CLINICAL RESEARCH
Platelet microparticle number is associated with the extent of myocardial damage in acute myocardial infarction
 
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Submission date: 2014-07-08
 
 
Final revision date: 2014-09-06
 
 
Acceptance date: 2014-09-07
 
 
Online publication date: 2016-05-18
 
 
Publication date: 2016-05-16
 
 
Arch Med Sci 2016;12(3):529-537
 
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Introduction: Activated platelets generate microparticles. Increased platelet microparticles occur in acute myocardial infarction (AMI) and contribute to intracoronary thrombosis and subsequent myocardial injury. This study aimed to investigate the impact of platelet microparticles on intracoronary thrombosis by assessing the relationship between platelet microparticles and the extent of myocardial damage in AMI.
Material and methods: This was a cross sectional study. The subjects were patients with acute coronary syndrome (ACS). Forty-one consecutive subjects with ACS admitted to intensive cardiovascular care unit were enrolled. The clinical spectrum of ACS comprised AMI (n = 26), both ST-elevation AMI (STEMI) and non-ST-elevation AMI (NSTEMI), and unstable angina (n = 15). Platelet microparticles were isolated from peripheral venous blood and detected with anti-CD42b-PE by the flow cytometry method. The extent of myocardial damage was determined by measuring the peak level of serial cardiac enzymes within 24 h of admission.
Results: Subjects with AMI had a significantly higher number of platelet microparticles than those with unstable angina (4855 ±4509/µl vs. 2181 ±1923/µl respectively; p = 0.036). Subjects with STEMI had the highest number of platelet microparticles, but no significant difference was detected as compared to those with NSTEMI (5775 ±5680/µl vs. 3601 ±1632/µl). The number of platelet microparticles in AMI was positively associated with the extent of myocardial damage (peak CK-MB: r = 0.408, p = 0.019 and peak GOT: r = 0.384, p = 0.026).
Conclusions: The number of platelet microparticles was increased in AMI as compared to unstable angina and associated with the extent of myocardial damage.
eISSN:1896-9151
ISSN:1734-1922
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