Mechanisms of aPL-mediated thrombosis: Effects of aPL on endothelium and platelets

Vega-Ostertag, Mariano; Pierangeli, Silvia S.

doi:10.1007/s11926-007-0031-0

Cited by 43 publications

(33 citation statements)

References 49 publications

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“…There is a strong evidence that antibodies against b2GPI may be involved in most of the pathogenic mechanisms of the syndrome both in in vitro and ex-vivo experimental models [3,6,7]. Table 2 summarizes all the mechanisms in which antib2GPI antibodies have been reported to play a pathogenic role.…”

Section: Anti-b2gpi Autoantibodies: the Bridge Between Apl And The Tamentioning

confidence: 99%

Pathogenesis of the antiphospholipid syndrome: An additional example of the mosaic of autoimmunity

Meroni

2008

Journal of Autoimmunity

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Section: Anti-b2gpi Autoantibodies: the Bridge Between Apl And The Tamentioning

confidence: 99%

Pathogenesis of the antiphospholipid syndrome: An additional example of the mosaic of autoimmunity

Meroni

2008

Journal of Autoimmunity

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“…Firstly, APS can cause endothelial dysfunction. The existing evidence has suggested a widespread endothelial dysfunction in APS patient, 7,8) while coronary endothelial dysfunction must play a major role in SCAD pathogenesis along with other factors such as increased coronary shear stress and localized vasculitis. 9) Secondly, APS is an important manifestration of various systemic inflammatory diseases, accelerating the process of atherosclerosis.…”

Section: Case Reportmentioning

confidence: 99%

Spontaneous Coronary Artery Dissection Accompanied with Antiphospholipid Syndrome and Leukemia

et al. 2018

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SummaryWe report a rare spontaneous coronary artery dissection (SCAD) case accompanied by antiphospholipid syndrome (APS) and leukemia which was treated successfully with drug-eluted stents (DES) implantation. This young SCAD patient was initially diagnosed of acute myocardial infarction (AMI); however, except for 6 packyears of smoking, there were no risk factors or family history of coronary artery disease. Subsequently, we screened other clinical status like autoimmune diseases and finally found APS. In general, APS was associated with thromboembolism events, not coronary artery dissection. Our case indicated that SCAD could be a rare manifestation of APS which should draw our attention. In addition, our bail-out therapy acquired the expected effect.(Int Heart J Advance Publication) Key words: Percutaneous coronary intervention, Intravascular ultrasound, Antithrombins S CAD is defined as spontaneous coronary artery layers separation producing true and false lumen without human intervention, triggered primarily by intimal-luminal interface disruption or vasa vasorum rupture.1) It remains an infrequent clinical entity, predominantly affecting young women. Interestingly, our SCAD case was a very young man with APS and a 19 year history of diagnosed leukemia. To our knowledge, this is the first time a SCAD case accompanied by APS and leukemia has been reported. Case ReportA 29-year old man who had no risk factors for coronary artery disease, except for 6 pack-years of smoking and a past medical history of diagnosed leukemia 19 years ago, presented to our cardiology department with severe chest pain for 13 days. The severe chest pain occurred 13 days ago while he was at rest, radiating to the left upper limb with profuse sweating. The symptom did not relieve until he received morphine and nitrates in the local hospital. The troponin I test was positive and ECG showed ST segment elevation in the anterior and lateral leads ( Figure 1), which led to a diagnosis of AMI. Accordingly, primary percutaneous coronary intervention was suggested, but it was refused by the patient. Standard drug therapy with low molecular heparin, double antiplatelet, statin, and other secondary prevention medicines was applied at the local hospital. Then, based on his wish, the patient was transferred 13 days later with a stable condition to our hospital (regional heart center). Cardiac catheterization was performed, which showed type-D dissection from ostium to the mid segment of the left anterior descending artery (LAD) with contrast retention and TIMI flow grade 2; the other coronary arteries were smooth without any stenosis. The cholesterol level was within normal range. The LDL-c level was 57.28 mg/dL. Echocardiogram showed severe hypokinesis of the anterior wall and the apical segment of left ventricle. The left ventricular ejection fraction value was 48%. Considering the low risk factors or family history of heart diseases, we screened further for other clinical status like autoimmune diseases. The ENA test was negative, while the an...

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“…Subsequently, in the presence of subactivating doses of thrombin, b 2 GPI-antibody complex induces the production of thromboxane B2 mainly through the activation of p38MAPK and subsequent phosphorylation of cytosolic phospholipase A2. In addition, aPL enhance the expression of platelet membrane glycoproteins, particularly glycoprotein (GP) IIb/IIIa and GPIIIa [12].…”

Section: Plateletsmentioning

confidence: 99%

Antiphospholipid syndrome: long-time research on pathogenic mechanisms has finally lead to new therapeutic strategies

Cervera¹,

Espinosa²

2010

Expert Opinion on Therapeutic Targets

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Mechanisms of aPL-mediated thrombosis: Effects of aPL on endothelium and platelets

Cited by 43 publications

References 49 publications

Pathogenesis of the antiphospholipid syndrome: An additional example of the mosaic of autoimmunity

Pathogenesis of the antiphospholipid syndrome: An additional example of the mosaic of autoimmunity

Spontaneous Coronary Artery Dissection Accompanied with Antiphospholipid Syndrome and Leukemia

Antiphospholipid syndrome: long-time research on pathogenic mechanisms has finally lead to new therapeutic strategies

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