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

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 immunomag netic separation, whether the pathological events in unstable angina (UA) o r acute myocardial infarction (AMI) could cause desquamation of endothelial cells in circulating blood compared with effort angina (EA) and noncoronar y chest pain. A high CEC count was found in AMI (median, 7.5 cells/mL; inte rquartile 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 ce lls/mL). CEC levels in serial samples peaked at 15.5 (2.7 to 39) cells/mL 1 8 to 24 hours after AMI (P < .05 repeated measures ANOVA), but fell steadil y after UA, Regardless of acute coronary events, the isolated cells display ed morphologic and immunologic features of vascular endothelium. The CECs w ere predominantly of macrovascular origin. They did not express the activat ion markers intercellular adhesion molecule (ICAM)-1, vascular cell adhesio n 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 presen ce of CECs provides direct evidence of endothelial injury in AMI and UA, bu t not in stable angina, confirming that these diseases have different etiop athogenic mechanisms, (C) 1999 by The American Society of Hematology.