Endothelial dysfunction in patients with antiphospholipid syndrome assessed with positron emission tomography

Alexánderson, Erick; Cruz, Phillip; Vargas, Angélica; Meave, Aloha; Ricalde, Alejandro; Talayero, Jose A.; Romero-Ibarra, José Luis; Goldson, Tove M.; Vera‐Lastra, Olga; Medina, Gabriela; Jara, Luis J.; Amigo, Mary‐Carmen

doi:10.1016/j.nuclcard.2007.05.003

Cited by 14 publications

(4 citation statements)

References 39 publications

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“…Once an embolic source was ruled unlikely, we can only hypothesize that the femoral lesion was a result of a local or a transient systemic inflammatory process related to his disease that led to endothelial dysfunction, complement and platelet activation, and ultimately, thrombus formation. [15][16][17][18] This lesion subsequently caused distal arterial embolism culminating as blue toe syndrome and toe ulcerations. Thrombosis due to premature or accelerated atherosclerosis in setting of traditional risk factors (smoking, diabetes, hypertension, and hypercholesterolemia) have been documented in APS patients.…”

Section: Discussionmentioning

confidence: 99%

Superficial femoral artery thrombosis as a cause for distal embolism in primary antiphospholipid syndrome

Lauvao

Goshima

León

et al. 2008

Journal of Vascular Surgery

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Antiphospholipid syndrome is a diagnosis with the clinical manifestations of thromboses in the presence of an antiphospholipid antibody. A 25-year-old man with a history of deep venous thrombosis, pulmonary emboli, and myocardial infarction, and receiving long-term anticoagulation with warfarin, all due to primary antiphospholipid syndrome, presented with blue toe syndrome from a primary superficial femoral artery thrombus. He was anticoagulated with fondaparinux in addition to dipyridamole and aspirin perioperatively. The area of thrombus was resected and reconstructed using a cephalic vein interposition graft. This report reviews antiphospholipid syndrome and identifies potential questions and problems relating to a rare clinical presentation.

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Section: Discussionmentioning

confidence: 99%

Superficial femoral artery thrombosis as a cause for distal embolism in primary antiphospholipid syndrome

Lauvao

Goshima

León

et al. 2008

Journal of Vascular Surgery

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“…The pathognomonic feature of this condition is recurrent thrombosis in both the arterial and venous circulations, and the possible causative mechanisms have been reviewed recently [8]. With particular reference to SCAD, recent evidence suggests a widespread endothelial dysfunction in APS [9]. Coronary endothelial dysfunction could therefore play a major role in the pathogenesis of SCAD along with other factors such as plaque or vasa vasorum rupture, localized vasculitis with eosinophilic infiltration, and increased shear stress.…”

Section: Discussionmentioning

confidence: 99%

Spontaneous coronary artery dissection presenting as an ischaemic stroke in a middle-aged man with anti-cardiolipin antibodies: a case report

2010

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IntroductionCerebrovascular disease is a major cause of mortality and morbidity worldwide. Ischemic stroke is the most common manifestation, encompassing a wide variety of causative mechanisms. We present the case of a middle-aged male patient with spontaneous coronary artery dissection in the presence of anti-cardiolipin antibodies, leading to left ventricular thrombus and presenting with stroke.Case presentationA 56-year-old Caucasian man presented with dysarthria and right-sided weakness. There was a history of chest pain with autonomic symptoms four days earlier. Examination revealed right-sided hemiparesis. Electrocardiogram showed sinus rhythm with anterior Q waves. Magnetic resonance imaging of the brain showed large left parietal and smaller multiple cerebral infarcts. Echocardiogram showed anterior wall and apical akinesis with a large mural thrombus. Anti-cardiolipin antibodies immunoglobulin G and immunoglobulin M were strongly positive. Coronary angiography showed dissection of the mid left anterior descending artery with normal flow down the distal vessel. He was treated conservatively with anticoagulation and secondary prevention. He was in good health when seen in clinic four months later.ConclusionWe highlight the importance of a comprehensive approach at obtaining the correct diagnosis, input of different specialities and the fact that the presence of anti-cardiolipin antibodies is associated with coronary artery dissection in a middle-aged male patient whose presentation was stroke.

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“…50 A substantial reduction of endothelial-derived coronary flow reserve measure by PET was found in APS in comparison with healthy controls. 51 Stress myocardial perfusion fibrosis evaluation by CMR has been successfully applied to identify subendocardial perfusion defects in SLE patients free of overt coronary artery disease. 52 In addition, CMR with late gadolinium enhancement (LGE) has been used for detecting occult localized myocardial scarring 53 and diffuse endomyocardial fibrosis 54 in APS patients.…”

Section: Ischemic Heart Diseasementioning

confidence: 99%

Cardiac Manifestations of Antiphospholipid Syndrome: Clinical Presentation, Role of Cardiac Imaging, and Treatment Strategies

Tufano

Minno

Guida

et al. 2019

Semin Thromb Hemost

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by the presence of antiphospholipid antibodies, vascular thrombosis (venous, arterial, or small vessels), and/or pregnancy morbidity. Diagnosis of APS is based on the presence of at least one clinical criterion (thrombotic events or pregnancy morbidity) and at least one of the laboratory criteria (persistently medium/high titer immunoglobulin G [IgG]/immunoglobulin M [IgM] anticardiolipin antibodies, and/or medium/high titer IgG/IgM anti-β2-glycoprotein I antibodies, and/or a positive lupus anticoagulant test), confirmed after repetition at least 12 weeks apart. The clinical spectrum of APS encompasses additional (extracriteria) clinical manifestations, including cardiac diseases. Heart involvement may become evident as a consequence of direct (autoimmune-mediated) or indirect (thrombosis) mechanisms, and include valve heart disease (vegetations and/or thickening associated with functional abnormalities) and intracardiac thrombosis, coronary, and vascular accelerated atherosclerosis, along with ischemic heart disease. APS can also cause pulmonary arterial hypertension, left ventricular dysfunction, and heart failure. This review describes the major cardiac manifestations of APS and illustrates the role of cardiac imaging for diagnosing subclinical and overt heart involvement and addressing management of these patients. The possible role of therapeutic strategies in cardiac manifestations of APS is also discussed.

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Endothelial dysfunction in patients with antiphospholipid syndrome assessed with positron emission tomography

Abstract: The CPT results obtained in this study showed that the PAPS patients studied have endothelial dysfunction.

Cited by 14 publications

References 39 publications

Superficial femoral artery thrombosis as a cause for distal embolism in primary antiphospholipid syndrome

Superficial femoral artery thrombosis as a cause for distal embolism in primary antiphospholipid syndrome

Spontaneous coronary artery dissection presenting as an ischaemic stroke in a middle-aged man with anti-cardiolipin antibodies: a case report

Cardiac Manifestations of Antiphospholipid Syndrome: Clinical Presentation, Role of Cardiac Imaging, and Treatment Strategies

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