| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 2001;72:982
© 2001 The Society of Thoracic Surgeons
a Cardiothoracic Unit, 6th Floor, New Guy’s House, Guy’s Hospital, St Thomas’ St, London, England SE1 9RT, United Kingdom
b University of Glasgow, Department of Cardiac Surgery, The Royal Infirmary, 10 Alexandra Parade, Glasgow, Scotland G31 2ER, United Kingdom
e-mail: elijah.muriithi{at}gstt.sthames.nhs.uk
To the Editor
The letter by Misawa and colleagues presents data in which they demonstrate an increase in platelet aggregate size after heparinization in vivo. They consider that this contradicts the observation we made, in the study they quote and in an earlier study [1], that in vivo heparinization inhibited platelet macroaggregation. We note that in their current study, the authors stimulated platelets in vitro with ADP (0.3 µmol/L) and failed to detect macroaggregation before heparinization. In their previous studies [2], they used a higher concentration of ADP (2.5 µmol/L) and macroaggregation occurred under similar conditions to those described in their letter.
In their current study, Misawa and colleagues observed that after heparinization platelets formed macroaggregates in response to stimulation with the low concentration of ADP (0.3 µmol/L). This occurred because heparin has proaggregatory actions that increase existent platelet microaggregation ex vivo [3]. This increase in the activation state of unstimulated platelets would amplify platelet autocrine positive feedback responses to stimulation. Weak agonists depend upon these autocrine responses to induce a full aggregatory response, therefore platelet macroaggregation occurring after stimulation by weak agonists is largely the result of platelet secretion of ADP, thromboxane A2, and serotonin. The authors did not mention the in vitro anticoagulant they used. If it were citrate, this too would have exaggerated platelet responses; this has been pointed out to the authors before.
Unfortunately, despite the authors clearly pointing out that the inhibitory effect of heparin on platelet macroaggregation, which we detected, developed over time, they neglected to state how soon after heparinization they sampled blood or the time lag between sampling and aggregometry in their study. These time intervals may have been insufficient for the development of the inhibitory effect of in vivo heparin on platelet macroaggregation. Previous workers have observed that increasing the intensity of stimulation, in the presence of inhibitors of platelet macroaggregation, did not increase the size of the aggregates that formed, although the number of aggregates increased [4]. We therefore suggest that had the authors allowed the inhibitory effect of heparin on platelet macroaggregation to develop before performing aggregometry they may have made similar observations. The lack of attention to these considerations is a major flaw in their study which raises questions as to the validity of their conclusions.
In reply to the authors’ comments about the different techniques of aggregometry, we state that impedance aggregometry is a reliable measure of macroaggregation which correlates well with optical aggregometry, which itself is a measure of the coalescence of microaggregates into macroaggregates [5]. The previous study conducted by the authors confirms that optical aggregometry detects macroaggregation, but not microaggregation [2]. Furthermore, in our studies, we observed that even a 62% reduction in platelet count due to microaggregation did not cause alterations in the electrical impedance of whole blood [1].
References
Related Article
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
