Filtered platelet concentrates from pooled buffy coats show comparable storage lesions when stored for 9 d at 20-24 degrees C or when supplemented with thromboSol at 2-6 degrees C

The present study investigated the quality of platelet concentrates from pooled buffy coat (PCBC) along different production steps and during storage to characterize storage lesions reflected by platelet activation, changing metabolic and cell turnover status (pH, LDH activity). These criteria were compared in conventionally stored PCBCs (20-24 degrees C, n = 8, Group I) to cold stored PCBCs (2-6 degrees C, n = 8, Group II) when supplemented with ThromboSol. Platelet activation was measured on days 1, 3, 7 and 9 by flow cytometry using fluoresceinisothiocyanate-labeled monoclonal antibodies (mAbs) against glycoprotein IIb/IIIa (CD41a, PAC-1 and LIBS-1), P-selectin (CD62P) or CD40 ligand receptor (CD40L) in combination with a phycoerythrin-labeled panspecific platelet marker against GPIb (CD42b). The platelet activation assessed with mAbs PAC-1, CD41a, LIBS-1 and CD40L showed an overall activation of 98 +/- 4% (mean value +/- 1 SD) at day 7 in both groups, except for CD62P, which was significantly lower in Group II. A storage-dependent greater platelet loss occurred in Group II compared to Group I, 42% vs. 19% (p < 0.05 on day 9). We could demonstrate that platelets stored in ThromboSol show about the same in-vitro activation as conventionally stored PCBCs, but their clinical usefulness needs to be investigated.     

Pharmacodynamic comparison of low-dose ticagrelor to low-dose prasugrel in patients with prior myocardial infarction: the ALTIC-2 study

Abstract

Given that patients with prior myocardial infarction and features of high ischemic and low bleeding risk may benefit by extending dual antiplatelet therapy beyond 1 year, we aimed of assessing platelet reactivity provided by ticagrelor 60 mg bid versus prasugrel 5 mg od in 20 such patients participating in a randomized, crossover study. The primary end point of platelet reactivity at the end of the two treatment periods (by VerifyNow, in PRU) was significantly lower for ticagrelor (31.9 PRU [95% CI 12.3–51.4]) compared with prasugrel (132.1 PRU [111.9–152.3]) with a least squares mean difference of –100.2 PRU (72.1–128.3, P < .001). This dedicated pharmacodynamic study showed that in post-myocardial infarction patients with high atherothrombotic risk and receiving P2Y₁₂ receptor antagonist beyond 1 year, low-dose ticagrelor results in a significantly lower platelet reactivity compared to low-dose prasugrel.     

Thrombosis formation on atherosclerotic lesions and plaque rupture

Atherosclerosis is a silent chronic vascular pathology that is the cause of the majority of cardiovascular ischaemic events. The evolution of vascular disease involves a combination of endothelial dysfunction, extensive lipid deposition in the intima, exacerbated innate and adaptive immune responses, proliferation of vascular smooth muscle cells and remodelling of the extracellular matrix, resulting in the formation of an atherosclerotic plaque. High‐risk plaques have a large acellular lipid‐rich necrotic core with an overlying thin fibrous cap infiltrated by inflammatory cells and diffuse calcification. The formation of new fragile and leaky vessels that invade the expanding intima contributes to enlarge the necrotic core increasing the vulnerability of the plaque. In addition, biomechanical, haemodynamic and physical factors contribute to plaque destabilization. Upon erosion or rupture, these high‐risk lipid‐rich vulnerable plaques expose vascular structures or necrotic core components to the circulation, which causes the activation of tissue factor and the subsequent formation of a fibrin monolayer (coagulation cascade) and, concomitantly, the recruitment of circulating platelets and inflammatory cells. The interaction between exposed atherosclerotic plaque components, platelet receptors and coagulation factors eventually leads to platelet activation, aggregation and the subsequent formation of a superimposed thrombus (i.e. atherothrombosis) which may compromise the arterial lumen leading to the presentation of acute ischaemic syndromes. In this review, we will describe the progression of the atherosclerotic lesion along with the main morphological characteristics that predispose to plaque rupture, and discuss the multifaceted mechanisms that drive platelet activation and subsequent thrombus formation. Finally, we will consider the current scientific challenges and future research directions.     

Practical guidance for the management of adults with immune thrombocytopenia during the COVID-19 pandemic

This document aims to provide practical guidance for the assessment and management of patients with thrombocytopenia, with a particular focus on immune thrombocytopenia (ITP), during the COVID-19 pandemic. The intention is to support clinicians and, although recommendations have been provided, it is not a formal guideline. Nor is there sufficient evidence base to conclude that alternative approaches to treatment are incorrect. Instead, it is a consensus written by clinicians with an interest in ITP or coagulation disorders and reviewed by members of the UK ITP forum.     

Hemostatic laboratory derangements in COVID-19 with a focus on platelet count

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the coronavirus disease in 2019 (COVID-19) which rapidly evolved from an outbreak in Wuhan, China into a pandemic that has resulted in over millions of infections and over hundreds of thousands of mortalities worldwide. Various coagulopathies have been reported in association with COVID-19, including disseminated intravascular coagulation (DIC), sepsis-induced coagulopathy (SIC), local microthrombi, venous thromboembolism (VTE), arterial thrombotic complications, and thrombo-inflammation. There is a plethora of publications and conflicting data on hematological and hemostatic derangements in COVID-19 with some data suggesting the link to disease progress, severity and/or mortality. There is also growing evidence of potentially useful clinical biomarkers to predict COVID-19 progression and disease outcomes. Of those, a link between thrombocytopenia and COVID-19 severity or mortality was suggested. In this opinion report, we examine the published evidence of hematological and hemostatic laboratory derangements in COVID-19 and the interrelated SARS-CoV-2 induced inflammation, with a focussed discussion on platelet count alterations. We explore whether thrombocytopenia could be a potential disease biomarker and we provide recommendations for future studies in this regard.     

超声弹性成像在下肢深静脉血栓形成分期中的应用价值

目的 探讨超声弹性成像在下肢深静脉血栓形成分期中的应用价值。方法 选取我院110例下肢深静脉血栓患者,其中急性期43例、亚急性期37例、慢性期30例。应用超声弹性成像获取弹性成像评分及杨氏模量平均值（Emean）,比较急性期、亚急性期、慢性期下肢深静脉血栓形成患者弹性成像评分、Emean及实验室指标的差异;分析弹性成像评分、Emean与实验室指标的相关性。应用Logistic回归分析下肢深静脉血栓形成分期的影响因素;绘制受试者工作特征（ROC）曲线分析弹性成像评分联合Emean对下肢深静脉血栓形成急性期的诊断效能。结果 急性期下肢深静脉血栓形成患者弹性成像评分、Emean均减低,活化部分凝血活酶时间（aPTT）、凝血酶原时间（PT）、纤维蛋白原（Fbg）均增高,与亚急性期、慢性期血栓形成患者比较差异均有统计学意义（均P<0.05）。相关性分析显示,弹性成像评分、Emean与aPTT、PT、Fbg均呈负相关（均P<0.05）。Logistic回归分析显示,弹性成像评分、Emean均为下肢深静脉血栓形成分期的独立影响因素（OR=2.136,1.201,均P<0.05）。R...