Prostacyclin analogues decrease platelet aggregation but have no effect on thrombin generation, fibrin clot structure, and fibrinolysis in pulmonary arterial hypertension: PAPAYA coagulation
Aleksander Siniarski,
Aleksandra Gąsecka,
Miłosz Starczyński,
Marta Banaszkiewicz,
Szymon Darocha,
Adam Torbicki,
Marcin Kurzyna,
Krzysztof J. Filipiak,
Jadwiga Nessler,
Grzegorz Gajos
Affiliations
Aleksander Siniarski
Institute of Cardiology, Jagiellonian University Medical College, John Paul II Hospital
Aleksandra Gąsecka
Medical University of Warsaw
Miłosz Starczyński
Medical University of Warsaw
Marta Banaszkiewicz
Department of Pulmonary Circulation, Thromboembolic Diseases and Cardiology, Centre of Postgraduate Medical Education, European Health Centre Otwock, Poland
Szymon Darocha
Department of Pulmonary Circulation, Thromboembolic Diseases and Cardiology, Centre of Postgraduate Medical Education, European Health Centre Otwock, Poland
Adam Torbicki
Department of Pulmonary Circulation, Thromboembolic Diseases and Cardiology, Centre of Postgraduate Medical Education, European Health Centre Otwock, Poland
Marcin Kurzyna
Department of Pulmonary Circulation, Thromboembolic Diseases and Cardiology, Centre of Postgraduate Medical Education, European Health Centre Otwock, Poland
Krzysztof J. Filipiak
Maria Sklodowska-Curie Medical Academy
Jadwiga Nessler
Institute of Cardiology, Jagiellonian University Medical College, John Paul II Hospital
Grzegorz Gajos
Institute of Cardiology, Jagiellonian University Medical College, John Paul II Hospital
Prostacyclin (PGI2) analogues (epoprostenol, treprostonil, iloprost) are the cornerstone of pulmonary arterial hypertension (PAH) treatment. PGI2 analogues inhibit platelet reactivity, but their impact on coagulation and fibrinolysis parameters has not been elucidated. We compared platelet reactivity, thrombin generation, clot permeation, and lysis properties in patients with PAH treated with PGI2 analogues (n = 20) and those not receiving PGI2 analogues (n = 20). Platelet reactivity was lower in patients treated with PGI2 analogues, compared to the control group, as evaluated with arachidonic acid (ASPI), adenosine diphosphate (ADP), and thrombin receptor-activating peptide-6 (TRAP) tests (p = .009, p = .02, p = .007, respectively). In the subgroup analysis, both treprostinil and epoprostenol decreased platelet reactivity to the similar extent. There were no differences regarding thrombin generation, clot permeation, and lysis parameters in patients receiving and not receiving PGI2 analogues (p ≥ .60 for all). In the subgroup analysis, there were no differences regarding coagulation and fibrinolysis parameters between treprostinil, epoprostenol, and no PGI2 analogues. To conclude, patients with PAH treated with PGI2 analogues have reduced platelet reactivity, but similar clot formation and lysis parameters, compared to patients not receiving PGI2 analogues. Further randomized clinical trials are required to confirm these findings.
