Procoagulant inflammatory responses of monocytes after direct balloon angioplasty in acute myocardial infarction

被引:72
作者
Ott, I [1 ]
Neumann, FJ [1 ]
Kenngott, S [1 ]
Gawaz, M [1 ]
Schömig, A [1 ]
机构
[1] Tech Univ Munich, Deutsch Herzzentrum, D-80636 Munich, Germany
关键词
D O I
10.1016/S0002-9149(98)00509-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
This study sought to investigate monocyte procoagulant activity and Mac-1 expression after successful percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (AMI). An increased leukocyte count is an important risk factor for subsequent adverse cardiac events in AMI. Cellular procoagulant responses may contribute to the risk of thrombotic events after AMI. In 20 patients with AMI serial venous blood samples were obtained before, 4, 8 hours, and daily after direct PTCA. Twenty patients with elective PTCA served as a control group. We measured leukocyte procoagulant activity with a 1-stage clotting assay, Mac-1 expression of monocytes by flow cytometry, concentrations of tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, and IL-8 using immunoassays. Forty-eight hours after PTCA in patients with AMI, an increase in systemic IL-6 and C-reactive concentrations was found (p = 0,001, p = 0.008) associated with an increase in monocyte Mac-1 expression by 49 +/- 18% (p = 0.04) and followed by an increase in monocyte procoagulant activity by 140 +/- 63% 72 hours after PTCA (p = 0.01). None of these changes were detectable in the central group. No changes in the concentrations of the cytokines IL-1 beta, tumor necrosis factor-alpha, or IL-8 were found. The present study demonstrates an increase in procoagulant activity along with an increase in Mac-1 expression on circulating monocytes after successful PTCA in AMI associated with an increase in systemic IL-6. These cellular procoagulant responses may limit the clinical benefit from timely reperfusion. (C) 1998 by Excerpta Medica, Inc.
引用
收藏
页码:938 / 942
页数:5
相关论文
共 29 条
  • [1] ABE Y, 1993, BRIT HEART J, V70, P132
  • [2] OLIGOSPECIFICITY OF THE CELLULAR ADHESION RECEPTOR MAC-1 ENCOMPASSES AN INDUCIBLE RECOGNITION SPECIFICITY FOR FIBRINOGEN
    ALTIERI, DC
    BADER, R
    MANNUCCI, PM
    EDGINGTON, TS
    [J]. JOURNAL OF CELL BIOLOGY, 1988, 107 (05) : 1893 - 1900
  • [3] ADHESIVE RECEPTOR MAC-1 COORDINATES THE ACTIVATION OF FACTOR-X ON STIMULATED CELLS OF MONOCYTIC AND MYELOID DIFFERENTIATION - AN ALTERNATIVE INITIATION OF THE COAGULATION PROTEASE CASCADE
    ALTIERI, DC
    MORRISSEY, JH
    EDGINGTON, TS
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1988, 85 (20) : 7462 - 7466
  • [4] SERUM TUMOR-NECROSIS-FACTOR LEVELS IN ACUTE MYOCARDIAL-INFARCTION AND UNSTABLE ANGINA-PECTORIS
    BASARAN, Y
    BASARAN, MM
    BABACAN, KF
    ENER, B
    OKAY, T
    GOK, H
    OZDEMIR, M
    [J]. ANGIOLOGY, 1993, 44 (04) : 332 - 337
  • [5] Cell biology of tissue factor, the principal initiator of blood coagulation
    Camerer, E
    Kolsto, AB
    Prydz, H
    [J]. THROMBOSIS RESEARCH, 1996, 81 (01) : 1 - 41
  • [6] CASTELL JV, 1989, ANN NY ACAD SCI, V557, P87
  • [7] CRUICKSHANK A, 1994, LANCET, V343, P947
  • [8] LEUKOCYTES AND THE RISK OF ISCHEMIC DISEASES
    ERNST, E
    HAMMERSCHMIDT, DE
    BAGGE, U
    MATRAI, A
    DORMANDY, JA
    [J]. JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1987, 257 (17): : 2318 - 2324
  • [9] SERUM INTERLEUKIN-6 LEVELS BECOME ELEVATED IN ACUTE MYOCARDIAL-INFARCTION
    IKEDA, U
    OHKAWA, F
    SEINO, Y
    YAMAMOTO, K
    HIDAKA, Y
    KASAHARA, T
    KAWAI, T
    SHIMADA, K
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1992, 24 (06) : 579 - 584
  • [10] EVIDENCE FOR TIME-DEPENDENT ACTIVATION OF MONOCYTES IN THE SYSTEMIC CIRCULATION IN UNSTABLE ANGINA BUT NOT IN ACUTE MYOCARDIAL-INFARCTION OR IN STABLE ANGINA
    JUDE, B
    AGRAOU, B
    MCFADDEN, EP
    SUSEN, S
    BAUTERS, C
    LEPELLEY, P
    VANHAESBROUCKE, C
    DEVOS, P
    COSSON, A
    ASSEMAN, P
    [J]. CIRCULATION, 1994, 90 (04) : 1662 - 1668