Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction

OBJECTIVES We investigated whether elevated levels of circulating monocyte-platelet aggregates (MPA) can be used to identify patients with acute myocardial infarction (AMI). BACKGROUND Commonly used blood markers of AMI reflect myocardial cell death, but do not reflect the earlier pathophysiologic p...

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Bibliographic Details
Published in:Journal of the American College of Cardiology 2001-10, Vol.38 (4), p.1002-1006
Main Authors: Furman, Mark I, Barnard, Marc R, Krueger, Lori A, Fox, Marsha L, Shilale, Elizabeth A, Lessard, Darleen M, Marchese, Peter, Frelinger, A.L, Goldberg, Robert J, Michelson, Alan D
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cardiology. Vascular system
Coronary heart disease
Creatine Kinase - blood
Creatine Kinase, MB Form
Female
Flow Cytometry
Heart
Humans
Isoenzymes - blood
Male
Medical sciences
Middle Aged
Monocytes - physiology
Myocardial Infarction - diagnosis
Myocardial Infarction - physiopathology
P-Selectin - analysis
Platelet Activation - physiology
Platelet Aggregation - physiology
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Summary:OBJECTIVES We investigated whether elevated levels of circulating monocyte-platelet aggregates (MPA) can be used to identify patients with acute myocardial infarction (AMI). BACKGROUND Commonly used blood markers of AMI reflect myocardial cell death, but do not reflect the earlier pathophysiologic processes of plaque rupture, platelet activation and resultant thrombus formation. Circulating MPA form after platelet activation. METHODS In a single center between October 1998 and November 1999, we measured circulating MPA in a blinded fashion by whole blood flow cytometry in 211 consecutive patients who presented to the emergency department (ED) with chest pain and were admitted to rule out AMI. Acute myocardial infarction was diagnosed by a CK-MB fraction greater than three times control. RESULTS Patients with AMI (n = 61), as compared with those without AMI (n = 150), had significantly higher numbers of circulating MPA (11.6 ± 11.4 vs. 6.4 ± 3.6, mean ± SD, p < 0.0001). After controlling for age, the adjusted odds of developing AMI for patients in the 2nd, 3rd and 4th quartiles of MPA, in comparison with patients in the lowest quartile (odds ratio = 1.0), were 2.1 (95% confidence interval [CI]: 0.7, 6.8), 4.4 (95% CI: 1.5, 13.1) and 10.8 (95% CI: 3.6, 32.0), respectively. The number of circulating MPA in patients with AMI presenting within 4 h of symptom onset (14.4) was significantly greater than those presenting after 4 h (9.4) and after 8 h (7.0), (p < 0.001). Of the 61 patients with AMI, 35 (57%) had a normal creatine kinase isoenzyme ratio at the time of presentation to the ED, but had high levels of circulating MPA (13.3). CONCLUSIONS Circulating MPA are an early marker of AMI.
ISSN:0735-1097
1558-3597
DOI:10.1016/S0735-1097(01)01485-1