Background Determining the cause of a cerebrovascular event (CVE) can greatly influence further management of the patient. Testing for hypercoagulable states is an important part in etiologic evaluation, which comprises also testing for antiphospholipid antibodies (aPL).
Objectives The primary aim was to determine the frequency of patients experiencing CVE and fulfilling the criteria for antiphospholipid syndrome (APS)  or non-criteria APS (when persistently positive for non-criteria aPL against anti-cardiolipin (aCL) IgA, anti-β2 glycoprotein I (anti-β2GPI) IgA, anti-phosphatidylserine/prothrombin (aPS/PT) and/or anti-annexinV (aANXV) - all isotypes). The second aim was to determine whether persistence of aPL-positivity is a risk factor for experiencing an episode of CVE.
Methods Eighty-nine consecutive patients (mean age 48 years, range 18-67) with acute CVE (transitory ischemic attack, ischemic cerebrovascular insult or venous sinus thrombosis) were prospectively followed for one year after the index event. In the comparative group, there were 25 patients with migraine (mean age 40 years, range 18-58) and 20 patients with Huntington's disease (mean age 53 years, range 32-67 years). Demographic data on smoking, hypertension, hyperlipidemia, diabetes and the use of oral contraceptives were obtained by an interview and examinations. For all patients at least two sera taken 3 months apart were tested for lupus anticoagulants, aCL, anti-β2GPI, aPS/PT and aANXV of IgG, IgM and IgA isotypes [2-5]. Data were analysed with multiple logistic regression model.
Results We found that 20/89 (22%) CVE patients were persistently positive (at least twice, with the first testing not earlier than 3 months after CVE) for one or more isotypes of tested aPL, 17/20 had criteria aPL and 3/20 non-criteria aPL; comparing to 3/45 (7%) positive in comparative group. Using TOAST CVE classification  with aPL, the cause of CVE could be consecutively explained in 16% of the patients with formerly unexplained CVE (Figure 1). We found significant association between persistently present aPL (of any class or isotype) and CVE (cumulative OR 4.62; 95% CI 1.09 to 19.66). Among other risk factors, only hypertension and hyperlipidemia showed a significant association with CVE (OR 4.31; 95% CI 1.33 to 13.92 for hypertension and OR 15.23; 95% CI 4.13 to 56.15 for hyperlipidemia).
Conclusions aPL are one of the possible etiologic factors for CVE. In our group of patients 16% of formerly unexplained CVE could be explained with the persistent presence of aPL (as required to fulfill the APS criteria). Furthermore, aPL are not only a diagnostic parameter, but they themselves represent an independent risk factor for thrombosis. They should be tested, especially in cases without other recognized common etiologic factors for CVE.
Miyakis S, et al. J Thromb Haemost 2006; 4: 295-306.
Brandt JT, et al. Thromb Haemost 1995; 74: 1185-90.
Cucnik S, et al. Clin Chem Lab Med 2000; 38: 777-783.
Avcin T, et al. Rheumatology 2001; 40: 565-573.
Zigon P, et al. Clin Chem Lab Med 2011; 49: 1011-1018.
Adams HP Jr, et al. Stroke 1993; 24; 24: 35-41.
Disclosure of Interest None declared