Therapeutic concentrations of heparin augment platelet activation at the time of coronary angiography

Tasneem Zehra Naqvi, P. K. Shah, P. A. Ivey, M. D. Molloy, P. Linn, M. Linker-Israeli, B. Cercek, S. Kaul

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Background: Besides its anticoagulant effects, heparin is known to alter platelet (PLT) function. We examined the effects of unfractionated heparin on PLT function in patients with stable coronary artery disease (CAD). Methods and Results: PLT function was evaluated by whole-blood flow cytometry to detect PLT CD62 expression and by impedance aggregometry to assess platelet aggregation (PA) before and after bolus intravenous administration of low- dose heparin (2713 ± 1231 U) in 16 patients undergoing coronary angiography (group 1) and high-dose heparin (7937 ± 2414 U) in 16 patients undergoing coronary angioplasty (group 2). Activated clotting time (ACT) and plasma antifactor-Xa heparin levels also were measured. Heparin increased PLT CD62 expression, which was significantly more pronounced in group 1 patients with plasma heparin levels less than 0.7 U/mL and ACT of 222 ± 52 seconds compared with group 2 patients with heparin levels greater than 0.7 U/mL and ACT of 365 ± 86 seconds (8 ± 9 v -1 ± 4% change in resting PLTs, P = .01, and 11 ± 12 v 1 ± 6% increase in adenosine diphosphate (ADP) [5 μM]- stimulated PLTs, P = .02). Heparin produced a slight increase in PA in group 1 patients (1.4 ± 5.3 ohms) as compared with the group 2 patients, where it significantly suppressed PA (-3.0 ± 5.3 ohms, P < .05 v group l). A strong and statistically significant negative correlation between change in platelet CD62 expression and heparin concentration was observed in group 1 patients (r = -.5, P = .05, -ADP; r = -.65, P = .006, +ADP), whereas this relationship was weak and did not reach statistical significance in group 2 patients (r = -0.4, P = .2, -ADP; r = .11, P = 0.9; + ADP). Conclusion: Bolus administration of intravenous heparin augmented PLT activation in patients at clinically relevant anticoagulant concentrations (<0.7 U/mL). These findings may have implications for optimal dosing strategy for heparin as an antithrombotic agent in clinical situations characterized by platelet- dependent thrombotic events.

Original languageEnglish (US)
Pages (from-to)91-102
Number of pages12
JournalJournal of Cardiovascular Pharmacology and Therapeutics
Volume3
Issue number2
StatePublished - 1998
Externally publishedYes

Fingerprint

Platelet Activation
Coronary Angiography
Heparin
Blood Platelets
Adenosine Diphosphate
Therapeutics
Platelet Aggregation
Intravenous Administration
Anticoagulants
Fibrinolytic Agents
Electric Impedance
Angioplasty
Coronary Artery Disease
Flow Cytometry

Keywords

  • Aggregation
  • Coagulation
  • Flow cytometry
  • Platelets

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Naqvi, T. Z., Shah, P. K., Ivey, P. A., Molloy, M. D., Linn, P., Linker-Israeli, M., ... Kaul, S. (1998). Therapeutic concentrations of heparin augment platelet activation at the time of coronary angiography. Journal of Cardiovascular Pharmacology and Therapeutics, 3(2), 91-102.

Therapeutic concentrations of heparin augment platelet activation at the time of coronary angiography. / Naqvi, Tasneem Zehra; Shah, P. K.; Ivey, P. A.; Molloy, M. D.; Linn, P.; Linker-Israeli, M.; Cercek, B.; Kaul, S.

In: Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 3, No. 2, 1998, p. 91-102.

Research output: Contribution to journalArticle

Naqvi, TZ, Shah, PK, Ivey, PA, Molloy, MD, Linn, P, Linker-Israeli, M, Cercek, B & Kaul, S 1998, 'Therapeutic concentrations of heparin augment platelet activation at the time of coronary angiography', Journal of Cardiovascular Pharmacology and Therapeutics, vol. 3, no. 2, pp. 91-102.
Naqvi, Tasneem Zehra ; Shah, P. K. ; Ivey, P. A. ; Molloy, M. D. ; Linn, P. ; Linker-Israeli, M. ; Cercek, B. ; Kaul, S. / Therapeutic concentrations of heparin augment platelet activation at the time of coronary angiography. In: Journal of Cardiovascular Pharmacology and Therapeutics. 1998 ; Vol. 3, No. 2. pp. 91-102.
@article{fc4b37edd88e4fe084dab8b1b485571d,
title = "Therapeutic concentrations of heparin augment platelet activation at the time of coronary angiography",
abstract = "Background: Besides its anticoagulant effects, heparin is known to alter platelet (PLT) function. We examined the effects of unfractionated heparin on PLT function in patients with stable coronary artery disease (CAD). Methods and Results: PLT function was evaluated by whole-blood flow cytometry to detect PLT CD62 expression and by impedance aggregometry to assess platelet aggregation (PA) before and after bolus intravenous administration of low- dose heparin (2713 ± 1231 U) in 16 patients undergoing coronary angiography (group 1) and high-dose heparin (7937 ± 2414 U) in 16 patients undergoing coronary angioplasty (group 2). Activated clotting time (ACT) and plasma antifactor-Xa heparin levels also were measured. Heparin increased PLT CD62 expression, which was significantly more pronounced in group 1 patients with plasma heparin levels less than 0.7 U/mL and ACT of 222 ± 52 seconds compared with group 2 patients with heparin levels greater than 0.7 U/mL and ACT of 365 ± 86 seconds (8 ± 9 v -1 ± 4{\%} change in resting PLTs, P = .01, and 11 ± 12 v 1 ± 6{\%} increase in adenosine diphosphate (ADP) [5 μM]- stimulated PLTs, P = .02). Heparin produced a slight increase in PA in group 1 patients (1.4 ± 5.3 ohms) as compared with the group 2 patients, where it significantly suppressed PA (-3.0 ± 5.3 ohms, P < .05 v group l). A strong and statistically significant negative correlation between change in platelet CD62 expression and heparin concentration was observed in group 1 patients (r = -.5, P = .05, -ADP; r = -.65, P = .006, +ADP), whereas this relationship was weak and did not reach statistical significance in group 2 patients (r = -0.4, P = .2, -ADP; r = .11, P = 0.9; + ADP). Conclusion: Bolus administration of intravenous heparin augmented PLT activation in patients at clinically relevant anticoagulant concentrations (<0.7 U/mL). These findings may have implications for optimal dosing strategy for heparin as an antithrombotic agent in clinical situations characterized by platelet- dependent thrombotic events.",
keywords = "Aggregation, Coagulation, Flow cytometry, Platelets",
author = "Naqvi, {Tasneem Zehra} and Shah, {P. K.} and Ivey, {P. A.} and Molloy, {M. D.} and P. Linn and M. Linker-Israeli and B. Cercek and S. Kaul",
year = "1998",
language = "English (US)",
volume = "3",
pages = "91--102",
journal = "Journal of Cardiovascular Pharmacology and Therapeutics",
issn = "1074-2484",
publisher = "SAGE Publications Ltd",
number = "2",

}

TY - JOUR

T1 - Therapeutic concentrations of heparin augment platelet activation at the time of coronary angiography

AU - Naqvi, Tasneem Zehra

AU - Shah, P. K.

AU - Ivey, P. A.

AU - Molloy, M. D.

AU - Linn, P.

AU - Linker-Israeli, M.

AU - Cercek, B.

AU - Kaul, S.

PY - 1998

Y1 - 1998

N2 - Background: Besides its anticoagulant effects, heparin is known to alter platelet (PLT) function. We examined the effects of unfractionated heparin on PLT function in patients with stable coronary artery disease (CAD). Methods and Results: PLT function was evaluated by whole-blood flow cytometry to detect PLT CD62 expression and by impedance aggregometry to assess platelet aggregation (PA) before and after bolus intravenous administration of low- dose heparin (2713 ± 1231 U) in 16 patients undergoing coronary angiography (group 1) and high-dose heparin (7937 ± 2414 U) in 16 patients undergoing coronary angioplasty (group 2). Activated clotting time (ACT) and plasma antifactor-Xa heparin levels also were measured. Heparin increased PLT CD62 expression, which was significantly more pronounced in group 1 patients with plasma heparin levels less than 0.7 U/mL and ACT of 222 ± 52 seconds compared with group 2 patients with heparin levels greater than 0.7 U/mL and ACT of 365 ± 86 seconds (8 ± 9 v -1 ± 4% change in resting PLTs, P = .01, and 11 ± 12 v 1 ± 6% increase in adenosine diphosphate (ADP) [5 μM]- stimulated PLTs, P = .02). Heparin produced a slight increase in PA in group 1 patients (1.4 ± 5.3 ohms) as compared with the group 2 patients, where it significantly suppressed PA (-3.0 ± 5.3 ohms, P < .05 v group l). A strong and statistically significant negative correlation between change in platelet CD62 expression and heparin concentration was observed in group 1 patients (r = -.5, P = .05, -ADP; r = -.65, P = .006, +ADP), whereas this relationship was weak and did not reach statistical significance in group 2 patients (r = -0.4, P = .2, -ADP; r = .11, P = 0.9; + ADP). Conclusion: Bolus administration of intravenous heparin augmented PLT activation in patients at clinically relevant anticoagulant concentrations (<0.7 U/mL). These findings may have implications for optimal dosing strategy for heparin as an antithrombotic agent in clinical situations characterized by platelet- dependent thrombotic events.

AB - Background: Besides its anticoagulant effects, heparin is known to alter platelet (PLT) function. We examined the effects of unfractionated heparin on PLT function in patients with stable coronary artery disease (CAD). Methods and Results: PLT function was evaluated by whole-blood flow cytometry to detect PLT CD62 expression and by impedance aggregometry to assess platelet aggregation (PA) before and after bolus intravenous administration of low- dose heparin (2713 ± 1231 U) in 16 patients undergoing coronary angiography (group 1) and high-dose heparin (7937 ± 2414 U) in 16 patients undergoing coronary angioplasty (group 2). Activated clotting time (ACT) and plasma antifactor-Xa heparin levels also were measured. Heparin increased PLT CD62 expression, which was significantly more pronounced in group 1 patients with plasma heparin levels less than 0.7 U/mL and ACT of 222 ± 52 seconds compared with group 2 patients with heparin levels greater than 0.7 U/mL and ACT of 365 ± 86 seconds (8 ± 9 v -1 ± 4% change in resting PLTs, P = .01, and 11 ± 12 v 1 ± 6% increase in adenosine diphosphate (ADP) [5 μM]- stimulated PLTs, P = .02). Heparin produced a slight increase in PA in group 1 patients (1.4 ± 5.3 ohms) as compared with the group 2 patients, where it significantly suppressed PA (-3.0 ± 5.3 ohms, P < .05 v group l). A strong and statistically significant negative correlation between change in platelet CD62 expression and heparin concentration was observed in group 1 patients (r = -.5, P = .05, -ADP; r = -.65, P = .006, +ADP), whereas this relationship was weak and did not reach statistical significance in group 2 patients (r = -0.4, P = .2, -ADP; r = .11, P = 0.9; + ADP). Conclusion: Bolus administration of intravenous heparin augmented PLT activation in patients at clinically relevant anticoagulant concentrations (<0.7 U/mL). These findings may have implications for optimal dosing strategy for heparin as an antithrombotic agent in clinical situations characterized by platelet- dependent thrombotic events.

KW - Aggregation

KW - Coagulation

KW - Flow cytometry

KW - Platelets

UR - http://www.scopus.com/inward/record.url?scp=0032454382&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032454382&partnerID=8YFLogxK

M3 - Article

VL - 3

SP - 91

EP - 102

JO - Journal of Cardiovascular Pharmacology and Therapeutics

JF - Journal of Cardiovascular Pharmacology and Therapeutics

SN - 1074-2484

IS - 2

ER -