Heparin-induced thrombocytopenia requiring VA-ECMO management during percutaneous coronary intervention for acute coronary syndrome: A case report

UNLABELLED: Heparin-induced thrombocytopenia (HIT) is an immune-mediated disease with severe thromboembolic complications. HIT during percutaneous coronary intervention (PCI) can be fatal without prompt treatment. We report an unusual case of HIT observed during PCI for acute coronary syndrome (ACS). A 74-year-old female with a history of pulmonary embolism managed with unfractionated heparin (UFH) 2 years previously presented with intermittent chest pain. Coronary angiography revealed total occlusion of the mid-right coronary artery. Before and during the primary PCI, 14000 UFH units were administered. However, abundant thrombus formation in the non-culprit lesion was refractory to repeated thrombus aspiration. We suspected HIT, discontinued UFH, and administered argatroban. Despite repeated thrombus aspirations and balloon dilatation, coronary obstruction persisted; consequently, ventricular fibrillation refractory to multiple cardioversions occurred. Therefore, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) was required. Platelet counts rapidly decreased to <50 % of the baseline value, and serum was highly positive for IgG-specific antiplatelet factor 4/heparin antibodies. The patient was discharged with independent gait and no major neurological disorders. This is a clinically noteworthy case of rapidly developing HIT during primary PCI for ACS, requiring VA-ECMO management, with no major neurological complications. HIT may occur immediately after re-exposure to heparin long after the first exposure. LEARNING OBJECTIVE: Without prompt treatment, heparin-induced thrombocytopenia (HIT) during percutaneous coronary intervention (PCI) can be fatal. It may lead to refractory coronary obstruction, which may need to be managed by veno-arterial extracorporeal membrane oxygenation (VA-ECMO). We present a clinically noteworthy case of rapidly developing HIT during primary PCI for acute coronary syndrome, requiring VA-ECMO management, with no major neurological complications. Physicians must be mindful that HIT may occur immediately after re-exposure to heparin long after the first exposure.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Peer-reviewed clinical and outcomes research relevant to anticoagulation, leech therapy, and microsurgical flap management. Indexed in PubMed and verified against the NCBI record.

Leech-derived molecules this paper discusses, each with a full profile in the ASH compound registry:

Explore cómo esta investigación se conecta con la práctica clínica

More peer-reviewed studies in Ensayos clínicos.

• Leech Therapy for Knee Osteoarthritis — The Landmark RCT — Michalsen et al. (2003)
• Leech-Assisted Flap Salvage — Systematic Review of 277 Cases — Whitaker et al. (2012)
• Effects of hirudotherapy on liver functions, lipid profile, and insulin sensitivity in rats with metabolic syndrome — Bilden A et al. (2026)
• HIRUDOTHERAPY IN PRESBYACUZIS PRAECOX IN CLEAN-UP WORKERS AFTER THE CHORNOBYL ACCIDENT DURING THE POST-CATASTROPHE YEARS — Zabolotnyi D, Mishchanchuk N (2019)
• Wound healing potential of bark paste of Pongamia pinnata along with hirudotherapy: A case report — Balasooriya D, Karunarathna C, Uluwaduge I (2021)
• AIF-1 and RNASET2 Play Complementary Roles in the Innate Immune Response of Medicinal Leech — Baranzini N et al. (2019)
• Study on the effect of medicinal leech therapy (Hirudo medicinalis) on full-thickness excisional wound healing in the animal model — Zakian A et al. (2022)
• [Hirudo medicinalis-leech applications in plastic and reconstructive microsurgery--a literature review] — Knobloch K et al. (2007)
• The duration of rest and feeding greatly affects the re-breeding of ectoparasites: Hirudo verbana, Hirudo medicinalis and Hirudo orientalis — Aminov R, Frolov A, Aminova A (2022)
• Recombinant hirudin in clinical practice: focus on lepirudin — Greinacher A, Lubenow N (2001)

Browse all ASH-analysed research →