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The Beckman Coulter® DXH900 uses the impedance method to measure the total leukocytes count. In presence of platelet aggregates, the device identifies the structural changes and associates an alarm with the leukocytes result. The aim of this study was to evaluate the influence of platelet aggregates using the principle of flow cytometry as a second assessment of the white blood cell count. Total leukocytes count was evaluated in 49 specimens with presence of platelet aggregates and 32 without anomaly. The differences between total leukocyte count by the two automatic methods (impedance and flow cytometry) and the microscopic method were compared. Without platelet aggregates, the median values were 5.6 (microscopic cell count), 5.4 (impedance) and 5.4 (flow cytometry) and no discordance was observed. In presence of platelet aggregates, the median values were 5.6, 6.4 and 5.1 respectively. The graphical analysis with the allowable total error range of ± 25.7% showed substantial analytical discrepancies (15/49) using impedance method while the flow cytometry method revealed minor disagreements (3/49). Analytical discordances versus WBC reference ranges showed 88% agreement and a substantial Kappa coefficient of 0.70 by impedance, while the flow cytometry method had 94% agreement and a perfect Kappa coefficient of 0.83. The formation of platelet aggregates increased the total leukocyte count performed DXH900 impedance method. Our study has shown that DXH 900 flow cytometry method may be an alternative to exclude the presence of pseudoleukocytosis. In case flags are generated, the microscopic method may be needed for the confirmation of WBC count. [ABSTRACT FROM AUTHOR]

COVID-19 is characterised by a broad spectrum of clinical and pathological features. Natural killer (NK) cells play an important role in innate immune responses to viral infections. Here, we analysed the phenotype and activity of NK cells in the blood of COVID-19 patients using flow cytometry, single-cell RNA-sequencing (scRNA-seq), and a cytotoxic killing assay. In the plasma of patients, we quantified the main cytokines and chemokines. Our cohort comprises COVID-19 patients hospitalised in a low-care ward unit (WARD), patients with severe COVID-19 disease symptoms hospitalised in intensive care units (ICU), and post-COVID-19 patients, who were discharged from hospital six weeks earlier. NK cells from hospitalised COVID-19 patients displayed an activated phenotype with substantial differences between WARD and ICU patients and the timing when samples were taken post-onset of symptoms. While NK cells from COVID-19 patients at an early stage of infection showed increased expression of the cytotoxic molecules perforin and granzyme A and B, NK cells from patients at later stages of COVID-19 presented enhanced levels of IFN-γ and TNF-α which were measured ex vivo in the absence of usual in vitro stimulation. These activated NK cells were phenotyped as CD49a+CD69a+CD107a+ cells, and their emergence in patients correlated to the number of neutrophils, and plasma IL-15, a key cytokine in NK cell activation. Despite lower amounts of cytotoxic molecules in NK cells of patients with severe symptoms, majority of COVID-19 patients displayed a normal cytotoxic killing of Raji tumour target cells. In vitro stimulation of patients blood cells by IL-12+IL-18 revealed a defective IFN-γ production in NK cells of ICU patients only, indicative of an exhausted phenotype. ScRNA-seq revealed, predominantly in patients with severe COVID-19 disease symptoms, the emergence of an NK cell subset with a platelet gene signature that we identified by flow and imaging cytometry as aggregates of NK cells with CD42a+CD62P+ activated platelets. Post-COVID-19 patients show slow recovery of NK cell frequencies and phenotype. Our study points to substantial changes in NK cell phenotype during COVID-19 disease and forms a basis to explore the contribution of platelet-NK cell aggregates to antiviral immunity against SARS-CoV-2 and disease pathology.

During the last decade, significant progress has been made in understanding thrombus composition and organization in the setting of acute ischemic stroke (AIS). In particular, thrombus organization is now described as highly heterogeneous but with 2 preserved characteristics: the presence of (1) two distinct main types of areas in the core—red blood cell (RBC)-rich and platelet-rich areas in variable proportions in each thrombus—and (2) an external shell surrounding the core composed exclusively of platelet-rich areas. In contrast to RBC-rich areas, platelet-rich areas are highly complex and are mainly responsible for the thrombolysis resistance of these thrombi for the following reasons: the presence of platelet-derived fibrinolysis inhibitors in large amounts, modifications of the fibrin network structure resistant to the tissue plasminogen activator (tPA)-induced fibrinolysis, and the presence of non-fibrin extracellular components, such as von Willebrand factor (vWF) multimers and neutrophil extracellular traps. From these studies, new therapeutic avenues are in development to increase the fibrinolytic efficacy of intravenous (IV) tPA-based therapy or to target non-fibrin thrombus components, such as platelet aggregates, vWF multimers, or the extracellular DNA network.

Platelet clumps present in anticoagulant specimens may generate a falsely decreased platelet count and lead to an incorrect diagnosis. A clear understanding of the ability of a haematology analyser (HA) to detect platelet clumps is important for routine work in the clinical laboratory. Citrate-anticoagulated whole-blood samples were collected from various patients as a negative group. Adenosine diphosphate (ADP)-induced platelet aggregation was performed on those negative samples to mimic platelet-clump-containing (positive) samples. The 'platelet clumps' and 'platelet abnormal' flags generated by the Sysmex XN-10 instrument were used to assess the flagging performance of this HA and demonstrate its flagging features. The complete blood count (CBC) results of paired negative and positive samples were compared to evaluate the impact of platelet clumps on the CBC parameters. A total of 187 samples were eligible for this study. The total accuracy, sensitivity, and specificity of the platelet clumps flag were 0.786, 0.626, and 0.947, respectively. The total accuracy, sensitivity, and specificity of the platelet abnormal flag were 0.631, 0.348, and 0.914, respectively. A separate assessment focusing on the positive samples with low platelet counts showed that the total sensitivities of the platelet clumps and platelet abnormal flags were 0.801 and 1.000, respectively. Platelet clumps may interfere with the leukocyte count and with platelet and erythrocyte indices. Platelet clumps can influence not only platelet indices but also leukocyte and erythrocyte counts. The Sysmex XN-10 instrument is sensitive to positive samples with low platelet counts but insensitive to those with high platelet counts. [ABSTRACT FROM AUTHOR]

Platelet aggregates has been used in surgery for many years. The primary goal of these 'Autologous Preparation' was to aggregate platelets and their growth factors and to convey it to a surgical site, to improve healing only. The latest research work shows that the PRF also can be used for Protection of Graft, neo-angiogenesis, vascularization locally and release of various growth factors apart from healing. Platelet rich fibrin (PRF) is considered as the new generation of platelet concentrate. "Choukroun's PRF" or Leucocyte PRF (L-PRF) is the new development, which was first developed by Choukroun's et al. in 2001 as an 'Autologous biomaterial.' A systematic literature search was performed to identify relevant articles that describes the use of PRF, through PubMed and Scopus databases. The focus of this article is to explore the role of PRF in esthetic facial surgery. [ABSTRACT FROM AUTHOR]

Introduction: An apico-marginal defect is a combined endodontic periodontal lesion that poses a challenge to the healing outcome and therefore often leads to the decreased prognosis of periapical surgery. This systematic review aims to analyze clinical studies and case reports that show evidence of the effect of autologous platelet aggregates on the healing outcome of apico-marginal defects. Materials and Methods: Literature search strategy was performed to find relevant clinical studies and case reports according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses checklist. The question was “healing outcome of apico-marginal defects treated using autologous platelet aggregates.” The review involved a search of electronic databases of Pubmed, Scopus, Ebsco host, as well as manual search. Results: Five relevant literature published between 1990 and June 2019 were selected after thorough analysis and exclusion according to the strict criteria. The included studies were related to clinical and radiographic healing outcome of apico-marginal defects with autologous platelet aggregates. Conclusion: The collected data suggested that autologous platelet aggregates give a favorable healing outcome for the management of apico-marginal defects.

There are two types of fibrinoids within the placenta, fibrin-type and matrix-type. The clinical importance of these fibrinoids is poorly understood. Design: Fibrinoid deposits occurring in normal and complicated pregnancies were studies with H&E stain and CD42b as a marker for platelet aggregates. Results: Fibrin-like fibrinoid was associated with platelet aggregates positive by CD42b immunostaining in the subchorionic and basal plate areas, facing the maternal circulation and intervillous spaces. Matrix-type fibrinoid did not stain with CD42b, and it was found in the intervillous spaces, trophoblastic cysts, intravillous tissue areas, and vascular walls in decidual vasculopathy. Conclusion: Fibrin-type fibrinoid within the intervillous spaces are mostly from maternal circulation and these fibrinoids are likely the result of the laminar flow change at specific anatomic locations, leading to activation of coagulatory cascades. The pathogenesis of matrix-like fibrinoid is unclear. CD42b immunostaining is helpful in differentiation of the types of fibrinoid in difficult cases. [ABSTRACT FROM AUTHOR]

Inflammatory mechanisms are activated, and thrombotic complications occur during the initial months after coronary artery bypass grafting (CABG). Therefore, changes over time of platelet activation and platelet–leukocyte interactions after CABG are of interest. Whole-blood flow cytometry was performed before, and 4–6 days, one month, and three months after elective CABG in 54 men with stable coronary artery disease treated with acetylsalicylic acid (ASA). Single platelets and platelet–leukocyte aggregates (PLAs) among monocytes (P-Mon), neutrophils (P-Neu), and lymphocytes (P-Lym) were studied without and with stimulation by submaximal concentrations of ADP, thrombin, and the thromboxane analog U46619. White blood cell counts were increased during the initial postoperative course, and platelet counts were increased after one month. Platelet P-selectin expression was significantly enhanced at one month when stimulated by thrombin and U46619 and at three months with ADP and thrombin. All PLAs subtypes were increased at one month without stimulation in vitro. P-Mon and P-Neu stimulated by ADP, thrombin, or U46619 were significantly increased one month after the operation but decreased compared to baseline at three months. Agonist stimulated P-Lyms were increased at one month and remained increased at three months after ADP stimulation. There was significant platelet activation and formation of PLAs unstimulated and after agonist stimulation by ADP, thrombin, and a thromboxane analog after CABG in patients with stable coronary artery disease irrespective of ASA treatment. Changes observed up to three months after CABG support further studies of the clinical implications of protracted increases in platelet activation and platelet–leukocyte interactions.

Inflammatory mechanisms are activated, and thrombotic complications occur during the initial months after coronary artery bypass grafting (CABG). Therefore, changes over time of platelet activation and platelet–leukocyte interactions after CABG are of interest. Whole-blood flow cytometry was performed before, and 4–6 days, one month, and three months after elective CABG in 54 men with stable coronary artery disease treated with acetylsalicylic acid (ASA). Single platelets and platelet–leukocyte aggregates (PLAs) among monocytes (P-Mon), neutrophils (P-Neu), and lymphocytes (P-Lym) were studied without and with stimulation by submaximal concentrations of ADP, thrombin, and the thromboxane analog U46619. White blood cell counts were increased during the initial postoperative course, and platelet counts were increased after one month. Platelet P-selectin expression was significantly enhanced at one month when stimulated by thrombin and U46619 and at three months with ADP and thrombin. All PLAs subtypes were increased at one month without stimulation in vitro. P-Mon and P-Neu stimulated by ADP, thrombin, or U46619 were significantly increased one month after the operation but decreased compared to baseline at three months. Agonist stimulated P-Lyms were increased at one month and remained increased at three months after ADP stimulation. There was significant platelet activation and formation of PLAs unstimulated and after agonist stimulation by ADP, thrombin, and a thromboxane analog after CABG in patients with stable coronary artery disease irrespective of ASA treatment. Changes observed up to three months after CABG support further studies of the clinical implications of protracted increases in platelet activation and platelet–leukocyte interactions. [ABSTRACT FROM AUTHOR]

Background: Severe COVID-19 is associated with an excessive immunothrombotic response and thromboinflammatory complications. Vaccinations effectively reduce the risk of severe clinical outcomes in patients with COVID-19, but their impact on platelet activation and immunothrombosis during breakthrough infections is not known., Objectives: To investigate how preemptive vaccinations modify the platelet-immune crosstalk during COVID-19 infections., Methods: Cross-sectional flow cytometry study of the phenotype and interactions of platelets circulating in vaccinated ( n  = 21) and unvaccinated patients with COVID-19, either admitted to the intensive care unit (ICU, n  = 36) or not (non-ICU, n  = 38), in comparison to matched SARS-CoV-2-negative patients ( n  = 48), was performed., Results: In the circulation of unvaccinated non-ICU patients with COVID-19, we detected hyperactive and hyperresponsive platelets and platelet aggregates with adaptive and innate immune cells. In unvaccinated ICU patients with COVID-19, most of whom had severe acute respiratory distress syndrome, platelets had high P-selectin and phosphatidylserine exposure but low capacity to activate integrin αIIbβ3, dysfunctional mitochondria, and reduced surface glycoproteins. In addition, in the circulation of ICU patients, we detected microthrombi and platelet aggregates with innate, but not with adaptive, immune cells. In vaccinated patients with COVID-19, who had no acute respiratory distress syndrome, platelets had surface receptor levels comparable to those in controls and did not form microthrombi or platelet-granulocyte aggregates but aggregated avidly with adaptive immune cells., Conclusion: Our study provides evidence that vaccinated patients with COVID-19 are not associated with platelet hyperactivation and are characterized by platelet-leukocyte aggregates that foster immune protection but not excessive immunothrombosis. These findings advocate for the importance of vaccination in preventing severe COVID-19., (© 2023 The Author(s).)

Background Diverse variables are involved in apheresis platelet collection, processing and storage. This survey shows how these are realized in Spain. Method An analysis of collected data was performed in a questionnaire completed by ten Transfusion Centers (TC) which perform between 50 and 520 apheresis procedures per month. This information comprises the procedures used to collect, inspect and store apheresis platelet concentrates (PC), and quality control data. Results Macroscopic inspection of PC is performed in all TC, especially during the first few hours post-collection and before distribution. The type of processor, duration of post-collection resting periods and temperature from the time of collection until distribution are similar in all TC. In 80% of TC, PC with small and scarce aggregates are distributed to transfusion services. The presence of clumps is influenced by type of processor, female donor, cold ambient temperature and collection of hyperconcentrated platelets, and is often recurrent in the same donor, although some TC have not found any influential variables. Overall, no objective inspection methods are followed, although there are exceptions. The degree of compliance with quality control parameters, such as the number of units studied, mean platelet yield, residual leukocyte counts and pH at expiry date, is acceptable in all TC. Compliance in terms of number of microbiological culture samples is variable. Discussion The usual practice in Spanish TC with respect to the collection, post-collection handling and storage of apheresis PC can be considered uniform, although some specific aspects of analyses should follow more objective methods. [ABSTRACT FROM AUTHOR]

Objectives: to determine the association between organic alteration and pathological morphological findings in peripheral blood smears of patients with preeclampsia-eclampsia syndrome. Methods: It is framed in a quantitative, descriptive and transversal approach, which shows 54 patients from a study population of 137 patients admitted with diagnosis of preeclampsia at the Hospital Materno Infantil German Urquidi, between May and December Of 2016. It is consisted of a documented review through a checklist of the clinicallaboratory alterations of each one of the patients; as the microscopic visualization of the spread of peripheral blood smear in search of schistocytes, equinocytes and platelet aggregates, it was performed in a laboratory authorized by SEDES. Results: of 54 patients, 85% presented schistocytes, equinocytes and platelet aggregates, considered as a positive result; the remaining 15% did not present any of these alterations considering as a negative result. Taking these results and comparing with the clinical-laboratory alterations in this study group, it was possible to determine that there is an association between positive smear and organic alteration; The odds ratio (OR) being 66; Translated in probabilities is equal to 98.5% risk of organic alteration with a positive peripheral blood smear (Table 1). Conclusions: The search for schistocytes, equinocytes and platelet aggregates in smears of peripheral blood is a simple, economical and fast method to perform; which shows the probability of developing some organic alteration when the smear of peripheral blood is positive; thus anticipating the exacerbation of clinical and biochemical manifestations in patients with preeclampsia. [ABSTRACT FROM AUTHOR]

Type 2B von Willebrand disease (VWD) is frequently associated with distinct platelet morphology. Here we present a familial case of type 2B VWD with a novel VWF mutation (p.R1308S), which caused neonatal thrombocytopenia. The mother had been treated for refractory immune thrombocytopenia (ITP) for more than 20 years. The most important hematological features of this case were large platelets and platelet aggregates detected on peripheral blood smears. Hemostatic tests showed enhanced ristocetin-induced platelet agglutination at low-ristocetin concentrations, absence of high-molecular weight von Willebrand factor (VWF) multimers, and low VWF cofactor activity/antigen ratio. In patients with intractable ITP, family history of ITP and consecutive neonatal thrombocytopenia, the differential diagnosis of congenital thrombocytopenia is mandatory. For this purpose, the identification of large platelets and platelet aggregates on peripheral blood smears is the key aspect of type 2B VWD diagnosis. [ABSTRACT FROM AUTHOR]

Pathogen reduction technology (PRT) is associated with increased blood safety through the inactivation of virus, bacteria and parasites. Dilution of platelet (PLT) concentrates in platelet additive solution (PAS) is a requirement for applying PRT, and that it is associated with various practical issues: increasing PLT target yields to compensate for loss of PLTs through PRT, extended apheresis donation time due to PAS addition at the end of the procedure, and the appearance of PLT aggregates. We proposed to program higher target PLT yields for plateletpheresis donations to compensate for PLTs lost due to PRT processing. To verify the feasibility of this approach, a paired study of the Amicus 3.11 and Trima 5.22 apheresis separators was performed using 196 procedures carried out on the same 98 donors. The Amicus 3.11 presented a higher collection efficiency (CE: 78.02 vs. 69.63; p < 0.0001) and collection rate (CR: 8.3 vs. 7.00; p < 0.0001); it was also faster (56.92 vs. 62.60; p < 0.0001) than the Trima 5.22 apheresis device. However, analysis of the donor group with higher pre-procedure PLT counts showed similar productivity results for the Amicus and Trima. The percentage of PLT aggregates detected was higher with the TA than the AM (8.62% vs. 3.88%, p = 0.04). Overall, both separators are entirely suitable for collecting hyper-concentrated PLTs that are subsequently diluted in PAS for PRT, without excessively increasing the donation time. PLT aggregation can occur after apheresis collection but most of them disappear by day 1. Further investigation is needed to study the clinical impact of PLT aggregation. [ABSTRACT FROM AUTHOR]

COVID-19 is characterised by a broad spectrum of clinical and pathological features. Natural killer (NK) cells play an important role in innate immune responses to viral infections. Here, we analysed the phenotype and activity of NK cells in the blood of COVID-19 patients using flow cytometry, single-cell RNA-sequencing (scRNA-seq), and a cytotoxic killing assay. In the plasma of patients, we quantified the main cytokines and chemokines. Our cohort comprises COVID-19 patients hospitalised in a low-care ward unit (WARD), patients with severe COVID-19 disease symptoms hospitalised in intensive care units (ICU), and post-COVID-19 patients, who were discharged from hospital six weeks earlier. NK cells from hospitalised COVID-19 patients displayed an activated phenotype with substantial differences between WARD and ICU patients and the timing when samples were taken post-onset of symptoms. While NK cells from COVID-19 patients at an early stage of infection showed increased expression of the cytotoxic molecules perforin and granzyme A and B, NK cells from patients at later stages of COVID-19 presented enhanced levels of IFN-γ and TNF-α which were measured ex vivo in the absence of usual in vitro stimulation. These activated NK cells were phenotyped as CD49a + CD69a + CD107a + cells, and their emergence in patients correlated to the number of neutrophils, and plasma IL-15, a key cytokine in NK cell activation. Despite lower amounts of cytotoxic molecules in NK cells of patients with severe symptoms, majority of COVID-19 patients displayed a normal cytotoxic killing of Raji tumour target cells. In vitro stimulation of patients blood cells by IL-12+IL-18 revealed a defective IFN-γ production in NK cells of ICU patients only, indicative of an exhausted phenotype. ScRNA-seq revealed, predominantly in patients with severe COVID-19 disease symptoms, the emergence of an NK cell subset with a platelet gene signature that we identified by flow and imaging cytometry as aggregates of NK cells with CD42a + CD62P + activated platelets. Post-COVID-19 patients show slow recovery of NK cell frequencies and phenotype. Our study points to substantial changes in NK cell phenotype during COVID-19 disease and forms a basis to explore the contribution of platelet-NK cell aggregates to antiviral immunity against SARS-CoV-2 and disease pathology., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Malengier-Devlies, Filtjens, Ahmadzadeh, Boeckx, Vandenhaute, De Visscher, Bernaerts, Mitera, Jacobs, Vanderbeke, Van Mol, Van Herck, Hermans, Meersseman, Wilmer, Gouwy, Garg, Humblet-Baron, De Smet, Martinod, Wauters, Proost, Wouters, Leclercq, Lambrechts, Wauters and Matthys.)

The article presents a letter to the editor in response to a study which compared the performance of the low platelet count by two detection methods, the impedance method and the optical method, between a novel hematological analyzer Mindray and the used Sysmex XE-2100 analyzer.

Endothelial cells that cover the lumen of all blood vessels have the inherent capacity to express both pro and anticoagulant molecules. However, under normal physiological condition, they generally function to maintain a non-thrombogenic surface for unobstructed blood flow. In response to injury, certain stimuli, or as a result of dysfunction, endothelial cells release a highly adhesive procoagulant protein, von Willebrand factor (VWF), which plays a central role in formation of platelet aggregates and thrombus generation. Since VWF expression is highly restricted to endothelial cells, regulation of its levels is among the most important functions of endothelial cells for maintaining hemostasis. However, with aging, there is a significant increase in VWF levels, which is concomitant with a significant rise in thrombotic events. It is not yet clear why and how aging results in increased VWF levels. In this review, we have aimed to discuss the age-related increase in VWF, its potential mechanisms, and associated coagulopathies as probable consequences. [ABSTRACT FROM AUTHOR]

Platelets are essential mediators of inflammation and thrombosis. Chronic obstructive pulmonary disease (COPD) is a heterogeneous multisystem disease, causing significant morbidity and mortality worldwide. Recent evidence suggests that the lung is an important organ for platelet biogenesis. Cigarette smoking has been shown to induce platelet aggregation and decrease the capacity of mitochondrial electron transport system in platelets. Preclinical and clinical studies have suggested that platelets may contribute to the development of COPD through the breakdown of lung elastin by platelet factor 4, platelet activation and formation of platelet aggregates, and modulation of hypoxia signaling pathways. Recent large population studies have produced encouraging results indicating a potential role for aspirin in preventing exacerbations and delaying disease progression in patients with COPD. This review summarizes the information about the lung as an organ for platelet production, pathophysiological functions of platelets and platelet mediators in the development of COPD, and the most updated evidence on the utility of aspirin in patients with COPD., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Although antiplatelet drugs are widely used for the prevention and treatment of atherothrombosis, clinical tests capable of evaluating their efficacy have not been established. Focusing on platelet aggregates in blood, we announced the world's first basic technology, an intelligent Image-Activated Cell Sorter (iIACS), that can exhaustively and rapidly identify cells one-by-one using image analysis with high-speed imaging and deep learning to sort specific cells according to the analysis results. This technology has even enabled the detection of single platelets with a size of 2 µm in blood samples and the quantification of the proportion of platelet aggregates by size. Furthermore, by applying this technique, we discovered different morphological features of platelet aggregates formed by different types of agonists that activate platelets. Here, we discuss this application in the early diagnosis of thrombotic microangiopathy (TMA). In the early stage of TMA, consumptive thrombocytopenia is caused by excessive platelet activation. Therefore, the detection of excessive platelet aggregates can lead to early TMA diagnosis.

Hyperglycemia alone may not explain the increased risk of cardiovascular diseases (CVDs) in patients with type 1 diabetes (T1D) compared with type 2. This study emphases on the evaluation of some platelet activity markers in patients with T1D, with relevance to some metabolic disorders as hyperlipidemia and hyperglycemia. This study was performed on 35 patients with T1D and 20 healthy controls. All participants were subjected to full history taking, clinical examination and assay of glycated hemoglobin (HbA1c), and lipid profile. The expression of CD62P and CD36 on platelets and the frequency of platelet–monocyte, and platelet–neutrophil aggregates were assessed by flow cytometry. Patients showed significantly higher expression of CD62P and CD36 than the control group. Platelets aggregates with monocytes were also higher among patients than the control group. Levels of CD36+ platelets, CD62P+ platelets, and platelet–monocyte aggregates revealed significant correlations with the levels of HbA1c, total cholesterol, low-density lipoprotein, and triglycerides. Hyperlipidemia and hyperglycemia accompanying T1D have a stimulatory effect on platelet activation which probably makes those patients vulnerable to CVD than nondiabetics. [ABSTRACT FROM AUTHOR]