Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.


Decreased Fibrin Clot Porosity in Patients with Antifosfolipid Syndrome.

Vikerfors2,  Anna, Antovic1,  Aleksandra, Svenungsson2,  Elisabet, Bremme3,  Katarina, Holmstrom4,  Margareta

Department of Clinical Sciences, Karolinska Institutet/Danderyd Hospital, Stockholm, Sweden
Department of Medicine, Rheumatology Unit, Karolinska Institutet/Karolinska University Hospital, Stockholm, Sweden
Department of Woman and Child Health, Division of Obstetrics and Gynaecology, Karolinska Institutet/Karolinska University Hospital, Stockholm, Sweden
Hematology Division, Department of Medicine, Karolinska Institutet/Karolinska University Hospital, Stockholm, Sweden

Background:

It has been reported that patients with type 1 diabetes and young males with myocardial infarction form a fibrin clot which is tighter and more resistant to fibrinolysis in comparison to the fibrin clot formed by healthy controls. The structure/porosity of the fibin clot in patients with the Antiphospholipid syndrome (APS) has not previously been investigated and we hypothesised that a tight fibrin clot may contribute to the procoagulant state in these patients.

Materials and Methods:

We thus evaluated fibrin clot porosity in plasma-samples from 47 patients with Antifosfolipid Syndrome (APS), strictly fulfilling the Sydney criteria for APS. Previously established flow measurement technique was used to determine the fibrin clot porosity, as expressed as the Darcy constant (Ks). A low Ks level indicates a tighter fibrin clot. Ks-levels were compared to reference Ks values used in our laboratory obtained from healthy individuals. Within the APS-group, associations between Ks-levels and clinical manifestations, specificities of antiphospholipid antibodies (aPL) were explored. For a majority of the patients data regarding markers of inflammation and on-going medication was available to guide interpretation.

Results:

The mean Ks-levels were significantly lower in the samples from patients with APS (6.7, +/-2.9) as compared to reference Ks values (10.7+/-1.6), indicating a tighter fibrin network, p<0,0001. Within the APS-group Ks-levels did not vary depending on different clinical APS manifestations or aPL pattern. There was however a trend towards lower Ks-levels for the 20 patients with previous obstetric morbidity (5.7, +/-2,0) as compared to the 27 patients without this clinical manifestation (7.4 +/-3.2), p=0,09.

CRP-levels were generally low in the APS-patients (median 1.06, range 0–7.4, n=28). A majority of the patients were treated with anticoagulants: either vitamin K-antagonits or dalteparin (19/34) and many with statins (7/34). Patients treated with these two groups of drugs had all experienced a previous arterial or venous tromboembolic event. Almost half of the patients (15/34) were treated with low-dose ASA, sometimes in combination with vitamin K-antagonists or dalteparin. The majority of the ASA-treated patients (12/15) had a previous tromboembolic manifestation.

Conclusion:

APS-patients form a tighter and more stable fibrin clot as estimated by Ks levels, which measure in vitro fibrin clot porosity. There was a significant difference compared to reference material obtained from healthy individuals, even though a majority of the APS-patients were treated with low dose ASA, warfarin, dalteparin, statins or a combination of these drugs. To our knowledge this is a new finding.

We observed a trend towards a tighter fibrin network in APS-patients with obstetric morbidity compared to other individuals with APS. This finding could be attributed to differences in medications between the two groups.

Future studies including larger patient materials and controls may shed further light on the aetiology of APS and may thereby contribute to better risk assessment and management for APS patients.

To cite this abstract, please use the following information:
Vikerfors, Anna, Antovic, Aleksandra, Svenungsson, Elisabet, Bremme, Katarina, Holmstrom, Margareta; Decreased Fibrin Clot Porosity in Patients with Antifosfolipid Syndrome. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :7
DOI: 10.1002/art.27777

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