Inserm, Institut national de la santé et de la recherche médicale
Faculté de pharmacie, Aix Marseille Université

Accueil » Publications » Communications internationales » Direct evidence of endothelial injury in acute myocardial infarction and (...)

Direct evidence of endothelial injury in acute myocardial infarction and unstable angina by demonstration of circulating endothelial cells

Mutin, M., Canavy, I., Blann, A., Bory, M., Sampol, J., Dignat-George, F. (1999) Blood 93, 2951-8. IF : 9.9.

Résumé/Abstract

Circulating endothelial cells (CECs) have been detected in association with endothelial injury and therefore represent proof of serious damage to the vascular tree. Our aim was to investigate, using the technique of immunomagnetic separation, whether the pathological events in unstable angina (UA) or acute myocardial infarction (AMI) could cause desquamation of endothelial cells in circulating blood compared with effort angina (EA) and noncoronary chest pain. A high CEC count was found in AMI (median, 7.5 cells/mL ; interquartile range, 4.1 to 43.5, P <.01 analysis of variance [ANOVA]) and UA (4.5 ; 0.75 to 13.25 cells/mL, P <.01) within 12 hours after chest pain as compared with controls (0 ; 0 to 0 cells/mL) and stable angina (0 ; 0 to 0 cells/mL). CEC levels in serial samples peaked at 15.5 (2.7 to 39) cells/mL 18 to 24 hours after AMI (P <.05 repeated measures ANOVA), but fell steadily after UA.

Regardless of acute coronary events, the isolated cells displayed morphologic and immunologic features of vascular endothelium. The CECs were predominantly of macrovascular origin. They did not express the activation markers intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, and E-selectin, although some were positive for tissue factor.

CECs failed to exhibit characteristics of apoptosis (TUNEL assay) excluding this event as a possible mechanism of cell detachment. The presence of CECs provides direct evidence of endothelial injury in AMI and UA, but not in stable angina, confirming that these diseases have different etiopathogenic mechanisms.

http://www.ncbi.nlm.nih.gov/pubmed/10216090