BACKGROUND AND AIM OF THE STUDY: The recent clinical history and experimental studies of the Medtronic Parallel (MP) valve suggest that bileaflet valve leakage flow is a primary initiator of thrombosis. These studies investigated the effects of physiologic leakage flow through a MP valve on various markers of blood damage. METHODS: A centrifugal pump was used to drive whole, human blood anticoagulated with PPACK through a circuit containing a MP 27 mm valve in the closed position (experimental runs) or a MP 27 mm valve in the open position (control runs). Samples were taken at set time intervals after the start of the pump. These samples were analyzed by cell counting, flow cytometry, and ELISA. RESULTS: Cell counts remained relatively constant in both the experimental and control runs. Increases in plasma hemoglobin concentration and the percentage of glycophorin A-positive fragments in the cell population were not significant in either the experimental or the control runs. Plasma platelet factor 4 activity and the percentage of the CD41-positive population which was positive for annexin V increased significantly (p <0.05) in the experimental runs compared with the control runs. CONCLUSION: The results indicate that bileaflet valve leakage flow causes significant platelet disruption, that erythrocytes are more resistant to disruption by leakage flow than platelets and granulocytes, and that annexin V binding to platelets and plasma platelet factor 4 activity are more sensitive markers of leakage induced blood damage than plasma hemoglobin concentration.
BACKGROUND AND AIM OF THE STUDY: The recent clinical history and experimental studies of the Medtronic Parallel (MP) valve suggest that bileaflet valve leakage flow is a primary initiator of thrombosis. These studies investigated the effects of physiologic leakage flow through a MP valve on various markers of blood damage. METHODS: A centrifugal pump was used to drive whole, human blood anticoagulated with PPACK through a circuit containing a MP 27 mm valve in the closed position (experimental runs) or a MP 27 mm valve in the open position (control runs). Samples were taken at set time intervals after the start of the pump. These samples were analyzed by cell counting, flow cytometry, and ELISA. RESULTS: Cell counts remained relatively constant in both the experimental and control runs. Increases in plasma hemoglobin concentration and the percentage of glycophorin A-positive fragments in the cell population were not significant in either the experimental or the control runs. Plasma platelet factor 4 activity and the percentage of the CD41-positive population which was positive for annexin V increased significantly (p <0.05) in the experimental runs compared with the control runs. CONCLUSION: The results indicate that bileaflet valve leakage flow causes significant platelet disruption, that erythrocytes are more resistant to disruption by leakage flow than platelets and granulocytes, and that annexin V binding to platelets and plasma platelet factor 4 activity are more sensitive markers of leakage induced blood damage than plasma hemoglobin concentration.