Thrombosis research
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Pregnancy-associated high-risk pulmonary embolism (PE) is among the most frequent causes of maternal mortality in the Western world, by causing hemodynamic instability and circulatory failure through a large thrombotic pulmonary obstruction. The very challenging management of these dramatic situations comprises the need to quickly select a therapy of pulmonary reperfusion or hemodynamic replacement, while taking into account both maternal and fetal risks. ⋯ For women in the peripartum and early post-partum period, non-fibrinolytic treatments may be preferred as a first-line treatment, if available, because of the particularly high bleeding risk. In all cases, pregnancy-associated high-risk PE requires a multidisciplinary approach involving PE response teams and obstetricians.
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Thrombosis research · Aug 2021
ReviewSpontaneous HIT syndrome: Knee replacement, infection, and parallels with vaccine-induced immune thrombotic thrombocytopenia.
Heparin-induced thrombocytopenia (HIT) is characterized clinically by thrombocytopenia, hypercoagulability, and increased thrombosis risk, and serologically by platelet-activating anti-platelet factor 4 (PF4)/heparin antibodies. Heparin-"induced" acknowledges that HIT is usually triggered by a proximate immunizing exposure to heparin. However, certain non-heparin medications (pentosan polysulfate, hypersulfated chondroitin sulfate, fondaparinux) can trigger "HIT". ⋯ Vaccine-induced immune thrombotic thrombocytopenia (VITT) features unusual thromboses (cerebral venous thrombosis, splanchnic vein thrombosis) similar to those seen in spontaneous HIT syndrome. The emerging concept is that classic HIT reflects platelet-activating anti-PF4/heparin antibodies whereas spontaneous HIT syndrome and other atypical "autoimmune HIT" presentations (delayed-onset HIT, persisting HIT, heparin "flush" HIT) reflect heparin-independent platelet-activating anti-PF4 antibodies-although the precise relationships between PF4 epitope targets and the clinical syndromes remain to be determined. Treatment of spontaneous HIT syndrome includes non-heparin anticoagulation (direct oral Xa inhibitors favored over direct thrombin inhibitors) and high-dose immunoglobulin.