The Effect of Hematocrit on Platelet Adhesion: Experiments and Simulations

Spann, Andrew; Campbell, James E.; Fitzgibbon, Sean; Rodríguez, Armando; Andrew, P.; Blackbourne, Lorne H.; Shaqfeh, Eric S. G.

doi:10.1016/j.bpj.2016.06.024

Cited by 59 publications

(44 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The risk of VTE in the Tromsø and ARIC general population studies, however, appears to be increased at hematocrit levels much lower than for polycythemia vera. Mechanistically, high hematocrit increases platelet margination and adhesiveness . However, a more important mechanism by which hematocrit may increase VTE risk is via increased blood viscosity and venous stasis …”

Section: Discussionmentioning

confidence: 99%

“…Mechanistically, high hematocrit increases TA B L E 3 Hazard ratios (95% CIs) of total, provoked, and unprovoked VTE by groups of Visit 1 hematocrit, ARIC, 1987-1989 through 2015 Hematocrit (percentiles based on sex-race specific cut points) platelet margination and adhesiveness. [20][21][22] However, a more important mechanism by which hematocrit may increase VTE risk is via increased blood viscosity and venous stasis. 1,23 A previous population-based control study suggested iron deficiency anemia is associated with a 40% increase in VTE, 24 and, although not statistically significant, spline analysis in the Copenhagen Study suggested that VTE may be elevated in those with low hematocrit.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Hematocrit and incidence of venous thromboembolism

Folsom

Wang

Parikh

et al. 2020

Research and Practice in Thrombosis and Haemostasis

View full text Add to dashboard Cite

Background Patients with polycythemia vera with high hematocrit have increased risk of venous thromboembolism (VTE). Objective To determine whether high hematocrit in the general population is also associated with elevated VTE risk. Methods The prospective Atherosclerosis Risk in Communities Study performed a complete blood count in 13 891 adults aged 45 to 64 in 1987 to 1989. We identified incident hospitalized VTEs through 2015 and performed proportional hazards regression analyses using race‐sex–specific categorization of hematocrit percentiles (ie, <5th, 5th to <25th, 25th to <75th, 75th to <95th, and 95th‐100th percentiles, with the 25th to <75th percentile serving as the reference). Results Over a median follow‐up of 26 years, 800 participants had an incident venous thrombosis of the leg and/or a pulmonary embolism. There was a nonlinear association of hematocrit with VTE incidence, with risk elevated 72% for participants above the 95th percentile of hematocrit compared with the reference. Specifically, hazard ratios (95% confidence intervals) of incident VTE were 1.27 (0.91‐1.76), 1.06 (0.87‐1.28), 1 (reference), 1.17 (0.98‐1.40) and 1.72 (1.30‐2.27) across the 5 hematocrit percentiles, adjusted for age, race, sex, body mass index, smoking status and pack‐years, and other confounding variables. The association of high hematocrit with VTE was limited to provoked VTE, with little evidence for unprovoked VTE. Hemoglobin above the 95th percentile also was associated with an increased risk of VTE. In contrast, there were no significant associations of platelet, leukocyte, neutrophil, or lymphocyte counts with VTE incidence. Conclusion High hematocrit and hemoglobin in a general middle‐aged population sample were associated with increased long‐term risk of VTE, particularly provoked VTE.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hematocrit and incidence of venous thromboembolism

Folsom

Wang

Parikh

et al. 2020

Research and Practice in Thrombosis and Haemostasis

View full text Add to dashboard Cite

show abstract

“…However, data to support the use of fresh red blood cells preferentially for critically-ill patients is lacking (74). Hematocrit also contributes to platelet margination to the vessel wall under flow and low hematocrit is associated with increased bleeding time (75,76). …”

Section: Blood Transfusion To Treat Blood Failurementioning

confidence: 99%

Hemorrhagic blood failure

White

Ward

Pati

et al. 2017

Journal of Trauma and Acute Care Surgery

Self Cite

View full text Add to dashboard Cite

Our understanding of the events taking place within the blood following severe injury with hemorrhagic shock is quickly evolving. Traditional concepts have given way to a detailed and nuanced understanding of coagulopathy, bleeding, and shock at the cellular and biochemical levels. In doing so, the tremendous complexity of events taking place within the blood have been illuminated and present an additional challenge. In this review, we seek to understand shock, endotheliopathy, and coagulopathy not as isolated events, but rather as the result of changes taking place within a single dynamic organ system. This review will highlight the key linkages existing between blood and endothelium and how these processes are perturbed by hemorrhagic shock to produce a syndrome that we call “hemorrhagic blood failure.” From this perspective, it may be regarded that the blood organ system fails in providing its vital functions predictably after injury. We review how accumulation of oxygen debt during shock leads to endotheliopathy and coagulopathy, and how current transfusion strategies may impact the syndrome of hemorrhagic blood failure.

show abstract

“…This layer is known to contribute in the reduction of the blood viscosity or plasma skimming as blood perfuses the smaller vessels (Freund, 2014;Pries and Secomb, 2003). In addition, the migration of the red blood cells induces the margination of stiffer platelets by volume exclusion (Spann et al, 2016;Fitzgibbon et al, 2015;Reasor et al, 2013;Vahidkhah, 2015;Haga et al, 1998;Bächer et al, 2018). These marginated platelets are now better located to participate in reactions with the endothelial cells in the event of an injury when the clotting cascade begins (Mitrophanov et al, 2014;Govindarajan et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Effect of Cytoplasmic Viscosity on Red Blood Cell Migration in Small Arteriole-level Confinements

Saadat

Guido

Shaqfeh³

2019

Preprint

View full text Add to dashboard Cite

The dynamics of red blood cells in small arterioles are important as these dynamics affect many physiological processes such as hemostasis and thrombosis. However, studying red blood cell flows theoretically is challenging due to the complex shapes of red blood cells and the non-trivial viscosity contrast of a red blood cell. To date little progress has been made studying small arteriole flows (20-40µm) with a hematocrit (red blood cell volume fraction) of 10-20% and a physiological viscosity contrast. In this work, we present the results of large-scale simulations that show how the channel size, viscosity contrast of the red blood cells, and hematocrit effect cell distributions and the cell free layer in these systems. We utilize a massively-parallel immersed boundary code coupled to a finite volume solver to capture particle resolved physics in these systems. We show that channel size qualitatively changes how the cells distribute in the channel. Our results also indicate that at a hematocrit of 10% that the viscosity contrast is not negligible when calculating the cell free layer thickness. We explain this result by comparing lift and collision trajectories of cells at different viscosity contrasts.

show abstract

The Effect of Hematocrit on Platelet Adhesion: Experiments and Simulations

Cited by 59 publications

References 56 publications

Hematocrit and incidence of venous thromboembolism

Hematocrit and incidence of venous thromboembolism

Hemorrhagic blood failure

Effect of Cytoplasmic Viscosity on Red Blood Cell Migration in Small Arteriole-level Confinements

Contact Info

Product

Resources

About