INCREASED EXPRESSION OF NEUTROPHIL AND MONOCYTE ADHESION MOLECULES LFA-1 AND MAC-1 AND THEIR LIGAND ICAM-1 AND VLA-4 THROUGHOUT THE ACUTE-PHASE OF MYOCARDIAL-INFARCTION - POSSIBLE IMPLICATIONS FOR LEUKOCYTE AGGREGATION AND MICROVASCULAR PLUGGING

Objectives, This study sought to evaluate expression of adhesion molec ules on neutrophils and monocytes throughout the acute phase of myocar dial infarction.Background. Neutrophil and monocyte counts increase wi thin days from onset of acute myocardial infarction, Because leukocyte s are recruited to the involved myocardial region, we postulated that these activated cells would display an increased expression of adhesio n molecules necessary for effective endothelial transmigration. Method s. We measured the expression of neutrophil and monocyte lymphocyte fu nction associated antigen-1 (LFA-1), Mac-1, very late after activation antigen-4 (VLA-4) and intercellular adhesion molecule-1 (ICAM-1) by f low cytometry throughout the acute phase of acute myocardial infarctio n in 25 patients and 10 age-matched control subjects. Results. Express ion of Mac-1 on neutrophils increased significantly, whereas no expres sion of VLA-4 and ICAM-1 was detected. The expression of LFA-1, Mac-1, VLA-4 and ICAM-1 on the monocyte cell membrane in patients with an ac ute myocardial infarction was increased compared with that in control subjects by 228 (on day 7), 67%, 13% and 44% (all on day 4), respectiv ely (all p < 0.001), Elevated density of monocyte-specific CD14 in the AMI versus the control group was also shown (30%, p < 0.001). Conclus ions. Increased expression of neutrophil and monocyte adhesion molecul es may contribute to their adhesion to endothelium in the ischemic ter ritory, This adhesion could feasibly precipitate vasoconstriction or a dd a local thrombotic effect due to tissue factor expression secondary to Mac-1 engagement. In addition, the manifestation of increased dens ity of LFA-1 and Mac-1 by activated leukocytes with monocytes also exp ressing ICAM-1 suggests that leukocytes may form microaggregates that could cause microvascular plugging, This mechanism may facilitate the occurrence of the ''no-reflow'' phenomenon or slow coronary filling af ter acute myocardial infarction. (C) 1998 by the American College of C ardiology.