Platelet hyperresponsiveness and increased platelet-neutrophil aggregates in dogs with myxomatous mitral valve disease and pulmonary hypertension.
Autor: | Duler L; William R. Pritchard Veterinary Medicine Teaching Hospital, School of Veterinary Medicine, University of California Davis, Davis, California, USA., Visser L; Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado, USA., Nguyen N; Department of Surgical and Radiological Science, School of Veterinary Medicine, University of California Davis, Davis, California, USA., Johnson LR; Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California Davis, Davis, California, USA., Stern JA; Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California Davis, Davis, California, USA.; Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA., Li RHL; Department of Surgical and Radiological Science, School of Veterinary Medicine, University of California Davis, Davis, California, USA. |
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Jazyk: | angličtina |
Zdroj: | Journal of veterinary internal medicine [J Vet Intern Med] 2024 Jul-Aug; Vol. 38 (4), pp. 2052-2063. Date of Electronic Publication: 2024 May 21. |
DOI: | 10.1111/jvim.17067 |
Abstrakt: | Background: Pulmonary hypertension (PH) in dogs with myxomatous mitral valve disease (MMVD) is caused by increased pulmonary venous pressure. Thrombosis, vascular remodeling, and vasoconstriction mediated by platelets could exacerbate PH. Hypothesis: Dogs with PH will exhibit a hypercoagulable state, characterized by increased platelet activation, platelet-leukocyte, and platelet-neutrophil aggregate formation. Animals: Eleven dogs (≥3.5 kg) diagnosed with MMVD and PH and 10 dogs with MMVD lacking PH. Methods: Prospective cohort ex vivo study. All dogs underwent echocardiographic examination, CBC, 3-view thoracic radiographs, and heartworm antigen testing. Severity of PH and MMVD were assessed by echocardiography. Viscoelastic monitoring of coagulation was assessed using thromboelastography (TEG). Platelet activation and platelet-leukocyte/platelet-neutrophil interactions were assessed using flow cytometry. Plasma serotonin concentrations were measured by ELISA. Results: Unstimulated platelets from dogs with MMVD and PH expressed more surface P-selectin than MMVD controls (P = .03). Platelets from dogs with MMVD and PH had persistent activation in response to agonists. The number of platelet-leukocyte aggregates was higher in dogs with MMVD and PH compared with MMVD controls (P = .01). Ex vivo stimulation of whole blood resulted in higher numbers of platelet-neutrophil aggregates in dogs with MMVD and PH (P = .01). Assessment of hypercoagulability based on TEG or plasma serotonin concentrations did not differ between groups. Conclusion and Clinical Importance: Platelet hyperresponsiveness and increased platelet-neutrophil interaction occur in dogs with MMVD and PH, suggesting that platelets play a role of in the pathogenesis of PH. Clinical benefits of antiplatelet drugs in dogs with MMVD and PH require further investigation. (© 2024 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.) |
Databáze: | MEDLINE |
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