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Blood, Vol. 93 No. 9 (May 1), 1999:
pp. 2951-2958
Direct Evidence of Endothelial Injury in Acute Myocardial
Infarction and Unstable Angina by Demonstration of Circulating
Endothelial Cells
Murielle Mutin,
Isabelle Canavy,
Andrew Blann,
Michel Bory,
José Sampol, and
Françoise Dignat-George
From the Laboratoire d'Hématologie et d'Immunologie, U.F.R.
de Pharmacie, Marseille Cedex; Laboratoire d'Hématologie,
Hôpital de la Conception, Marseille Cedex; Service de cardiologie
A, centre hospitalier et universitaire de la Timone, Marseille Cedex,
France; and Haemostasis, Thrombosis and Vascular Biology Unit,
University Department of Medicine, City Hospital, Birmingham, UK.
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.
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