Cardiovascular disease risk in antiphospholipid syndrome: Thrombo-inflammation and atherothrombosis

Tektonidou, Maria G.

doi:10.1016/j.jaut.2022.102813

Cited by 59 publications

(44 citation statements)

References 121 publications

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“…Generally, aPLs-mediated in ammation and thrombosis are considered as important pathogenetic mechanisms of APS. Moreover, aPLs-induced atherothrombosis might cause hypertension during pregnancy by stimulating platelet, endothelial cell and monocyte activation, inducing cytokines and adhesion molecules production, complement activation, and neutrophil extracellular traps (NETs) formation [19,20]. Consistently, our study showed that the prevalence of hypertension during pregnancy was signi cantly higher in the adverse outcomes group than the non-adverse outcomes group (32.7% vs. 4.3%, p = 0.001).…”

Section: Discussionsupporting

confidence: 79%

Risk factors for adverse pregnancy outcomes in obstetric antiphospholipid syndrome

Yang

Wang

et al. 2022

Preprint

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Background: Antiphospholipid syndrome (APS) causes adverse obstetric outcomes in the affected patients. Our study aimed to investigate the risk factors for adverse pregnancy outcomes (APOs) in women with APS. Methods: This retrospective study included 143 pregnant women with APS admitted to Peking University People’s Hospital. Based on the presence of APOs, pregnant women were divided into the adverse outcomes group (n=49) and the non-adverse outcomes group (n=94). Clinical data were extracted from medical records. Univariate and multivariate logistic regression analyses were used to identify the risk factors associated with APOs. Results: We found that the low platelet count (≤50×109/L), hypertension during pregnancy, and single-positivity of antiphospholipid antibody (aPLs) were the risk factors of APOs after adjusting age, the number of prior spontaneous miscarriages, weight change during pregnancy, gestational diabetes, thrombosis, oligohydramnios, and aPLs status (model I). Of importance, hypertension during pregnancy and single-positivity of aPLs remained the risk factors for adverse outcomes, but the low platelet count (≤50×109/L) was no longer a risk factor after adding the adjustments of the time of diagnosis and treatment during pregnancy (model II). And the number of platelets increased after delivery under the treatment (87.53±49.81 vs. 65.06±41.3 vs. 52.75±20.70 vs. 110.19±55.30; p<0.05). Therefore, treatment could effectively decrease the risk of adverse outcomes in pregnant APS patients with thrombocytopenia. Conclusion: APS increases the risk of adverse outcomes during pregnancy. Thrombocytopenia, hypertension during pregnancy, and single-positivity of aPLs were the risk factors of APOs in women with APS. Treatment can significantly reduce the risk of adverse outcomes by upregulating platelet count during pregnancy in APS patients with thrombocytopenia.

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Section: Discussionsupporting

confidence: 79%

Risk factors for adverse pregnancy outcomes in obstetric antiphospholipid syndrome

Yang

Wang

et al. 2022

Preprint

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“…However, a proportion of patients present with late onset APS, typically over the age of 65 years [ 70 ]. Mitochondrial dysfunction, oxidative stress and inflammation have been implicated in the pathogenesis of APS [ 71 , 72 , 73 ]. As an alternative to anticoagulant based therapy, research has focused on anti-inflammatory agents such as CoQ10, which in view of its antioxidant and anti-inflammatory functions, may be an appropriate candidate therapy for this disorder [ 1 , 2 ].…”

Section: Late Onset Antiphospholipid Syndromementioning

confidence: 99%

Coenzyme Q10: Role in Less Common Age-Related Disorders

Mantle

Hargreaves

2022

Antioxidants

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In this article we have reviewed the potential role of coenzyme Q10 (CoQ10) in the pathogenesis and treatment of a number of less common age-related disorders, for many of which effective therapies are not currently available. For most of these disorders, mitochondrial dysfunction, oxidative stress and inflammation have been implicated in the disease process, providing a rationale for the potential therapeutic use of CoQ10, because of its key roles in mitochondrial function, as an antioxidant, and as an anti-inflammatory agent. Disorders reviewed in the article include multi system atrophy, progressive supranuclear palsy, sporadic adult onset ataxia, and pulmonary fibrosis, together with late onset versions of Huntington’s disease, Alexander disease, lupus, anti-phospholipid syndrome, lysosomal storage disorders, fibromyalgia, Machado-Joseph disease, acyl-CoA dehydrogenase deficiency, and Leber’s optic neuropathy.

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“…But the mitochondrial phospholipid cardiolipin is a component of atheromas and a target of an autoimmune response in a number of diseases with impaired hemostasis. For example, autoantibodies to cardiolipin are present in atherosclerosis and aneurysms of the abdominal aorta [32]. Damage to mitochondria with the release of their DNA (mtDNA) is a potential result of SARS-CoV-2 infection.…”

Section: Respiratory Failure and Mixed Hypoxiamentioning

confidence: 99%

Aterosclerosis, Cardiovascular Disorders And Covid-19: Comorbid Pathogenesis

Makarova¹,

Ryabkova²,

Салухов³

et al. 2022

Preprint

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The article describes how atherosclerosis and coronavirus disease 19 (COVID-19) may affect each other. The features of this comorbid pathogenesis at various levels (vascular, cellular and molecular) are considered. A bidirectional influence of these conditions is described: the presence of cardiovascular diseases affects different individual susceptibility to viral infection. In turn, SARS-CoV-2 can have a negative effect on the endothelium and cardiomyocytes, causing blood clotting, secretion of pro-inflammatory cytokines, and thus exacerbating the development of atherosclerosis. In addition to the established entry into cells via ACE2 принимая во внимание его влияние на, other mechanisms of SARS-CoV-2 entry are currently under investigation, for example, through CD147. Pathogenesis of comorbidity can be determined by the influence of the virus on various links which are meaningful for atherogenesis: generation of oxidized forms of LDL, launch of a cytokine storm, damage to the endothelial glycocalyx, and mitochondrial injury. The transformation of a stable plaque into an unstable one plays an important role in the pathogenesis of atherosclerosis complications and can be triggered by COVID-19. The impact of SARS-CoV-2 on large vessels such as aorta is more complex than previously thought considering its impact on vasa vasorum. Current information on the mutual influence of the medicines used in the treatment of atherosclerosis and acute COVID-19 is briefly summarized

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Cardiovascular disease risk in antiphospholipid syndrome: Thrombo-inflammation and atherothrombosis

Cited by 59 publications

References 121 publications

Risk factors for adverse pregnancy outcomes in obstetric antiphospholipid syndrome

Risk factors for adverse pregnancy outcomes in obstetric antiphospholipid syndrome

Coenzyme Q10: Role in Less Common Age-Related Disorders

Aterosclerosis, Cardiovascular Disorders And Covid-19: Comorbid Pathogenesis

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