This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wesley, M. C. Articles by DiNardo, J. A. Search for Related Content PubMed PubMed Citation Articles by Wesley, M. C. Articles by DiNardo, J. A. Related Collections Cardiovascular Monitoring (Cardiac) Coagulation Pharmacology

---

CARDIOVASCULAR ANESTHESIOLOGY

The Effect of Milrinone on Platelet Activation as Determined by TEG® Platelet Mapping^TM

Mark C. Wesley, MD^*, Francis X. McGowan, MD^*, Robert A. Castro, MT^*, Sheahan Dissanayake, MT^*, David Zurakowski, PhD, and James A. DiNardo, MD^*

From the Departments of *Anesthesia, Perioperative and Pain Medicine, and Orthopaedic Surgery and Biostatistics, Children’s Hospital Boston and Harvard Medical School, Boston, Massachusetts.

Address correspondence and reprint requests to James A. DiNardo, MD, Department of Anesthesia, Children’s Hospital Boston, 300 Longwood Avenue, Boston, MA 02115. Address e-mail to james.dinardo{at}childrens.harvard.edu.

Abstract

BACKGROUND: Milrinone is a phosphodiesterase III inhibitor that increases intracellular cyclic adenosine monophosphate resulting in improved ventricular function and vasodilation. Increased intracellular levels of cyclic adenosine monophosphate also inhibit adenosine diphosphate (ADP) and arachidonic acid (AA)-induced platelet aggregation. We hypothesized that inhibition of ADP and AA-induced platelet activation by therapeutic blood concentrations of milrinone could be quantified using TEG® Platelet Mapping^TM.

METHODS: Blood was taken from 15 healthy adults who had not been taking antiplatelet medications. Milrinone was added to whole blood in three clinically relevant concentrations (30, 100, and 300 ng/mL). Conventional thromboelastography (TEG®) and TEG Platelet Mapping were performed on whole blood without milrinone and at each of these three concentrations.

RESULTS: Increased blood concentrations of milrinone were associated with increased inhibition of ADP and AA-induced platelet activation (P < 0.0001). Milrinone at a blood concentration of 300 ng/mL markedly impaired the platelet activation response to ADP and AA.

CONCLUSIONS: Therapeutic blood concentrations of milrinone exhibit a significant inhibitory effect on ADP and AA-induced platelet activation as determined by TEG Platelet Mapping, without affecting the conventional kaolin-activated TEG.

We suggest that TEG Platelet Mapping results be interpreted with caution in patients being treated with milrinone, and other drugs that modify platelet cyclic nucleotide concentrations.