Platelet activation during dobutamine stress echocardiography

M. T. Galloway, T. G. Paglieroni, Theodore Wun, F. J. Arena, W. R. Lewis

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Background: Dobutamine stress echocardiography (DSE) is a common, useful test for the evaluation of coronary artery disease. Two of 650 patients who underwent DSE at our institution sustained nonfatal myocardial infarction either during DSE or shortly thereafter. Although DSE is associated with low morbidity rates, this rate is higher than our experience with exercise treadmill testing (ETT). Methods: Six individuals who did not undergo DSE or ETT were enrolled to evaluate direct in vitro effects of dobutamine on platelets. Nine patients undergoing DSE and seven patients undergoing ETT were enrolled to evaluate in vive platelet activation. We used flow cytometry and fluorescent-labeled monoclonal antibodies to activation-dependent platelet antigens to detect dobutamine-associated platelet activation both in vitro and in vivo. Results: In vitro we found a synergistic increase in epinephrine-induced CD62 expression in the presence of dobutamine. The response to the combination of dobutamine and epinephrine was 151% to 565% of the expected response. In vivo there was a dose- and time-dependent rise in the percentage of platelets expressing CD62 in all nine subjects undergoing DSE. The median percentage of platelets expressing CD62 was 1.6% (range 0.1% to 6.8%), 6.5% (range 0.2% to 11.7%), 11.6% (range 5.9% to 19.1%), and 11.4% (range 7.2% to 25.0%) in the samples obtained at baseline, 20 μg/kg/min of dobutamine, 40 μg/kg/min of dobutamine, and during the recovery phase, respectively (repeated measures analysis of variance, p = 0.02). There was no increase in CD62 expression on platelets obtained from seven patients at peak ETT. The median percentage of CD62 at baseline ETT was 1.9% (range 0.2% to 7.3%) and at peak was 2.6% (range 0.4% to 7.0%) (p = 0.156, Wilcoxon signed rank test). Conclusion: We conclude that platelet activation occurs in vive in patients undergoing DSE and that this may be caused by a synergistic effect of dobutamine with physiologic platelet agonists.

Original languageEnglish (US)
Pages (from-to)888-900
Number of pages13
JournalAmerican Heart Journal
Volume135
Issue number5 I
DOIs
StatePublished - 1998

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Stress Echocardiography
Platelet Activation
Dobutamine
Blood Platelets
Exercise
Epinephrine
Nonparametric Statistics
Coronary Artery Disease
Analysis of Variance
Flow Cytometry
Myocardial Infarction
Monoclonal Antibodies
Morbidity
Antigens

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Galloway, M. T., Paglieroni, T. G., Wun, T., Arena, F. J., & Lewis, W. R. (1998). Platelet activation during dobutamine stress echocardiography. American Heart Journal, 135(5 I), 888-900. https://doi.org/10.1016/S0002-8703(98)70051-1

Platelet activation during dobutamine stress echocardiography. / Galloway, M. T.; Paglieroni, T. G.; Wun, Theodore; Arena, F. J.; Lewis, W. R.

In: American Heart Journal, Vol. 135, No. 5 I, 1998, p. 888-900.

Research output: Contribution to journalArticle

Galloway, MT, Paglieroni, TG, Wun, T, Arena, FJ & Lewis, WR 1998, 'Platelet activation during dobutamine stress echocardiography', American Heart Journal, vol. 135, no. 5 I, pp. 888-900. https://doi.org/10.1016/S0002-8703(98)70051-1
Galloway, M. T. ; Paglieroni, T. G. ; Wun, Theodore ; Arena, F. J. ; Lewis, W. R. / Platelet activation during dobutamine stress echocardiography. In: American Heart Journal. 1998 ; Vol. 135, No. 5 I. pp. 888-900.
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abstract = "Background: Dobutamine stress echocardiography (DSE) is a common, useful test for the evaluation of coronary artery disease. Two of 650 patients who underwent DSE at our institution sustained nonfatal myocardial infarction either during DSE or shortly thereafter. Although DSE is associated with low morbidity rates, this rate is higher than our experience with exercise treadmill testing (ETT). Methods: Six individuals who did not undergo DSE or ETT were enrolled to evaluate direct in vitro effects of dobutamine on platelets. Nine patients undergoing DSE and seven patients undergoing ETT were enrolled to evaluate in vive platelet activation. We used flow cytometry and fluorescent-labeled monoclonal antibodies to activation-dependent platelet antigens to detect dobutamine-associated platelet activation both in vitro and in vivo. Results: In vitro we found a synergistic increase in epinephrine-induced CD62 expression in the presence of dobutamine. The response to the combination of dobutamine and epinephrine was 151{\%} to 565{\%} of the expected response. In vivo there was a dose- and time-dependent rise in the percentage of platelets expressing CD62 in all nine subjects undergoing DSE. The median percentage of platelets expressing CD62 was 1.6{\%} (range 0.1{\%} to 6.8{\%}), 6.5{\%} (range 0.2{\%} to 11.7{\%}), 11.6{\%} (range 5.9{\%} to 19.1{\%}), and 11.4{\%} (range 7.2{\%} to 25.0{\%}) in the samples obtained at baseline, 20 μg/kg/min of dobutamine, 40 μg/kg/min of dobutamine, and during the recovery phase, respectively (repeated measures analysis of variance, p = 0.02). There was no increase in CD62 expression on platelets obtained from seven patients at peak ETT. The median percentage of CD62 at baseline ETT was 1.9{\%} (range 0.2{\%} to 7.3{\%}) and at peak was 2.6{\%} (range 0.4{\%} to 7.0{\%}) (p = 0.156, Wilcoxon signed rank test). Conclusion: We conclude that platelet activation occurs in vive in patients undergoing DSE and that this may be caused by a synergistic effect of dobutamine with physiologic platelet agonists.",
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N2 - Background: Dobutamine stress echocardiography (DSE) is a common, useful test for the evaluation of coronary artery disease. Two of 650 patients who underwent DSE at our institution sustained nonfatal myocardial infarction either during DSE or shortly thereafter. Although DSE is associated with low morbidity rates, this rate is higher than our experience with exercise treadmill testing (ETT). Methods: Six individuals who did not undergo DSE or ETT were enrolled to evaluate direct in vitro effects of dobutamine on platelets. Nine patients undergoing DSE and seven patients undergoing ETT were enrolled to evaluate in vive platelet activation. We used flow cytometry and fluorescent-labeled monoclonal antibodies to activation-dependent platelet antigens to detect dobutamine-associated platelet activation both in vitro and in vivo. Results: In vitro we found a synergistic increase in epinephrine-induced CD62 expression in the presence of dobutamine. The response to the combination of dobutamine and epinephrine was 151% to 565% of the expected response. In vivo there was a dose- and time-dependent rise in the percentage of platelets expressing CD62 in all nine subjects undergoing DSE. The median percentage of platelets expressing CD62 was 1.6% (range 0.1% to 6.8%), 6.5% (range 0.2% to 11.7%), 11.6% (range 5.9% to 19.1%), and 11.4% (range 7.2% to 25.0%) in the samples obtained at baseline, 20 μg/kg/min of dobutamine, 40 μg/kg/min of dobutamine, and during the recovery phase, respectively (repeated measures analysis of variance, p = 0.02). There was no increase in CD62 expression on platelets obtained from seven patients at peak ETT. The median percentage of CD62 at baseline ETT was 1.9% (range 0.2% to 7.3%) and at peak was 2.6% (range 0.4% to 7.0%) (p = 0.156, Wilcoxon signed rank test). Conclusion: We conclude that platelet activation occurs in vive in patients undergoing DSE and that this may be caused by a synergistic effect of dobutamine with physiologic platelet agonists.

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