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Published on: June 29, 2015
[ST-segment elevation myocardial infarction in a patient with thrombophilia taking new oral anticoagulants]
Mauro Li Calzi1, Angelo Placci1, Daniela Lina1
1U.O.C. Cardiologia, Azienda Ospedaliero-Universitaria di Parma, Parma.
Insights
A patient with a Factor II gene mutation experienced myocardial infarction despite rivaroxaban treatment. Warfarin plus aspirin was effective, suggesting novel oral anticoagulants may be insufficient for Factor II G20210A mutation-related thrombosis.
Area of Science:
- Cardiology
- Hematology
- Pharmacology
Background:
- Novel oral anticoagulants (NOACs) are increasingly used for thrombotic conditions.
- Factor II G20210A mutation is a known prothrombotic risk factor.
Observation:
- A 65-year-old woman on rivaroxaban for pulmonary embolism presented with ST-segment elevation myocardial infarction due to coronary artery thrombosis.
- Angiography revealed thrombotic occlusion without atherosclerosis, and genetic testing confirmed a Factor II G20210A mutation.
Findings:
- Rivaroxaban appeared ineffective in preventing acute coronary thrombosis in this patient with a Factor II G20210A mutation.
- Switching to warfarin plus low-dose aspirin resolved the issue, with no further ischemic events in 1 year.
Implications:
- Factor Xa inhibition by NOACs may be insufficient in thrombophilic states caused by Factor II G20210A mutation.
- This case highlights the need for individualized antithrombotic strategies in patients with genetic thrombophilia and acute coronary syndromes.
Abstract:
We report the case of a 65--year-old woman admitted for inferior ST-segment elevation myocardial infarction complicated by complete atrioventricular block. The patient was under treatment with a novel oral anticoagulant (NOAC, rivaroxaban) because of a history of recurrent idiopathic pulmonary embolism. Emergency angiography showed complete acute thrombotic occlusion of the right coronary artery. After manual thrombectomy, there was no angiographic evidence of underlying atherosclerosis, therefore no further percutaneous coronary intervention was performed. Subsequent clinical course was uneventful. Laboratory tests demonstrated the presence of a heterozygous mutation of the factor II gene (G20210A), confirming the clinical evidence of a thrombophilic state. As rivaroxaban seemed to be ineffective in preventing spontaneous coronary thrombosis in this patient, antithrombotic therapy was shifted to warfarin plus low-dose aspirin. No further ischemic events occurred during the 1-year follow-up. It can be hypothesized that factor Xa inhibition by NOACs, such as rivaroxaban, could be insufficient in case of a thrombophilic state due to thrombin mutation. A brief review of the current literature on use of NOACs in acute coronary syndromes is also reported.
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