Cardiac involvement in the antiphospholipid syndrome
Identifieur interne : 001E95 ( Main/Exploration ); précédent : 001E94; suivant : 001E96Cardiac involvement in the antiphospholipid syndrome
Auteurs : F. Tenedios [États-Unis] ; D. Erkan [États-Unis] ; M D Lockshin [États-Unis]Source :
- Lupus [ 0961-2033 ] ; 2005-09.
English descriptors
- Teeft :
- Abnormality, Anticardiolipin antibodies, Antiphospholipid, Antiphospholipid antibodies, Antiphospholipid antibody syndrome, Antiphospholipid syndrome, Atherosclerosis, Cardiac, Cardiac abnormalities, Cardiac manifestations, Carotid, Coronary artery disease, Diastolic, Diastolic dysfunction, Diastolic function, Dysfunction, Echocardiographic, Endothelial, Endothelial cell activation, Endothelial cells, Erythematosus, Fetal loss, Healthy controls, High prevalence, Hopkins lupus cohort, Hypertension, Independent risk factor, Infarction, Intracardiac, Intracardiac thrombi, Lesion, Lupus, Myocardial, Myocardial infarction, Oxidized, Primary antiphospholipid syndrome, Pulmonary hypertension, Rheum, Risk factor, Syndrome, Systemic lupus erythematosus, Tenedios, Thrombosis, Thrombus, Transesophageal echocardiography, Valve, Valve abnormalities, Valve disease, Valve lesions, Valvular, Ventricular, Ventricular dysfunction, Ventricular hypertrophy.
Abstract
Antiphospholipid syndrome (APS) is a systemic autoimmune disease, associated with a hypercoagulable state and fetal loss and with other clinical manifestations including cardiac involvement. Cardiac manifestations of APS are valve abnormalities (valve thickening and vegetations), occlusive arterial disease (atherosclerosis and myocardial infarction), intracardiac emboli, ventricular dysfunction, and pulmonary hypertension. Antiphospholipid antibodies (aPLs) may have a role in the accelerated atherosclerotic arterial disease observed in APS, related to their ability to induce endothelial activation. aPLs have been incriminated in the pathogenesis of heart valve lesions in APS patients. Markers of endothelial cell activation are up-regulated with prominent deposition of aPL in heart valves, suggesting aPL deposition initiates an inflammatory process that recruits complement leading to the valve lesion. Autoantibody-mediated endothelial cell activation probably plays a role in sustaining a proadhesive, proinflammatory, and procoagulant phenotype. The heterogeneity of APS clinical manifestations is likely linked to the varied effects that aPL can induce on endothelial cells and to the different functions that endothelial cells display depending on the anatomic localization.
Url:
DOI: 10.1191/0961203305lu2202oa
Affiliations:
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Erkan</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Rheumatology, Hospital for Special Surgery, Weill Medical College of Cornell University, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author wicri:is="90%"><name sortKey="Lockshin, M D" sort="Lockshin, M D" uniqKey="Lockshin M" first="M D" last="Lockshin">M D Lockshin</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Rheumatology, Hospital for Special Surgery, Weill Medical College of Cornell University, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Lupus</title><idno type="ISSN">0961-2033</idno><idno type="eISSN">1477-0962</idno><imprint><publisher>Sage Publications</publisher><pubPlace>Sage CA: Thousand Oaks, CA</pubPlace><date type="published" when="2005-09">2005-09</date><biblScope unit="volume">14</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="691">691</biblScope><biblScope unit="page" to="696">696</biblScope></imprint><idno type="ISSN">0961-2033</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0961-2033</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Abnormality</term><term>Anticardiolipin antibodies</term><term>Antiphospholipid</term><term>Antiphospholipid antibodies</term><term>Antiphospholipid antibody syndrome</term><term>Antiphospholipid syndrome</term><term>Atherosclerosis</term><term>Cardiac</term><term>Cardiac abnormalities</term><term>Cardiac manifestations</term><term>Carotid</term><term>Coronary artery disease</term><term>Diastolic</term><term>Diastolic dysfunction</term><term>Diastolic function</term><term>Dysfunction</term><term>Echocardiographic</term><term>Endothelial</term><term>Endothelial cell activation</term><term>Endothelial cells</term><term>Erythematosus</term><term>Fetal loss</term><term>Healthy controls</term><term>High prevalence</term><term>Hopkins lupus cohort</term><term>Hypertension</term><term>Independent risk factor</term><term>Infarction</term><term>Intracardiac</term><term>Intracardiac thrombi</term><term>Lesion</term><term>Lupus</term><term>Myocardial</term><term>Myocardial infarction</term><term>Oxidized</term><term>Primary antiphospholipid syndrome</term><term>Pulmonary hypertension</term><term>Rheum</term><term>Risk factor</term><term>Syndrome</term><term>Systemic lupus erythematosus</term><term>Tenedios</term><term>Thrombosis</term><term>Thrombus</term><term>Transesophageal echocardiography</term><term>Valve</term><term>Valve abnormalities</term><term>Valve disease</term><term>Valve lesions</term><term>Valvular</term><term>Ventricular</term><term>Ventricular dysfunction</term><term>Ventricular hypertrophy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Antiphospholipid syndrome (APS) is a systemic autoimmune disease, associated with a hypercoagulable state and fetal loss and with other clinical manifestations including cardiac involvement. Cardiac manifestations of APS are valve abnormalities (valve thickening and vegetations), occlusive arterial disease (atherosclerosis and myocardial infarction), intracardiac emboli, ventricular dysfunction, and pulmonary hypertension. Antiphospholipid antibodies (aPLs) may have a role in the accelerated atherosclerotic arterial disease observed in APS, related to their ability to induce endothelial activation. aPLs have been incriminated in the pathogenesis of heart valve lesions in APS patients. Markers of endothelial cell activation are up-regulated with prominent deposition of aPL in heart valves, suggesting aPL deposition initiates an inflammatory process that recruits complement leading to the valve lesion. Autoantibody-mediated endothelial cell activation probably plays a role in sustaining a proadhesive, proinflammatory, and procoagulant phenotype. The heterogeneity of APS clinical manifestations is likely linked to the varied effects that aPL can induce on endothelial cells and to the different functions that endothelial cells display depending on the anatomic localization.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><noRegion><name sortKey="Tenedios, F" sort="Tenedios, F" uniqKey="Tenedios F" first="F" last="Tenedios">F. Tenedios</name></noRegion><name sortKey="Erkan, D" sort="Erkan, D" uniqKey="Erkan D" first="D" last="Erkan">D. Erkan</name><name sortKey="Lockshin, M D" sort="Lockshin, M D" uniqKey="Lockshin M" first="M D" last="Lockshin">M D Lockshin</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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