PB1407 - No evidence of contact system activation after PICC placement in cancer patients: a prospective cohort study

Tuesday, June 25, 2024

13:45 – 14:45 ICT

Room: Exhibition Hall

Presenting Author(s)

Noori Guman, MD

MD, PhD Student
Amsterdam UMC location University of Amsterdam, Vascular Medicine, Amsterdam, Netherlands
Amsterdam, Noord-Holland, Netherlands

Co-Author(s)

Magdolna Nagy

PhD
Department of Biochemistry, Maastricht University Medical Center+, Maastricht, The Netherlands
Maastricht, Limburg, Netherlands
Henri M.H Spronk, PhD

Professor of Biochemistry of Atherothrombosis
Maastricht University
Maastricht, Limburg, Netherlands
Hugo ten Cate, MD, PHD

MD, PhD
Departments of Internal Medicine and Biochemistry, Maastricht University Medical Center+, Maastricht, The Netherlands
Maastricht, Limburg, Netherlands
Hv

Hanneke W. M. van Laarhoven

Professor, MD, PhD
Department of Medical Oncology, Amsterdam University Medical Centers, Amsterdam, The Netherlands
Amsterdam, Noord-Holland, Netherlands
Peter Verhamme, MD PhD

Professor
Department of Cardiovascular Diseases, University Hospitals Leuven, Leuven, Belgium
Leuven, Vlaams-Brabant, Belgium
HB

Harry Buller

emeritus professor
Amsterdam UMC location University of Amsterdam, Vascular Medicine, Amsterdam, Netherlands
Amsterdam, Noord-Holland, Netherlands
Michiel Coppens

MD, PhD
Department of Vascular Medicine, Amsterdam UMC location University of Amsterdam
Amsterdam, Noord-Holland, Netherlands
Nick van Es, MD PhD

Internist-vascular medicine
Department of Vascular Medicine, Amsterdam University Medical Centers, Amsterdam, the Netherlands
Amsterdam, Noord-Holland, Netherlands

Background: Activation of the intrinsic coagulation pathway through the contact system is thought to be a major driver of venous thromboembolism (VTE) related to peripherally inserted central venous catheters (PICCs) in cancer patients. Yet, data on contact system activation in this setting are scarce.

Aims: To measure the effect of PICC placement on contact system activation in cancer patients and subsequent PICC-related VTE.

Methods: Blood was collected from adult patients with cancer through antecubital venipuncture using a 21G needle into 3.2%(w/v) citrate and EDTA tubes just prior to PICC placement (V1), at day 7±3 (V2), and at day 20±5 (V3). Contact system activation was evaluated by measuring complexes of (activated) proteases (factor IXa, XIIa, XIa, prekallikrein [pKA], and thrombin with their natural inhibitors (antithrombin [AT] or C1-esterase inhibitors [C1-INH]. VTE was either symptomatic or asymptomatic detected by screening ultrasonography and CT venography at V3. Complex levels were compared between study visits, and patients with and without VTE after PICC placement using a Wilcoxon signed rank test, while maintaining a Bonferroni-corrected significance threshold of 0.007. The study was approved by a medical ethics committee and informed consent was obtained.

Results: Forty-one patients were included (Table) of whom 21 (51%) were diagnosed with VTE, including 19 (39%) upper-extremity DVTs, 2 (4.9%) pulmonary embolisms, and 4 (9.8%) superficial vein thrombosis. Complex levels of thrombin-antithrombin were higher at V3 compared with V1 (P=0.006); no differences were observed for the other complexes (Figure). Plasma levels at V1 were comparable in patients with and without VTE.

Conclusion(s): The study underlines the high risk of PICC-related VTE in cancer patients. No significant increase in contact system activation was observed after PICC placement, potentially indicating cancer-induced activation of the contact system prior to PICC placement. The results do not support use of the evaluated complexes to identify patients at high risk of VTE.