Antiplatelet drugs do not protect from platelet-leukocyte aggregation in coronary artery disease

Christian Schulte; Luise Pieper; Maike Frye; Christoph Waldeyer; Johannes T Neumann; Fabian J Brunner; Giordano Pula

doi:10.1016/j.jtha.2023.04.041

Antiplatelet drugs do not protect from platelet-leukocyte aggregation in coronary artery disease

Standard

Antiplatelet drugs do not protect from platelet-leukocyte aggregation in coronary artery disease. / Schulte, Christian ; Pieper, Luise ; Frye, Maike ; Waldeyer, Christoph ; Neumann, Johannes T ; Brunner, Fabian J; Pula, Giordano.

In: J THROMB HAEMOST, Vol. 22, No. 2, 02.2024, p. 553-557.

Research output: SCORING: Contribution to journal › Short publication › Research › peer-review

Harvard

Schulte, C , Pieper, L , Frye, M , Waldeyer, C , Neumann, JT , Brunner, FJ & Pula, G 2024, 'Antiplatelet drugs do not protect from platelet-leukocyte aggregation in coronary artery disease', J THROMB HAEMOST, vol. 22, no. 2, pp. 553-557. https://doi.org/10.1016/j.jtha.2023.04.041

APA

Schulte, C., Pieper, L., Frye, M., Waldeyer, C., Neumann, J. T., Brunner, F. J., & Pula, G. (2024). Antiplatelet drugs do not protect from platelet-leukocyte aggregation in coronary artery disease. J THROMB HAEMOST, 22(2), 553-557. https://doi.org/10.1016/j.jtha.2023.04.041

Vancouver

Schulte C , Pieper L , Frye M , Waldeyer C , Neumann JT , Brunner FJ et al. Antiplatelet drugs do not protect from platelet-leukocyte aggregation in coronary artery disease. J THROMB HAEMOST. 2024 Feb;22(2):553-557. https://doi.org/10.1016/j.jtha.2023.04.041

Bibtex

@article{d4bd0b53a17543e5b4b22435eb1170cd,

title = "Antiplatelet drugs do not protect from platelet-leukocyte aggregation in coronary artery disease",

abstract = "BACKGROUND: Despite advances in cardiovascular medicine, coronary artery disease (CAD) remains a leading cause of mortality. Among the pathophysiological features of this condition, platelet-leukocyte aggregates (PLAs) require further attention, either as diagnostic/prognostic disease markers or as potential interventional targets.OBJECTIVES: In this study, we characterized PLAs in patients with CAD. Primarily, we investigated the association of PLA levels with CAD diagnosis. In addition, the basal levels of platelet activation and degranulation were assessed in patients with CAD and controls, and their correlation with PLA levels was analyzed. Finally, the effect of antiplatelet treatments on circulating PLA numbers, basal platelet activation, and degranulation was studied in patients with CAD.METHODS: Participants were recruited at the Department of Cardiology of the University Heart and Vascular Centre Hamburg Eppendorf. Among patients admitted with severe chest pain, the diagnosis of CAD was made angiographically, and patients without CAD were used as controls. PLAs, platelet activation, and platelet degranulation were assessed by flow cytometry.RESULTS: Circulating PLAs and basal platelet degranulation levels were significantly higher in patients with CAD than in controls. Surprisingly, there was no significant correlation between PLA levels and platelet degranulation (or any other measured parameter). In addition, patients with CAD on antiplatelet therapy did not display lower PLA or platelet degranulation levels compared with those in controls.CONCLUSION: Overall, these data suggest a mechanism of PLA formation that is independent of platelet activation or degranulation and highlights the inefficiency of current antiplatelet treatments for the prevention of basal platelet degranulation and PLA formation.",

author = "Christian Schulte and Luise Pieper and Maike Frye and Christoph Waldeyer and Neumann, {Johannes T} and Brunner, {Fabian J} and Giordano Pula",

year = "2024",

month = feb,

doi = "10.1016/j.jtha.2023.04.041",

language = "English",

volume = "22",

pages = "553--557",

journal = "J THROMB HAEMOST",

issn = "1538-7933",

publisher = "Wiley-Blackwell",

number = "2",

}

RIS

TY - JOUR

T1 - Antiplatelet drugs do not protect from platelet-leukocyte aggregation in coronary artery disease

AU - Schulte, Christian

AU - Pieper, Luise

AU - Frye, Maike

AU - Waldeyer, Christoph

AU - Neumann, Johannes T

AU - Brunner, Fabian J

AU - Pula, Giordano

PY - 2024/2

Y1 - 2024/2

N2 - BACKGROUND: Despite advances in cardiovascular medicine, coronary artery disease (CAD) remains a leading cause of mortality. Among the pathophysiological features of this condition, platelet-leukocyte aggregates (PLAs) require further attention, either as diagnostic/prognostic disease markers or as potential interventional targets.OBJECTIVES: In this study, we characterized PLAs in patients with CAD. Primarily, we investigated the association of PLA levels with CAD diagnosis. In addition, the basal levels of platelet activation and degranulation were assessed in patients with CAD and controls, and their correlation with PLA levels was analyzed. Finally, the effect of antiplatelet treatments on circulating PLA numbers, basal platelet activation, and degranulation was studied in patients with CAD.METHODS: Participants were recruited at the Department of Cardiology of the University Heart and Vascular Centre Hamburg Eppendorf. Among patients admitted with severe chest pain, the diagnosis of CAD was made angiographically, and patients without CAD were used as controls. PLAs, platelet activation, and platelet degranulation were assessed by flow cytometry.RESULTS: Circulating PLAs and basal platelet degranulation levels were significantly higher in patients with CAD than in controls. Surprisingly, there was no significant correlation between PLA levels and platelet degranulation (or any other measured parameter). In addition, patients with CAD on antiplatelet therapy did not display lower PLA or platelet degranulation levels compared with those in controls.CONCLUSION: Overall, these data suggest a mechanism of PLA formation that is independent of platelet activation or degranulation and highlights the inefficiency of current antiplatelet treatments for the prevention of basal platelet degranulation and PLA formation.

AB - BACKGROUND: Despite advances in cardiovascular medicine, coronary artery disease (CAD) remains a leading cause of mortality. Among the pathophysiological features of this condition, platelet-leukocyte aggregates (PLAs) require further attention, either as diagnostic/prognostic disease markers or as potential interventional targets.OBJECTIVES: In this study, we characterized PLAs in patients with CAD. Primarily, we investigated the association of PLA levels with CAD diagnosis. In addition, the basal levels of platelet activation and degranulation were assessed in patients with CAD and controls, and their correlation with PLA levels was analyzed. Finally, the effect of antiplatelet treatments on circulating PLA numbers, basal platelet activation, and degranulation was studied in patients with CAD.METHODS: Participants were recruited at the Department of Cardiology of the University Heart and Vascular Centre Hamburg Eppendorf. Among patients admitted with severe chest pain, the diagnosis of CAD was made angiographically, and patients without CAD were used as controls. PLAs, platelet activation, and platelet degranulation were assessed by flow cytometry.RESULTS: Circulating PLAs and basal platelet degranulation levels were significantly higher in patients with CAD than in controls. Surprisingly, there was no significant correlation between PLA levels and platelet degranulation (or any other measured parameter). In addition, patients with CAD on antiplatelet therapy did not display lower PLA or platelet degranulation levels compared with those in controls.CONCLUSION: Overall, these data suggest a mechanism of PLA formation that is independent of platelet activation or degranulation and highlights the inefficiency of current antiplatelet treatments for the prevention of basal platelet degranulation and PLA formation.

U2 - 10.1016/j.jtha.2023.04.041

DO - 10.1016/j.jtha.2023.04.041

M3 - Short publication

C2 - 37225020

VL - 22

SP - 553

EP - 557

JO - J THROMB HAEMOST

JF - J THROMB HAEMOST

SN - 1538-7933

IS - 2

ER -