Journal
PLATELETS
Volume 33, Issue 1, Pages 132-140Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/09537104.2020.1859101
Keywords
Left ventricular assist device; mechanical circulatory support; platelet dysfunction; platelet-leukocyte interaction; systemic inflammation
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Funding
- AKF program of the University of Tubingen (Tubingen, Germany) [AKF-330-0-0]
- grant DFG CRC/TR 240 Platelets Molecular, cellular and systemic functions in health and disease [374031971]
- DFG [CRC/TR 240 Platelets - Molecular, cellular and sy]
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Blood flow through left ventricular assist devices may lead to platelet activation and dysfunction, causing inflammatory tissue damage. This observational study investigated patients undergoing LVAD implantation and control patients undergoing CABG/AVR surgery. The study found that LVAD implantation is associated with platelet dysfunction and proinflammatory platelet-leukocyte binding, with less pronounced changes observed in patients treated with the newer generation LVAD HM3.
Blood flow through left ventricular assist devices (LVAD) may induce activation and dysfunction of platelets. Dysfunctional platelets cause coagulation disturbances and form platelet-neutrophil conjugates (PNC), which contribute to inflammatory tissue damage. This prospective observational cohort study investigated patients, who underwent implantation of a LVAD (either HeartMate II (HM II) (n = 7) or HeartMate 3 (HM 3) (n = 6)) and as control patients undergoing coronary artery bypass grafting (CABG) and/or aortic valve replacement (AVR) (n = 10). We performed platelet and leukocyte flow cytometry, analysis of platelet activation markers, and platelet aggregometry. Platelet CD42b expression was reduced at baseline and perioperatively in HM II/3 compared to CABG/AVR patients. After surgery the platelet activation marker beta-thromboglobulin and platelet microparticles increased in all groups while platelet aggregation decreased. Platelet aggregation was more significantly impaired in LVAD compared to CABG/AVR patients. PNC were higher in HM II compared to HM 3 patients. We conclude that LVAD implantation is associated with platelet dysfunction and proinflammatory platelet-leukocyte binding. These changes are less pronounced in patients treated with the newer generation LVAD HM 3. Future research should identify device-specific LVAD features, which are associated with the least amount of platelet activation to further improve LVAD therapy.
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