Plasma indices of endothelial and platelet activation in Rheumatoid Disease: Relationship to cardiovascular co-morbidity

Bhatia, Gurbir; Sosin, Michael; Patel, Jeetesh V.; Grindulis, K. A.; Khattak, Fazal H.; Davis, Russell; Lip, Gregory Y.H.

doi:10.1016/j.ijcard.2008.01.038

Cited by 8 publications

(4 citation statements)

References 24 publications

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“…After excluding traditional risk factors for CVD, Esther Houri Levi et al demonstrated that RA was the main cause of CVD after RA (6). From a conventional aspect, inflammatory factors, such as von Willebrand factor (VWF), induced CVD through endothelial damage/dysfunction, platelet activation, hypercoagulability, and angiogenesis in patients with RA (31,32). It was also speculated that the pathogenesis of CVD in RA patients was different from that in non-RA patients.…”

Section: Discussionmentioning

confidence: 99%

Relationship between rheumatoid arthritis and cardiovascular comorbidity, causation or co-occurrence: A Mendelian randomization study

Min

Chao

Mei

et al. 2023

Front. Cardiovasc. Med.

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BackgroundIn recent years, the incidence rates of rheumatoid arthritis (RA) and heart disease (HD) have noticeably increased worldwide. Previous studies have found that patients with RA are more likely to develop HD, while the cause and effect have still remained elusive. In this study, Mendelian randomization (MR) analysis was used to indicate whether there was a potential association between RA and HD.MethodsData of RA, ischemic heart disease (IHD), myocardial infarction (MI), atrial fibrillation (AF), and arrhythmia were based on the genome-wide association study (GWAS) dataset. No disease group was intersected. Inverse-variance weighted (IVW) method was used to calculate MR estimates, and sensitivity analysis was performed.ResultsThe primary MR analysis showed that genetic susceptibility to RA was significantly associated with the risk of IHD and MI, rather than with AF and arrhythmia. Besides, there was no heterogeneity and horizontal pleiotropy between the primary and replicated analyses. There was a significant correlation between RA and the risk of IHD (odds ratio (OR), 1.0006; 95% confidence interval (CI), 1.000244–1.00104; P = 0.001552), meanwhile, there was a significant correlation between RA and the risk of MI (OR, 1.0458; 95% CI, 1.07061–1.05379; P = 0.001636). The results were similar to those of sensitivity analysis, and the sensitivity analysis also verified the conclusion. Furthermore, sensitivity and reverse MR analyses suggested that no heterogeneity, horizontal pleiotropy or reverse causality was found between RA and cardiovascular comorbidity.ConclusionRA was noted to be causally associated with IHD and MI, rather than with AF and arrhythmia. This MR study might provide a new genetic basis for the causal relationship between RA and the risk of CVD. The findings suggested that the control of RA activity might reduce the risk of cardiovascular disease.

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Section: Discussionmentioning

confidence: 99%

Relationship between rheumatoid arthritis and cardiovascular comorbidity, causation or co-occurrence: A Mendelian randomization study

Min

Chao

Mei

et al. 2023

Front. Cardiovasc. Med.

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“…Recent attempts to associate a single marker of platelet function (e.g., P-selectin, MPV) with accelerated atherosclerosis and CVD in RA have failed [70,105]. It is, therefore, important to further investigate shifts of several markers of platelet function in response to DMARDs and anti-platelets in RA.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have failed to provide evidence of direct involvement of soluble P-selectin in vasculitis, atherosclerotic disease or myocardial dysfunction in RA [33, 62,70]. However, these studies had some limitations, such as inappropriate case-control design, small number of patients, lack of representative population of patients, neglect of confounding effects of acute-phase reactants interacting with P-selectin or lack of correction required in the case of therapy with DMARDs and cardiovascular drugs, known to inhibit platelet function.…”

Section: Soluble P-selectinmentioning

confidence: 99%

Platelet function in rheumatoid arthritis: arthritic and cardiovascular implications

Gasparyan

Stavropoulos‐Kalinoglou

Mikhailidis

et al. 2010

Rheumatol Int

141

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Patients with rheumatoid arthritis (RA) are at high risk of cardiovascular events. Platelet biomarkers are involved in inflammation, atherosclerosis and thrombosis. Cardiovascular and RA-associated factors can alter the structure and function of platelets, starting from megakaryocytopoiesis. Reactive megakaryocytopoiesis increases circulating platelets count and triggers hyperactivity. Hyperactive platelets target synovial membranes with subsequent local rheumatoid inflammation. Hyperactive platelets interact with other cells, and target the vascular wall. Accumulating evidence suggests that disease modifying anti-rheumatic drugs (DMARD) decrease platelet activity.

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“…Furthermore, it has been shown that platelet, and not endothelium‐derived P‐selectin, promotes local inflammation by enhancing leucocyte recruitment and increasing leucocyte–endothelial interactions in antigen‐induced arthritis (AIA) . In addition, elevated soluble P‐selectin levels have been associated with atherosclerotic complications, it has been detected in synovial fluid of knee osteoarthritis patients where it correlated with disease severity and several studies identified soluble P‐selectin as a marker for systemic inflammation in RA . Taken together, platelet‐derived P‐selectin is competent to initiate and perpetuate endothelial inflammation and could be considered as a biomarker for several inflammatory diseases.…”

Section: Platelet Activationmentioning

confidence: 99%

Platelets and autoimmunity

Habets

Huizinga

Toes

2013

Eur J Clin Investigation

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Vascular injury is the initial manifestation of inflammation resulting in the recruitment and activation of various cell types. The integrity of the vascular wall is monitored by platelets that become activated in the presence of exposed subendothelium. Besides their well-established role in haemostasis, ample data are now emerging on the many immunoregulatory functions of platelets. Platelets store and release a large plethora of cytokines, chemokines and growth factors. They also represent the largest circulating pool of many inflammatory mediators like P-selectin, CD40L and non-neuronal serotonin. Furthermore, complement activation occurs on the platelet surface and deposition of complement results in platelet activation. Overall, platelets have multiple functions in both innate and adaptive immunity. Further insight into the multifaceted role of platelets could therefore provide important clues into how we could implement current platelet therapy to reduce both plateletinduced thrombosis and inflammation. In this review, we discuss the current perceptions of platelet involvement in various autoimmune diseases like rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis and multiple sclerosis.

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Plasma indices of endothelial and platelet activation in Rheumatoid Disease: Relationship to cardiovascular co-morbidity

Cited by 8 publications

References 24 publications

Relationship between rheumatoid arthritis and cardiovascular comorbidity, causation or co-occurrence: A Mendelian randomization study

Relationship between rheumatoid arthritis and cardiovascular comorbidity, causation or co-occurrence: A Mendelian randomization study

Platelet function in rheumatoid arthritis: arthritic and cardiovascular implications

Platelets and autoimmunity

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