Chapters authored
Is Restenosis/Reocclusion after Femoropopliteal Percutaneous Transluminal Angioplasty (PTA) the Consequence of Reduced Blood Flow, Inflammation, and/or Hemostasis Disturbances? By Mojca Božič-Mijovski, Vinko Boc, Vladka Salapura, Aleš Blinc and
Mojca Stegnar
Percutaneous transluminal angioplasty (PTA) is an established method for treatment of peripheral artery disease (PAD) of the femoropopliteal artery. However, in up to 50% of patients restenosis and/or reocclusion remain a frequent complication occurring in the first year after the procedure. In this study, we focused on the influence of compromised postprocedural infrapopliteal runoff of the affected limb, on the hypercoagulability as detected by a global hemostasis assay and on genetic predisposition to hypercoagulability and on the regulation of the inflammation through the nuclear receptor related 1 protein (NuRR1). Consecutive PAD patients treated by femoropopliteal PTA because of disabling claudication or critical limb ischemia were followed up by vascular ultrasound imaging at 1, 6, and 12 months after the procedure. Venous blood samples for hemostasis, inflammation, and gene analysis were obtained before and 24 h after PTA. One month after femoropopliteal PTA, 23% of patients with compromised runoff developed the combined end point restenosis/reocclusion in comparison to 11% with good runoff (p = 0.03). After 6 months, the differences were no longer significant. It was concluded that compromised postprocedural infrapopliteal runoff predisposes to early restenosis/reocclusion after femoropopliteal PTA and that the deterioration of infrapopliteal runoff in the year after femoropopliteal PTA is accompanied by worsening of long-term femoropopliteal patency. Patients were genotyped for the prothrombotic gene polymorphisms: platelet receptor glycoprotein IIIa T1565C, coagulation factor V G1691A, coagulation factor II G20210A, coagulation factor XII C(-4)T, and plasminogen activator inhibitor-1 4G5G. We were not able to show any association between these polymorphisms and the restenosis/reocclusion rate in patients treated with femoropopliteal PTA. Furthermore, no association between thrombin generation and restenosis/reocclusion rate was established. NuRR1 haplotypes significantly increased the restenosis/reocclusion rate after PTA (adjusted relative risks were 1.6, 95% CI 1.1–2.3 for haplotype 2 and 2.0, 95% CI 1.3–2.8 for haplotype 3). To conclude, this study suggested a significantly higher restenosis/reocclusion rate in patients with compromised runoff compared to patients with a good runoff 1 month after the procedure. Hypercoagulability was not associated with the restenosis/reocclusion rate, and the prothrombotic polymorphisms were equally distributed among patient with and without restenosis/reocclusion, suggesting minor or no role in restenosis/reocclusion. Haplotypes 2 and 3 in the NuRR1 gene significantly increased the restenosis/reocclusion rate, suggesting significant role of inflammation. In this ongoing study, further analysis on a larger group of patients is warranted.
Part of the book: Thrombosis, Atherosclerosis and Atherothrombosis
Laboratory Methodology Important in the Diagnosis and Prognosis of Antiphospholipid Syndrome By Polona Žigon, Mojca Božič-Mijovski, Mojca Frank Bertoncelj, Aleš
Ambrožič, Matija Tomšič, Alojzija Hočevar, Borut Božič, Snežna
Sodin Šemrl, Tanja Kveder and Saša Čučnik
Antiphospholipid syndrome (APS) is an autoimmune disease, characterized by thrombosis and pregnancy complications with persistently elevated levels of antiphospholipid antibodies (aPL). Recently, a unique mathematical calculation has been presented to assess the risk of thrombosis in patients with APS called antiphospholipid score or global antiphospholipid syndrome score (GAPSS). This new approach in the diagnosis of APS leads to the assessment of the risk of thrombosis considering the results of different aPL (lupus anticoagulants (LA), anticardiolipin antibodies (aCL), antibodies against β2GPI (anti-β2GPI), and phosphatidylserine-dependent antiprothrombin antibodies (aPS/PT) (isotypes IgG and IgM). This chapter provides an overview of the algorithm strategy for APS diagnosis with the aims of characterizing in detail the laboratory methodology of criteria aPL (LA, aCL, and anti-β2GPI) and noncriteria aPL, such as IgA aCL and IgA anti-β2GPI, anti-domain I β2GPI, and antiprothrombin antibodies. In order to improve APS diagnosis, several new approaches in aPL detection have recently been suggested, such as multiline immunodot assay, detection of aPL by flow cytometry using beads with particular surface properties, and the newly developed automated BioPlex system technology for parallel detection of aCL and anti-β2GPI antibodies of IgG, IgA, and IgM isotypes. A completely different and promising approach in future research lies in the potential of microRNAs as biomarkers for risk of thrombosis and/or obstetric complication.
Part of the book: Thrombosis, Atherosclerosis and Atherothrombosis