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Large platelets continue to circulate in an activated state after myocardial infarction
Author(s) -
SCHULTHEIß H. P.,
TSCHOEPE D.,
ESSER J.,
SCHWIPPERT B.,
ROESEN P.,
NIEUWENHUIS H. K.,
SCHMIDTSOLTAU C.,
STRAUER B.
Publication year - 1994
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1994.tb01081.x
Subject(s) - platelet , platelet activation , cd63 , medicine , myocardial infarction , percentile , mean platelet volume , flow cytometry , creatine kinase , cardiology , gastroenterology , immunology , chemistry , microrna , biochemistry , statistics , mathematics , microvesicles , gene
This study was intended to investigate the actual platelet activation status after an acute coronary event. The activation status of circulating platelets was assayed directly by measuring the membrane activation markers CD62 and CD63 with the Düssel‐dorf III flow cytometry test in 22 patients with the diagnosis of acute myocardial infarction during the 48‐h observation period following the acute event. The number of activated, marker‐positive sample platelets was significantly increased in the post‐MI patients: CD62: 5·8%× 2·25 ±1 vs. 3·5%× 2·32 ±1 , P ≤ 0·05; CD63: 18·7%× 1·77 ±1 vs. 4·6%× 2·16 ±1 , P ≤ 0·00·1. The platelet volume and count were concomitantly increased (12·1 ± 2·4 fl/ 236 ± 90 times 10 3 μl ‐1 compared to 8·3 ± 1·6 fl/187 ± 42 times 10 3 μl ‐1 ) in the control group. Particularly large platelets were identified as being activated documented by the exponential increase in the difference in CD63‐binding sites per sample platelet above the 90%‐percentile and below the 10%‐percentile of the volume distribution: Δ+ 1341 ± 903 (MI patients) vs. Δ+ 276 ± 126 (controls), P ≤ 0·00·1. Significant creatine kinase elevation and decrease in platelet count was found in the non‐survivor subset ( n = 5). We conclude that predominantly large platelets continue to circulate in an activated state after MI. This study provides direct evidence that the assumption of an increased thrombotic potential becomes operative in vivo in MI patients. Besides CK elevation and decrease in platelet count this might possibly constitute a prognostic factor for the short‐term outcome of the patients.