Tomasz Ciurus, Anetta Undas, Malgorzata Lelonek A B Figure 1. A mass attached to the aortic arch wall (arrow in the image) and closing brachiocephalic trunk ostium in MRI with a contrast injection (no amplification of the contrast in sequence of perfusion). A – a perfusion scan, B – a cine image Ao – aorta, LV – left ventricle a well-demarcated mass attached to the aortic arch wall and obstructing the brachiocephalic trunk ostium (Figure 1 A-B). There was no amplification of the contrast in the perfusion image of MRI, thus indicating the thrombus (Figure 1 A). The patient received intravenous unfractionat- ed heparin followed by vitamin K antagonist (VKA) administration with a target international normal- ized ratio of 2-3 that resulted in a slight reduction in thrombus size within the first 3 weeks of thera- py. At 12 months transoesophageal echocardiogra- phy, however, did not show any pathology in the aortic arch. Given the data showing altered fibrin clot prop- erties in patients with venous thromboembolism Table I. Comparisons of fibrin clot features Feature Ks [10–9 cm2] Compaction [%] Lag phase [s] ΔAbs (405 nm) t50% [min] D-D max [mg/l] Patient 6.8 49 43 0.89 9.7 3.98 Controls with INR 2-3 (n = 20) 8.6 ±1 63.8 ±6.2 46.2 ±3.4 0.72 (0.68-0.8) 7 ±1 3.1 (2.6-3.6) D-D rate [mg/l/min] 0.069 0.079 (0.075-0.085) Values are given as mean ± SD. Ks indicates permeability coefficient, ΔAbs (405 nm) – maximum absorbance of fibrin gel at 405 nm deter- mined by using turbidimetry, t50% – half-lysis time, D-D max – maxi- mum D-dimer levels in lysis assay 2, D-D rate – maximum rate of increase in D-dimer levels in lysis assay 2 [6] and ischemic stroke [7], we performed plasma fibrin structure/function analysis [6], which demon- strated markedly altered fibrin clot characteristics, including reduced clot permeability (a marker of pore size, Ks) and compaction (a marker of clot stiff- ness) combined with faster clot formation (short- er lag phase of fibrin formation) and impaired clot lysis (prolonged lysis time and slower rate of D-dimer release from clots) as compared to values obtained for anticoagulated patients with distal deep vein thrombosis (Table I). Traditional cardiovascular risk factors explain arterial thrombosis in older patients [1], especially after interventions [8]. In young patients without cardiac risk factors, mostly arterial thrombotic events occurred related to atrial fibrillation or fac- tor V Leiden. Thrombophilia screening fails to iden- tify predisposing factors in 30% to 50% of idiopathic thrombosis patients [3]. A new risk factor for pro- thrombotic events revealed in venous thromboem- bolism, altered fibrin clot properties, is rarely described in patients with arterial thrombosis [3]. This study is the first to demonstrate AAT in a man with altered clot properties and reduced sus- ceptibility to lysis. In the search for any cause of AAT in the patient with negative thrombophilia screening, abnormal features of plasma fibrin clot structure/function were detected. The propensity to faster formation of compact fibrin clots is asso- ciated with resistance to fibrinolysis, as evidenced by longer lysis time and lower lysis rate (Table I). By analogy to cryptogenic venous thrombosis [6] or stroke [7], such properties could also explain the 734 Arch Med Sci 4, August / 2012