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[Antiprothrombinase and myocardial infarction. Apropos of 2 cases]
P Philippe1, S Charmion, B Citron
1Service de Médicine interne, Hôpital Nord Cébazat, Clermont-Ferrand.
Insights
Antiprothrombinase antibodies, rare causes of myocardial infarction, were observed in two patients. These antibodies may play a primary role in arterial thrombosis, independent of systemic lupus erythematosus (SLE).
Area of Science:
- Cardiology
- Hematology
- Immunology
Background:
- Myocardial infarction (MI) is rarely associated with circulating anticoagulants of the antiprothrombinase type.
- Understanding the etiological factors of MI is crucial for effective prevention and treatment strategies.
Observation:
- Two cases of myocardial necrosis occurred in patients with antiprothrombinase antibodies.
- Coronary arteriography revealed no significant atherosclerotic lesions or vasculitis, suggesting the anticoagulant's direct role.
Findings:
- Antiprothrombinase antibodies were implicated as a predominant factor in the genesis of myocardial infarction.
- The presence of systemic lupus erythematosus (SLE) did not appear to be an independent risk factor for arterial thrombosis in these cases, unless vasculitis or corticosteroid therapy was involved.
- Antibodies against phospholipids may represent an independent risk factor for MI, irrespective of SLE diagnosis.
Implications:
- This study highlights a rare but significant cause of myocardial infarction, emphasizing the need to consider antiprothrombinase antibodies in thrombotic events.
- Further research is warranted to elucidate the precise mechanisms linking phospholipid antibodies to arterial thrombosis and MI.
- Clinical management should consider screening for these antibodies in specific patient populations presenting with unexplained arterial thrombosis.
Abstract:
Among the thrombotic events associated with a circulating anticoagulant of the antiprothrombinase type, myocardial infarction is exceptionally reported, which justifies the presentation of two cases. In both patients, myocardial necrosis occurred some time after the antiprothrombinase was discovered, and there was nothing special in its clinical features. No obvious atherosclerotic lesion and no image suggestive of vasculitis were found at coronary arteriography, which suggested that the antiprothrombinase played a predominant role in the genesis of infarction. Relationships between antiprothrombinase, arterial thrombosis (particularly of the coronary arteries) and the presence or absence of systemic lupus erythematosus (SLE) are discussed. As observed in thrombosis of other arteries, it is not certain that the presence of SLE constitutes an additional risk factor, except in cases with unquestionable vasculitis or if the treatment of SLE requires prolonged corticosteroid therapy. On the other hand, the appearance of an antibody directed against phospholipids is not necessarily related to the presence of SLE; in fact, this antibody itself might be a risk factor of myocardial infarction, as has recently been suggested.