary stenting by individualizing therapy. We randomly assigned 2440 patients scheduled for coronary stenting at 38 centers to a strategy of platelet-function monitoring, with drug adjustment in patients who had a poor response to antiplatelet therapy, or to a conventional strategy without monitoring and drug adjustment. The primary end point was the composite of death, myocardial infarction, stent thrombosis, stroke, or urgent revascularization 1 year after stent implantation. For patients in the monitoring group, the VerifyNow P2Y12 and aspirin point-of-care assays were used in the catheterization laboratory before stent implantation and in the outpatient clinic 2 to 4 weeks later. In the monitoring group, high platelet reactivity in patients taking clopidogrel (34.5% of patients) or aspirin (7.6%) led to the administration of an additional bolus of clopidogrel, prasugrel, or aspirin along with glycoprotein IIb/IIIa inhibitors during the procedure. The primary end point occurred in 34.6% of the patients in the monitoring group, as compared with 31.1% of those in the conventional-treatment group (hazard ratio, 1.13; 95% confidence interval [CI], 0.98 to 1.29; P=0.10). The main secondary end point, stent thrombosis or any urgent revascularization, occurred in 4.9% of the patients in the monitoring group and 4.6% of those in the conventional-treatment group (hazard ratio, 1.06; 95% CI, 0.74 to 1.52; P=0.77). The rate of major bleeding events did not differ significantly between groups. This study showed no significant improvements in clinical outcomes with platelet-function monitoring and treatment adjustment for coronary stenting, as compared with standard antiplatelet therapy without monitoring. (Funded by Allies in Cardiovascular Trials Initiatives and Organized Networks and others; ARCTIC ClinicalTrials.gov number, NCT00827411.).
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              Increasing cardiovascular disease burden due to diabetes mellitus: the Framingham Heart Study.

              Marked reductions in cardiovascular disease (CVD) morbidity and mortality have occurred in the United States over the last 50 years. We tested the hypothesis that the relative burden of CVD attributable to diabetes mellitus (DM) has increased over the past 5 decades. Participants aged 45 to 64 years from the Framingham Heart Study, who attended examinations in an "early" time period (1952 to 1974), were compared with those who attended examinations in a later time period (1975 to 1998). The risk of CVD events (n=133 among those with and 1093 among those without DM) attributable to DM in the 2 time periods was assessed with Cox proportional hazards models; population attributable risk of DM as a CVD risk factor was calculated for each time period. The age- and sex-adjusted hazard ratio for DM as a CVD risk factor was 3.0 (95% CI, 2.3 to 3.9) in the earlier time period and 2.5 (95% CI, 1.9 to 3.2) in the later time period. The population attributable risk for DM as a CVD risk factor increased from 5.4% (95% CI, 3.8% to 6.9%) in the earlier time period to 8.7% (95% CI, 5.9% to 11.4%) in the later time period (P for attributable risk ratio=0.04), although multivariable adjustment resulted in attenuation of these findings (P=0.12); most of these observations were found among men. The proportion of CVD attributable to DM has increased over the past 50 years in Framingham. These findings emphasize the need for increased efforts to prevent DM and to aggressively treat and control CVD risk factors among those with DM.
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                Author and article information

                Contributors
                Journal
                Thromb Res Suppl
                Thromb. Res. Suppl
                Thrombosis Research. Supplement
                Pergamon Press
                0049-3848
                1 May 2014
                May 2014
                : 133
                : 5
                : 880-885
                Affiliations
                [a ]Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK
                [b ]The Mount Sinai School of Medicine, NY, USA
                [c ]Freeman Hospital, Newcastle upon Tyne, UK
                Author notes
                [* ]Corresponding author at: Freeman Hospital, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK NE7 7DN. Tel.: + 44 191 213 7277; fax: + 44 191 223 1417. Azfar.zaman@ 123456nuth.nhs.uk
                [1]

                Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK NE2 4HH. Tel.: + 44 191 282 4210; fax: + 44 191 282 0064.

                [2]

                Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK, NE2 4HH. Tel.: + 44 191 222 7880.

                [3]

                Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK, NE2 4HH. Tel.: + 44 191 282 4210.

                [4]

                Cardiovascular Institute, The Mount Sinai School of Medicine, Atran Berg Laboratory Building, Floor 6, Room 20, 1428 Madison Avenue, New York, NY USA, 10029. Tel.: + 1 212 241 6500.

                Article
                S0049-3848(14)00057-7
                10.1016/j.thromres.2014.01.033
                4018991
                24582462
                dc3020d0-9323-4a7f-9fa3-88f3fe004cb8
                © 2014 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/).

                History
                : 16 October 2013
                : 27 December 2013
                : 27 January 2014
                Categories
                Regular Article

                Hematology
                aru, aspirin reactivity index,ci, clot index,hdl, high density lipoprotein,hotr, high on treatment platelet reactivity,ldl, low density lipoprotein,l parameter, thrombus lysis parameter,nste-acs, non st elevation acute coronary syndrome,pru, platelet reactivity index,sem, scanning electron microscopy,t2dm, type 2 diabetes mellitus,teg, thromboelastography,whole blood thrombus,type 2 diabetes mellitus,non st elevation acute coronary syndrome,thrombus kinetics,antiplatelet therapy,fibrin structure

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