Secondary Thromboprophylaxis in Hereditary Thrombophilia
Journal
Cardiology and Angiology: An International Journal
Date Issued
2018-02
Author(s)
DOI
10.9734/CA/2018/39718
Abstract
Aims: The aim of this study is to show how the coagulation laboratory and clinical findings worked
together in the management of a patient with hereditary thrombophilia and pulmonary embolism
(PE) in terms of diagnosis, the choice of anticoagulation treatment and the duration of secondary
thromboprophylaxis.
Study Design: A case report with the presentation of clinical and laboratory findings, treatment and
long-term follow up of the patient.
Place and Duration of Study: Institute of Transfusion Medicine and University Clinics of
Cardiology, St Cyril and Methodius University, Skopje, Macedonia in the period from February 2015
and December 2017.
Case Presentation: Computer tomography confirmed the diagnosis of PE in a 32-year-old man
who was admitted to the cardiology emergency department with D-dimer level of 5980 ng/mL after
an episode of syncope. After the initial anticoagulation with unfractionated heparin 30.000i.e./24 h,enoxaparin 80 mg/12 h and acenocoumarol were introduced. The therapeutic INR rang could not be
achieved so the acenocoumarol was switched to rivaroxaban 2x15 mg/day. One year later the
anticoagulation with rivaroxaban 20 mg/day was discontinued. Thrombophilia testing included:
prothrombin (PTB), Factor V Leiden and methylene tetrahydrofolate reductase (MTHFR) C677T
gene mutation, as well as antiphospholipid antibodies, antithrombin, protein C and S.
Results: The patient was homozygous for the PTB. His parents were heterozygous for the same
mutation; his mother also being heterozygous for MTHFR C677T. His brother was compound
heterozygote for PTB and MTHFR C677T and his sister was heterozygous for the PTB. Coagulation
status monitoring showed hypercoagulability (APTT was 24-26 seconds) and increment of D-dimer
(2100-2400 ng/ml) when rivaroxaban was discontinued and normal APTT (28-38 seconds) and Ddimer
(< 500 ng/mL) when it was reintroduced.
Conclusion: According to the laboratory findings and also having in mind that this was a second
episode of a thrombotic event, we decided for an extended secondary thromboprophylaxis. Although
it sometimes implies that it will be continued life-long we consider worthwhile to apply the patientoriented
approach to the decision when and whether to terminate anticoagulation.
together in the management of a patient with hereditary thrombophilia and pulmonary embolism
(PE) in terms of diagnosis, the choice of anticoagulation treatment and the duration of secondary
thromboprophylaxis.
Study Design: A case report with the presentation of clinical and laboratory findings, treatment and
long-term follow up of the patient.
Place and Duration of Study: Institute of Transfusion Medicine and University Clinics of
Cardiology, St Cyril and Methodius University, Skopje, Macedonia in the period from February 2015
and December 2017.
Case Presentation: Computer tomography confirmed the diagnosis of PE in a 32-year-old man
who was admitted to the cardiology emergency department with D-dimer level of 5980 ng/mL after
an episode of syncope. After the initial anticoagulation with unfractionated heparin 30.000i.e./24 h,enoxaparin 80 mg/12 h and acenocoumarol were introduced. The therapeutic INR rang could not be
achieved so the acenocoumarol was switched to rivaroxaban 2x15 mg/day. One year later the
anticoagulation with rivaroxaban 20 mg/day was discontinued. Thrombophilia testing included:
prothrombin (PTB), Factor V Leiden and methylene tetrahydrofolate reductase (MTHFR) C677T
gene mutation, as well as antiphospholipid antibodies, antithrombin, protein C and S.
Results: The patient was homozygous for the PTB. His parents were heterozygous for the same
mutation; his mother also being heterozygous for MTHFR C677T. His brother was compound
heterozygote for PTB and MTHFR C677T and his sister was heterozygous for the PTB. Coagulation
status monitoring showed hypercoagulability (APTT was 24-26 seconds) and increment of D-dimer
(2100-2400 ng/ml) when rivaroxaban was discontinued and normal APTT (28-38 seconds) and Ddimer
(< 500 ng/mL) when it was reintroduced.
Conclusion: According to the laboratory findings and also having in mind that this was a second
episode of a thrombotic event, we decided for an extended secondary thromboprophylaxis. Although
it sometimes implies that it will be continued life-long we consider worthwhile to apply the patientoriented
approach to the decision when and whether to terminate anticoagulation.
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