Background Patients with antiphospholipid syndrome (APS) are prone to thromboembolism. So far, the only predictive parameters for further complications are their number in patient’s history and perhaps the titre of aPL. Derived from clinical investigation of stroke and obvious analogies between cerebrovascular ischemia (CVI) in patients with carotid artery disease (CAD) and patients with APS, a novel non-invasive method using transcranial Doppler (TCD) is used for detection of so called ‘microembolic signals’ (MES) in the cerebral vasculature. In patients with CAD, these ‘microemboli’ proved to correlate with past and impending symptoms of CVI allowing for therapeutic stratification by their detectability. We found very similar signals in the cerebral bloodstream of APS patients with a history of CVI.
Detectability of MES in APS implies occlusive thromboembolism and not vasculitis as the underlying mechanism at least in arterial cerebrovascular manifestations of this state. However, Doppler signal properties (i.e. the reflected energy) do not allow for direct estimation of the signal’s substrate size or -composition.
Objectives To further elucidate the pathophysilogical substrate of MES in APS.
Methods Repeated TCD monitoring in a 38 year old female APS patient with ongoing transitory ischaemic attacks and high rate of MES before and after intravenous administration of Tirofiban, a potent, synthetic, highly selective and reversible inhibitor of platelet gpIIb/IIIa receptor which binds fibrinogen on the platelet’s surface.
Results Within one hour the rate of MES decreased from ~50/hr to <5/hr on three successive occasions accompanied by cessation of clinical symptoms. Using flowcytometry, platelet-leucocyte aggregates found increased before administration of Tirofiban were also reduced considerably.
Conclusion The finding that MES are influenced by blockade of the platelet gpIIb/IIIa receptor and correlate with platelet-leucocyte aggregates argues for a central role of thrombocytes in APS with CVI. This might favour to look for thrombocyte targeted prophylactic therapy in APS. Whether detection of MES can also serve to monitor such therapies has still to be proved.
Specker C, Rademacher J, Sohngen D, Sitzer M, Janda I, Siebler M, Steinmetz H, Schneider M. Cerebral microemboli in patients with antiphospholipid syndrome. Lupus 1997;6(8):638–44
Specker C, Perniok A, Brauckmann U, Siebler M, Schneider M. Detection of cerebral microemboli in APS – introducing a novel investigation method and implications of analogies with Carotid artery disease. Lupus 1998;7(Suppl 2):75–80
Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.