Background— Smoking is a potent cardiovascular risk factor and is associated with proinflammatory and prothrombotic responses. The CD40/CD40 ligand (CD40L) dyad and platelet-monocyte aggregation mediate a range of proinflammatory and prothrombotic processes thought to be important in atherothrombosis. We investigated whether expression of the CD40/CD40L dyad and platelet-monocyte aggregation are altered in cigarette smokers. Methods and Results— C-reactive protein (CRP), soluble (s) CD40L, and surface expression of CD40L on platelets and T cells and of CD40 on monocytes and platelet-monocyte aggregates were compared in 25 cigarette smokers and 25 age- and gender-matched nonsmokers. Cigarette smokers had increased serum CRP (2.47±2.60 versus 0.94±0.96 mg/L, P =0.008) and appeared to have elevated plasma sCD40L (0.8±1.09 versus 0.37±0.21 ng/mL, P =0.07) concentrations. Smokers also had increased surface expression of CD40 on monocytes (45.9±7.7% versus 39.9±6.5%, P =0.006), of CD40L on platelets (2.9±1.0% versus 2.3±0.6%, P =0.03), and of platelet-monocyte aggregates (26.6±10.9% versus 19.7±8.6%, P =0.02). Plasma cotinine concentrations correlated with monocyte CD40 expression, platelet CD40L expression, and platelet-monocyte aggregates. Conclusions— Cigarette smokers have upregulation of the CD40/CD40L dyad and platelet-monocyte aggregation that may account for the atherothrombotic consequences of this major cardiovascular risk factor.

Background: Diabetes mellitus is a major risk factor for cardiovascular disease and is associated with a proinflammatory and prothrombotic state. We investigated whether CD40 ligand (L) expression and platelet-monocyte aggregation are increased in patients with type 1 diabetes.Methods: Serum C-reactive protein (CRP) and soluble (s) CD40L concentrations, platelet surface CD40L expression and platelet-monocyte aggregates were measured in 22 patients with uncomplicated type 1 diabetes and 22 age- and sex-matched non-diabetic control subjects.Results: In comparison to controls, patients with type 1 diabetes had higher serum CRP concentrations (3.29 +/- 0.9 mg/L versus 0.99 +/- 0.2 mg/L, P = 0.01), serum sCD40L concentrations (10.0 +/- 1.4 ng/mL versus 4.6 +/- 0.6 ng/mL, P = 0.006), and platelet surface expression of CD40L (13.8 +/- 0.9% versus 8.5 +/- 1.1%, P < 0.001). Platelet-monocyte aggregates were also significantly elevated in type 1 diabetes (35.9 +/- 3.3% versus 26.4 +/- 2.9%, P 0.005; n = 10). We also observed a significant correlation between plasma glucose and serum CRP (r = 0.53, P = 0.01) as well as platelet-monocyte aggregates (r = 0.69, P = 0.03).Conclusions: Type 1 diabetes is associated with increased CD40L expression and platelet-monocyte aggregation, which may contribute to the proinflammatory and prothrombotic state as well as the accelerated atherogenesis associated with this disorder. (C) 2004 Elsevier Ireland Ltd. All rights reserved.

Platelet-monocyte binding and surface P-selectin expression are sensitive markers of platelet activation. Endothelium-derived factors are known to inhibit platelet activation and may confer important anti-atherothrombotic effects. We assessed the relationship between platelet activation and endothelium-dependent vasomotion in patients with coronary heart disease (CHD). Twenty male patients with stable CHD were compared with 20 healthy men. Platelet-monocyte binding and platelet surface expression of P-selectin were assessed using two-colour flow cytometry on whole blood. Forearm blood flow was assessed in patients using venous occlusion plethysmography during intra-arterial infusions of substance P, acetylcholine and sodium nitroprusside. Platelet activation was higher in patients than healthy men (platelet-monocyte binding, 27 +/- 3 vs. 20 +/- 1%; P < 0.05). In patients with CHD, there was an inverse correlation between maximal substance P induced vasodilatation and both platelet-monocyte binding (P = 0.003) and P-selectin expression (P = 0.02). A similar correlation was observed between platelet-monocyte binding and the vasomotor response to acetylcholine (P = 0.08) but not with sodium nitroprusside. In patients with stable coronary heart disease, there is a strong inverse relationship between markers of platelet activation and endothelium-dependent vasomotor function. This may explain the pathophysiological mechanism linking endothelial vasomotor dysfunction and the risk of acute atherothrombotic events.

Conference Abstract| March 01 2002 Increased Platelet/Monocyte Binding in Acute Coronary Syndromes: Novel Platelet Interactions in Inflammatory Vascular Injury? J Sarma; J Sarma 1MRC Centre for Inflammation Research & Wellcome Cardiovascular Research Initiative, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG Search for other works by this author on: This Site PubMed Google Scholar A Jha; A Jha 1MRC Centre for Inflammation Research & Wellcome Cardiovascular Research Initiative, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG Search for other works by this author on: This Site PubMed Google Scholar S Alam; S Alam 1MRC Centre for Inflammation Research & Wellcome Cardiovascular Research Initiative, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG Search for other works by this author on: This Site PubMed Google Scholar KA Laan; KA Laan 1MRC Centre for Inflammation Research & Wellcome Cardiovascular Research Initiative, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG Search for other works by this author on: This Site PubMed Google Scholar I Dransfield; I Dransfield 1MRC Centre for Inflammation Research & Wellcome Cardiovascular Research Initiative, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG Search for other works by this author on: This Site PubMed Google Scholar KAA Fox KAA Fox 1MRC Centre for Inflammation Research & Wellcome Cardiovascular Research Initiative, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (2002) 102 (s46): 4P. https://doi.org/10.1042/cs102004P Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation J Sarma, A Jha, S Alam, KA Laan, I Dransfield, KAA Fox; Increased Platelet/Monocyte Binding in Acute Coronary Syndromes: Novel Platelet Interactions in Inflammatory Vascular Injury?. Clin Sci (Lond) 1 March 2002; 102 (s46): 4P. doi: https://doi.org/10.1042/cs102004P Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 2002 The Biochemical Society and the Medical Research Society2002 Article PDF first page preview Close Modal You do not currently have access to this content.

Evidence on the role of antiplatelet agents in patients with non-ST elevation acute coronary syndrome is reviewed, and a strategy for their use in unstable angina is presented

Research in vitro and in animal models suggested that gold electroplating of stents can attenuate neointimal hyperplasia and reduce thrombogenicity. The objective of this study was to evaluate the safety and efficacy of the gold‐coated NIROYAL stent in the treatment of stenosed coronary arteries and bypass grafts. We retrospectively studied 181 consecutive patients undergoing deployment of NIR (n = 87) or NIROYAL (n = 94) coronary stents in a single tertiary referral center from July 1997 to December 1998. Mean follow‐up duration for the NIR and NIROYAL patient groups were 11.6 and 11.4 (range, 3–12) months, respectively. Stent thrombosis rates were 3/87 (3%) in the NIR and 0/94 (0%) in the NIROYAL group (P = 0.07). The need for target lesion revascularization (TLR) in the NIR patient group was 8/87 (9%) compared to 11/94 (12%) in the NIROYAL patient group (P = 0.6). The overall MACE rates for the NIR and NIROYAL patient groups were 24/87 (28%) and 22/94 (23%), respectively (P = 0.5). The present study, hence, implies equivalence between the stainless steel NIR and the gold‐plated NIROYAL stent with no significant difference in immediate and long‐term clinical performance profiles. Cathet Cardiovasc Intervent 2001;54:141–145. © 2001 Wiley‐Liss, Inc.