Influence of statin therapy on antiphospholipid antibodies and endothelial dysfunction in young patients with coronary artery disease and systemic lupus erythematosus

Mazurek, Adam; Gryga, Krzysztof; Bugała, Kamil; Iwaniec, Teresa; Musiał, Jacek; Podolec, Piotr; Płazak, Wojciech

doi:10.5114/aoms.2019.90271

Cited by 7 publications

(9 citation statements)

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“…The high level of prothrombotic activity in SLE was also described as an important factor that contributes to an increased risk of cardiovascular events [15]. It is suggested to be associated with endothelial damage and autoinflammation [27].…”

Section: Discussionmentioning

confidence: 99%

“…It appears that the rapid progression of atherosclerosis, a result of the pro-inflammatory state in rheumatic disorders, may also increase the probability of thrombotic events. Many studies have shown a cor-relation between prothrombotic activity and endothelial dysfunction, one of the early stages of atherosclerosis [15,33]. Thrombin formation has been shown to increase matrix metalloproteinase (MMS) enzymatic activity, contributing to the stiffness of the extracellular matrix of arteries [34].…”

Section: Discussionmentioning

confidence: 99%

“…Its blood concentration increases in endothelial damage, especially in diseases that accelerate atherosclerosis, such as arterial hypertension, hyperlipidaemia, and nicotinism [6,13]. Although elevated blood vWF concentration can also be found during pregnancy and after physical activity in otherwise healthy subjects, vWF is considered a good marker of endothelial damage [14,15]. The general advantage of vWF as an indicator of endothelial damage is that it is produced only by the endothelium and its level remains stable for weeks [14].…”

Section: Introduction Objectivesmentioning

confidence: 99%

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Arterial stiffness and atherosclerosis in systemic lupus erythematosus patients

et al. 2022

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Introduction: Systemic lupus erythematosus (SLE) is characterized by early atherothrombosis. Pulse wave velocity (PWV) is a promising tool for the diagnosis of early vascular remodelling and initial atherosclerotic plaque formation. Our objective was to evaluate PWV and its relationship with coronary atherosclerosis and thrombotic biomarkers in patients with SLE. Material and methods: In 26 patients with SLE with stable clinical conditions, mean age of 39.1 ±11.7 years and without a history of coronary artery disease, multidetector computed tomography (MDCT)-based coronary calcium scoring (CACS) was performed and PWV measured. Laboratory evaluation included serum levels of anticardiolipin and anti-β2-glycoprotein antibodies (anti-β2-GPI), lupus anticoagulant (LA), D-dimers, thrombin-antithrombin complexes (TAT), and von Willebrand factor (vWF). Results: Multidetector computed tomography revealed coronary calcifications in 8 (30.8%) patients and the median CACS was 52.4 HU (range 2-843.2). The mean PWV was 9.0 ±3.2 m/s and was higher in patients aged > 50 years (+33.7% vs. < 50 years), those with positive LA (+28.2% vs. LA negative), TAT ≥ 10 µg/l (+18.1% vs. < 10 µg/l), vWF ≥ 200 IU/dl (+51.8% vs. < 200 IU/dl) and with coronary atherosclerosis (CACS > 0; +21.4% vs. CACS = 0). In contrast, the duration of the disease, D-dimers, anticardiolipin, and anti-β2-GPI antibodies did not influence PWV. In the group without atherosclerosis (CACS = 0, n =18), patients with vWF ≥ 200 IU/dl had a 19.3% higher PWV compared to the rest. Conclusions: In patients with SLE, PWV was associated with the presence of coronary atherosclerotic lesions in MDCT. Furthermore, arterial stiffness was higher in patients with markers of endothelial dysfunction and a prothrombotic state, suggesting their contribution to the early stages of arterial remodelling in SLE.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introduction Objectivesmentioning

confidence: 99%

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Arterial stiffness and atherosclerosis in systemic lupus erythematosus patients

et al. 2022

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“…The activation or damage of the vascular endothelium is manifested by the elevation of ICAM-1 and vWF [ 55 , 56 ]. In patients with coronary calcifications, the levels of these molecules are significantly higher compared to those without calcium deposits in the coronary arteries [ 57 ]. Furthermore, the connection between the presence of calcified coronary plaque and the levels of selectin E, VCAM, or tumor necrosis factor-alpha (TNFα) levels was shown [ 55 ].…”

Section: Sle and Early Onset Atherosclerosismentioning

confidence: 99%

SARS-CoV-2 infection and SLE: endothelial dysfunction, atherosclerosis, and thrombosis

Płazak

Drabik

2023

Clin Rheumatol

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An increased risk of atherosclerotic and thrombotic complications characterizes connective tissue diseases. Endothelial dysfunction is the basis for the initiation and progression of atherosclerosis and thrombosis. We present systemic lupus erythematosus (SLE) as a model rheumatic disease with endothelial dysfunction and discuss its mechanisms, factors that influence the early onset and rapid progression of atherosclerosis, and the increased risk of thromboembolic events. We focus on established methods to improve endothelium function, including statins, antiplatelet, and antithrombotic therapy. Hypercoagulable and hypofibrinolitic states and a hyperinflammatory response characterize severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Several pathogenic mechanisms are typical for an acute phase of Covid-19 post-Covid syndrome and connective tissue diseases: endothelial dysfunction, elevated antiphospholipid antibody titer, activation of the complement system, and formation of extracellular neutrophil traps (NET). The current review discusses the mechanisms underlying SLE and the COVID-19 in the context of endothelial function, atherosclerosis, and thrombosis (Graphical abstract). Key Points• The pathophysiology of systemic lupus erythematosus (SLE) and Covid-19 shows some similarities, such as endothelial cell activation and dysfunction, the activation of complementary systems, the presence of antiphospholipid antibodies, and the formation of extracellular neutrophil traps.• Autoimmunity in both diseases creates the basis for hyperinflammatory, hypercoagulable, and hypofibrinolitic states and their thromboembolic complications.• This paper presents our perspective on the mechanisms behind the cardiovascular manifestations of SLE and COVID-19, with a particular emphasis on endothelial dysfunction. Graphical abstract Covid-19 and systemic lupus erythematosus—potential similarities in pathophysiology. Figures of the panel illustrate the clinical manifestations of endothelial dysfunction, atherosclerosis, and thromboembolism, including coronary artery disease ([A] coronary angiography with left anterior descending artery stenosis and [B] scintigraphy with reduced perfusion in the myocardial apical segments), stroke ([C] carotid angiography, left carotid artery occlusion) and pulmonary embolism ([D]computed tomography with thrombus in the right pulmonary artery).

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“…Besides reducing cholesterol levels, statins have pleiotropic effects, including modulating immune response, 4 , 5 reducing oxidative stress, 6 , 7 and improving endothelial function. 8 , 9 …”

Section: Introductionmentioning

confidence: 99%