Background: Rheumatoid Disease (RD) is associated with ischaemic heart disease (IHD). We sought to investigate whether abnormalities of endothelial function and platelet activation in patients with established RD were related to co-morbid cardiovascular risk factors.
Methods: In a cross-sectional study, RD patients with no cardiac risk factors and normal cardiac function (RD, n=73), those with cardiovascular disease or risk factors and normal cardiac function (RD-risk, n=59), and those with left ventricular systolic dysfunction (RD-LVSD, n=21) were recruited, and compared to healthy controls (HC, n=76). Plasma levels of von Willebrand factor (vWF, an index of endothelial damage/dysfunction), soluble E-selectin (sE-sel, a marker of endothelial activation), and soluble P-selectin (sP-sel, an index of platelet activation) were studied.
Results: Plasma levels of vWF and sP-sel (but not sE-sel) were significantly higher among 153 RD patients compared to controls (p=0.002 and p<0.001, respectively). Levels of vWF progressively rose with increasing cardiovascular risk across the four subgroups (p for trend<0.001). Previous IHD was independently associated with vWF levels, and diabetes mellitus (DM) was similarly associated with all three markers. RD itself and beta-blocker use were associated with sP-sel.
Conclusion: Plasma levels of vWF and sP-sel are higher among RD patients. Levels of vWF were particularly influenced by cardiac risk factor status, and associated with known IHD and DM.
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http://dx.doi.org/10.1016/j.ijcard.2008.01.038 | DOI Listing |
Catheter Cardiovasc Interv
January 2025
Department of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong, People's Republic of China.
Background: Platelet activation plays a central role in the pathogenesis of acute coronary syndrome (ACS). Platelet morphological parameters, including MPV, PDW, and P-LCR, are emerging as biomarkers for predicting the severity of ACS and prognosis.
Aims: This study aims to assess the relationship between these parameters and coronary severity and to evaluate their predicting adverse outcomes.
Proteomics Clin Appl
January 2025
SPHERE Research Group, Conway Institute, University College Dublin, Dublin, Ireland.
Purpose: Multiple Sclerosis is an inflammatory neurodegenerative disease characterised by blood-brain barrier dysfunction and leukocyte infiltration into the CNS. Platelets are best known for their contributions to haemostasis, however, upon activation, platelets release an abundance of soluble and vesicular-associated proteins, termed the platelet releasate (PR). This milieu contains numerous inflammatory and vasoactive proteins, that can attract leukocytes and alter endothelial permeability.
View Article and Find Full Text PDFZh Nevrol Psikhiatr Im S S Korsakova
January 2025
Pirogov City Clinical Hospital No. 1, Moscow, Russia.
Objective: To study the associations of genetic markers influencing the residual reactivity of platelets during antiplatelet therapy with acetylsalicylic acid, and clinical and laboratory parameters, including parameters of the platelet hemostasis, in patients with non-cardioembolic ischemic stroke (IS) for a deeper understanding of the pathogenetic mechanisms and prediction of response to therapy and clinical outcome.
Material And Methods: The study included 296 patients (average age 64.65 [55; 76] years) undergoing treatment at the City Clinical Hospital named after.
ACS Appl Bio Mater
January 2025
Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Beijing 100190, PR China.
Chitosan is generally considered to be a procoagulant effect, which may cause adverse phenomena such as blood clotting when used in small-diameter vascular grafts. However, it also shows good biocompatibility and anti-inflammatory properties, which can facilitate vascular reconstruction. Therefore, it is significant to transition the effect of chitosan from coagulation promotion to antiplatelet while still harnessing its bioactivity.
View Article and Find Full Text PDFGenes Cells
January 2025
Department of Animal Sciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Aichi, Japan.
The dysfunction of the innate immune system is well-described as a clinical characteristic of COVID-19. While several groups have reported human endogenous retroviruses (ERVs) as enhancing factors of immune reactivity, characterization of the COVID-19-specific ERVs has not yet been sufficiently conducted. Here, we revealed the transcriptome profile of more than 500 ERV subfamilies and innate immune response genes in eight different cohorts of platelet, peripheral blood mononuclear cells (PBMCs), lung, frontal cortex of brain, ventral midbrain, pooled human umbilical vein endothelial cells (pHUVECs), placenta, and cardiac microvascular endothelial cells (HCMEC) from COVID-19 patients (total; n = 124) and normal samples (total; n = 53) using publicly available datasets.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!