Congress of the International Society on Thrombosis and Haemostasis

Anticoagulation of a patient with hypertrophic cardiomyopathy and factor VII deficiency

Abstract number: PP-MO-120

Davidson¹ S.J., Turner¹ N., Tillyer¹ L.

¹¹Haematology, Royal Brompton Hospital, London, United Kingdom

How-to-cite Davidson SJ, Turner N, Tillyer L. Anticoagulation of a patient with hypertrophic cardiomyopathy and factor VII deficiency. Journal of Thrombosis and Haemostasis 2009; Volume 7, Supplement 2: Abstract PP-MO-120

A 50 year old male patient with hypertrophic cardiomyopathy and atrial fibrillation was anticoagulated with warfarin following insertion of a cardioverter defibrillator. He became markedly over anticoagulated after standard moderate induction doses of warfarin (INR 19.6). His baseline prothrombin time was prolonged and further investigation showed the patient to have a mild factor VII deficiency. He was restarted on low dose warfarin and successfully stabilised with a target INR of 3.0 (range 2.5 to 3.5). We used the data from factor VII levels and thrombin generation tests before and after anticoagulation to control dosage and to decide on a suitable therapeutic range for the INR. Molecular studies showed him to have two separate mutations in the factor VII gene. The first has been reported to reduce factor VII activity by 75% of normal (p.Arg412Gln); the second mis-sense mutation has not previously been reported on the factor VII mutation database (p.Arg60Gly)VII gene. The baseline pre-warfarin results were as follows; Prothrombin time 17.3s (NR 10.2-13.2s), factor VII activity recombinant Human TF 15u/dL (NR 70-130u/dL), VII activity rabbit TF 13u/dL (NR 70-130u/dL), factor VII:Ag 43% (NR 50-150%). Factors II, IX, X and protein C were all within normal limits. When the patient was stabilised on 3mg warfarin his INR was 3.1 factor VII acitvity was 2u/dL, and the thrombin potential had decreased by 50% of normal. This highlights the importance of noting the baseline prothrombin time before initiating oral anticoagulation, and describes how safe anticoagulation can be achieved in a patient with congenital factor VII deficiency.

Disclosure of interest: none declared.

To cite this abstract use the following format:

Journal of Thrombosis and Haemostasis 2007; Volume 5, Supplement 2: abstract number

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Date:	Unpresented
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Session name:	ISTH2009
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