Antiphospholipid Antibodies: Is There a Role in Cardiac Valvular Disease and Its Thromboembolic Complications?

Soscia, P Nardone; Romain, Paul L.

doi:10.1159/000174972

Cited by 8 publications

(3 citation statements)

References 21 publications

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“…. In addition, the association between aPL and IS or TIAs is strong1, [8][9][10][11][12][13][14][15]17,18,[28][29][30][31][32][33][34] if the exact pathophysiology of aPL-induced thrombosis is still unknown35, there is an urgent need for controlled prospective studies dealing with primary and secondary prevention of thrombosis in APS 12,16,[20][21][22][23][36][37][38][39][40][41][42][43][44][45][46] In situ thrombosis in veins or medium to large arteries, proliferative small vessel vasculopathy as well as embolism from cardiac valvular lesions have been reported iñ jpgi2,i6 Thus, thrombotic APS is an heterogenous syndrome in which either venous or arterial thromboembolic events are observed~'~'~~. Interestingly, 91% of Rosove's patients and 87.5% of our APS patients had repetitive thrombotic events of similar distribution when untreated.…”

Section: Patientsmentioning

confidence: 99%

Thrombosis and Antiphospholipid Syndrome: a Preliminary Assessment of Three Antithrombotic Treatments

Rivier

Herranz

Khamashta

1994

Lupus

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To assess retrospectively three antithrombotic treatments in the secondary prevention of thrombosis in the antiphospholipid syndrome (APS), 23 patients (six systemic lupus erythematosus, seven lupus-like disease and 10 primary antiphospholipid syndrome) were included in this study. Treatments assessed were: (1) aspirin 75 mg daily, (2) warfarin (international normalised ratios (INRs) 2.0-2.9) +/- aspirin 75 mg daily, and (3) warfarin (INRs > 2.9) +/- aspirin 75 mg daily. Where patients had received two or three of these treatments successively, the periods of time on each treatment were added and the number of patients with recurrence(s) on each treatment were compared by Fisher's exact probability test. 'High' anticoagulation (INRs > 2.9) +/- aspirin 75 mg daily was more effective than aspirin 75 mg daily, there was a trend in favour of 'high' anticoagulation (P = 0.066). No statistically significant difference could be demonstrated when comparing 'low' anticoagulation +/- aspirin 75 mg daily with aspirin 75 mg daily (P = 0.092). These results suggest that aggressive anticoagulation with or without low-dose aspirin is effective in preventing further thromboembolic events in APS.

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Section: Patientsmentioning

confidence: 99%

Thrombosis and Antiphospholipid Syndrome: a Preliminary Assessment of Three Antithrombotic Treatments

Rivier

Herranz

Khamashta

1994

Lupus

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“…I read with great interest the recent editorial by Nardone Soscia and Romain [ 1 ] on the role of anti phospholipid antibodies in cardiac valvular disease and its throm boembolic complications. That an tiphospholipid antibodies (APLA) can occur in patients without sys temic lupus erythematosus or other connective tissue diseases has been reported previously [2][3][4].…”

mentioning

confidence: 99%

“…That an tiphospholipid antibodies (APLA) can occur in patients without sys temic lupus erythematosus or other connective tissue diseases has been reported previously [2][3][4]. Their role in causing thromboembolic complications in valvular disease of the heart has only recently been implicated [1][2][3][4], Thromboembolism is a dread ed. though rare, complication of mitral valve prolapse (MVP), the commonest valvular disease in the world [5].…”

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confidence: 99%

Antiphospholipid Antibodies in Mitral Valve Prolapse

Cheng¹

1992

Cardiology

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Pulmonary arteritis with pulmonary arterial thrombosis and recurrent endopulmonary embolization

et al. 1993

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A 41-year-old woman underwent medical examination for superficial thrombophlebitis of both lower legs. Incidentally a chronic myelogenous leukemia was diagnosed and chemotherapeutically treated. Three weeks after the first attendance the patient again suffered superficial thrombophlebitides of all extremities. Clinically she exhibited symptoms of recurrent mild pulmonary embolization. Contrast venography revealed no signs of deep venous thrombosis of legs, pelvis, or cava inferior. Despite continuous full-dose intravenous heparin administration the patient died, with signs of fulminant pulmonary embolization. Surprisingly, necropsy revealed a complete thrombotic occlusion of the pulmonary arterial system caused by pulmonary arteritis with signs of recurrent pulmonary embolization from a parietal truncus pulmonalis thrombosis. In addition, an appositional growth of parietal thrombi central from peripheral arterial ramifications had occurred. Simultaneously, superficial thrombophlebitis of all extremities was observed without any additional signs of general vasculitis. There was no strong evidence for a causal relationship between the chronic myelogenous leukemia and pulmonary arteritis nor for any other underlying systemic disorder. Therefore we consider the pulmonary arteritis a possibly primary one. This very rare disease is discussed with respect to the literature.

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Antiphospholipid Antibodies: Is There a Role in Cardiac Valvular Disease and Its Thromboembolic Complications?

Cited by 8 publications

References 21 publications

Thrombosis and Antiphospholipid Syndrome: a Preliminary Assessment of Three Antithrombotic Treatments

Thrombosis and Antiphospholipid Syndrome: a Preliminary Assessment of Three Antithrombotic Treatments

Antiphospholipid Antibodies in Mitral Valve Prolapse

Pulmonary arteritis with pulmonary arterial thrombosis and recurrent endopulmonary embolization

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