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J Am Coll Cardiol, 1999; 34:983-988
© 1999 by the American College of Cardiology Foundation
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CLINICAL STUDIES

Angiotensin-converting enzyme inhibition reduces monocyte chemoattractant protein-1 and tissue factor levels in patients with myocardial infarction

Hirofumi Soejima, MD*, Hisao Ogawa, MD*, Hirofumi Yasue, MD*, Koichi Kaikita, MD*, Keiji Takazoe, MD*, Koichi Nishiyama, MD*, Kenji Misumi, MD*, Shinzo Miyamoto, MD*, Michihiro Yoshimura, MD*, Kiyotaka Kugiyama, MD*, Shin Nakamura, MD{dagger} and Ichiro Tsuji, PhD{ddagger}

* Department of Cardiovascular Medicine, Kumamoto University School of Medicine, Kumamoto, Japan
{dagger} Department of Molecular and Cellular Biology, Primate Research Institute, Kyoto University, Inuyama, Aichi, Japan
{ddagger} Chemo-Sero Therapeutic Research Institute, Kumamoto, Japan

Manuscript received January 4, 1999; revised manuscript received April 22, 1999, accepted June 11, 1999.

Reprint requests and correspondence: Dr. Hisao Ogawa, Department of Cardiovascular Medicine, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto City, 860-8556 Japan
ogawah{at}gpo.kumamoto-u.ac.jp


   Abstract
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 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES

We investigated the effects of enalapril therapy on plasma tissue factor (TF), tissue factor pathway inhibitor (TFPI) and monocyte chemoattractant protein-1 (MCP-1) levels in patients with acute myocardial infarction.

BACKGROUND

Macrophages express TF in human coronary atherosclerotic plaques. Both TF and TFPI are major regulators of coagulation and thrombosis. Monocyte chemoattractant protein-1 is a monocyte and macrophage chemotactic and activating factor.

METHODS

In a randomized, double-blind, placebo-controlled study beginning about two weeks after myocardial infarction, 16 patients received four weeks of placebo (placebo group) and another 16 patients received four weeks of enalapril 5 mg daily therapy (enalapril group). We performed blood sampling after administration of the doses.

RESULTS

There were no significant differences in the serum angiotensin-converting enzyme (ACE) activity, plasma TF, free TFPI or MCP-1 levels before administration between the enalapril and placebo groups. In the enalapril group, ACE activity (IU/liter) (14.0 before, 5.2 on day 3, 5.8 on day 7, 6.3 on day 28), TF levels (pg/ml) (223, 203, 182, 178) and MCP-1 levels (pg/ml) (919, 789, 790, 803) significantly decreased by day 28. However, the free TFPI levels (ng/ml) (28.2, 26.5, 26.8, 28.4) did not change. These four variables were unchanged during the study period in the placebo group.

CONCLUSIONS

This study demonstrated that administration of enalapril reduces the increased procoagulant activity in patients with myocardial infarction associated with inhibition of the activation and accumulation of macrophages and monocytes.

Abbreviations and Acronyms
  ACE = angiotensin-converting enzyme
  ECG = electrocardiogram
  HDL = high-density lipoprotein
  MCP-1 = monocyte chemoattractant protein-1
  TF = tissue factor
  TFPI = tissue factor pathway inhibitor

Data from large placebo-controlled studies have indicated that the administration of angiotensin-converting enzyme (ACE) inhibitors in patients with myocardial infarction is associated with an improvement in survival (1–3). Tissue factor (TF) is a low molecular weight glycoprotein that binds and acts on essential cofactor factor VII, and the resulting complex activates factor IX and X, and initiates the clotting cascade in vivo (4–6). There has been a report that hypercoagulability in patients with acute coronary syndromes is associated with TF induced on circulating monocytes (7). We have also demonstrated that plasma TF levels are elevated in patients with myocardial infarction and unstable angina (8–10). Annex et al. (11) reported that TF protein was expressed in directional atherectomy specimens from patients with acute coronary syndromes.

Furthermore, we have also shown that the expression of TF on macrophages is more frequent in the coronary atherosclerotic plaques in patients with unstable angina than in those with stable exertional angina, and fibrin deposition is mainly observed around massive infiltration of the TF-positive macrophages in patients with unstable angina (12). Recent data have shown that the instability of the atherosclerotic plaque is closely related to its macrophage content (13). Monocyte chemoattractant protein-1 (MCP-1) has a potent chemotactic activity for monocytes (14) and activates monocytes (15). We reported the elevation of plasma MCP-1 levels in patients with acute coronary syndromes (16).

In contrast, tissue factor pathway inhibitor (TFPI) regulates the initial step of the extrinsic coagulation pathway mediated by TF (17). Sandset et al. (18) demonstrated that the TFPI level increases in patients with acute coronary disease. We also showed that plasma levels of TFPI increased in the coronary circulation after coronary spasm (19). We investigated whether the administration of ACE inhibitor might modify plasma TF, free TFPI and MCP-1 levels in patients with myocardial infarction.


   Methods
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 Methods
Results
 Discussion
 References
 
Subjects.   This study was designed as a randomized, double-blind, placebo-controlled study. Entry into the study was two weeks after the onset of myocardial infarction to avoid any acute-phase response. Thirty-two patients with their first myocardial infarction were recruited two weeks after admission to the hospital. All patients were diagnosed as having acute myocardial infarction based on typical chest pain lasting >30 min with ST-segment elevation of >0.2 mV in >2 continuous leads on a standard 12-lead electrocardiogram (ECG) and an increase of creatine kinase level at least twice the upper level of normal. No patients had previously taken an ACE inhibitor. Patients took beta-adrenergic blocking agents, calcium antagonists, long-acting nitrates and aspirin daily from the time of admission. In addition, patients started to receive a placebo or 5 mg of enalapril each morning for four weeks. No patients had a significant hypotensive response or abnormal electrolytes during this study. Informed consent was obtained from each patient.

Sampling.   Blood samplings were performed on the day before the administration, and on days 3, 7 and 28 after the start of enalapril or placebo administration. All patients were supine, and a 21-gauge needle was inserted into a large antecubital vein. An initial 3 ml of blood was used for measuring lipid concentrations; an additional 4.5 ml of blood for TF, free TFPI and MCP-1 assay was drawn into a tube containing sodium citrate (0.13 mol/liter, pH 7.5). Subsequently, 5 ml of blood for measurement of ACE activity was drawn into a plain glass tube. The samples for TF, free TFPI and MCP-1 assay were immediately centrifuged at 3000 rpm for 10 min at 4°C. The samples for lipid concentrations and ACE activity assay were left in room air for 30 min and centrifuged in the same way. After centrifugation, the samples were immediately stored at –80°C until analysis.

Assays.   Serum ACE activity was measured by the ACE color method (Fujirevio, Tokyo). We previously reported using this kit (10). The normal value of ACE activity in our laboratory (n = 16) is 14.8 ± 3.9 (mean ± SD) IU/liter.

Plasma TF antigen levels were measured by the enzyme-linked immunosorbent assay (ELISA) kit (TF ELISA Kit "KAKETSUKEN") purchased from Sanko Junyaku (Tokyo). We previously reported using this kit (9). The normal TF value in our laboratory (n = 16) is 172 ± 32 (mean ± SD) pg/ml.

Plasma free TFPI antigen levels were measured by the ELISA kit (Free TFPI ELISA Kit "KAKETSUKEN") purchased from Sanko Junyaku . We previously reported using this kit (16). The normal free TFPI value in our laboratory (n = 16) is 24.1 ± 6.5 (mean ± SD) ng/ml.

Plasma MCP-1 level was measured using a recently described Hbt Human MCP-1 ELISA Kit developed by Hycult Biotechnology B.V. (Uden, The Netherlands). We previously reported using this Kit (19). The normal MCP-1 value in our laboratory (n = 16) is 531 ± 99 (mean ± SD) pg/ml.

Statistical analyses.   All data are shown as mean value ± SD. The clinical characteristics of the two patient groups with myocardial infarction were compared using an unpaired t test for continuous data and chi-square test for frequency data. Plasma TF, free TFPI and MCP-1 levels and serum ACE activity between the enalapril and placebo group before administration were compared using the Mann-Whitney U test. Those levels between the normal group and patient group were also compared using the Mann-Whitney U test. The plasma TF, free TFPI and MCP-1 levels and serum ACE activity levels over the time course in the two patient groups were, respectively, compared by two-way analysis of variance (ANOVA) for repeated measures that included treatment and stratum as main effects and treatment-by-stratum interactions. When the results were significant, the significance level for correlations is given after applying the Bonferroni method (20). A linear regression analysis was used to determine the correlations between the two variables. Probability levels less than 0.05 were considered significant.


   Results
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 Methods
 Results
Discussion
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Baseline characteristics.   The clinical characteristics of patients are listed in Table 1. There were no significant differences in frequencies of hypertension, obesity, diabetes mellitus and history of smoking, and in the levels of serum total cholesterol, triglyceride and high-density lipoprotein (HDL) cholesterol between the enalapril and placebo groups. There were also no significant differences in medications such as beta-blockers, calcium antagonists, long-acting nitrates and aspirin between the two patient groups.


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  		Table 1 Characteristics of the Two Patient Groups (mean ± SD)

 
The three variables before administration.   There were no differences in the mean level of ACE activity, TF, free TFPI and MCP-1 levels before the administration between the enalapril and placebo groups (enalapril, placebo: ACE [IU/liter]: 14.0 ± 5.7, 14.4 ± 5.7; TF [pg/ml]: 223 ± 58, 229 ± 54; free TFPI [ng/ml]: 28.2 ± 16.3, 29.1 ± 14.2; MCP-1 [pg/ml]: 919 ± 173, 932 ± 193). The TF and MCP-1 levels before the administration in patients with myocardial infarction were significantly higher than the normal values in our laboratory.

The three variables after administration.   The following were p values of the main effects and the interaction resulting from two-way repeated measures ANOVA. The main effect was p < 0.001 and interaction was p < 0.001 in the ACE activity; main effect was p = 0.036 and interaction was p = 0.005 in the TF levels; main effect was p < 0.001 and interaction was p = 0.020 in the MCP-1 levels; and main effect was p = 0.725 and interaction was p = 0.993 in the free TFPI levels.

The ACE activity (IU/liter) in the enalapril group significantly decreased from 14.0 ± 5.7 before the administration to 5.2 ± 3.5 on day 3 (Fig. 1). The activity on days 7 and 28 was also significantly lower. The ACE activity in the placebo group did not significantly change during the study period. Activity on days 3, 7 and 28 in the enalapril group was significantly lower than that in the placebo group.



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  		Figure 1 Serial changes in the serum levels of angiotensin-converting enzyme (ACE) activity in patients treated with enalapril and placebo (mean ± SEM). Solid circle = enalapril; open circle = placebo. **p < 0.01 vs. before administration; {dagger}{dagger}p < 0.01 vs. placebo.

 
The TF levels (pg/ml) in the enalapril group significantly decreased from 223 ± 58 before administration to 182 ± 39 on day 7 (Fig. 2). The levels on day 28 were also significantly lower. The TF levels in the placebo group did not significantly change during the study period. The levels on days 7 and 28 in the enalapril group were significantly lower than those in the placebo group.



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  		Figure 2 Serial changes in the plasma levels of tissue factor (TF) antigen in patients treated with enalapril and placebo (mean ± SEM). Solid circle = enalapril; open circle = placebo. *p < 0.05 vs. before administration; **p < 0.01 vs. before administration; {dagger}{dagger}p < 0.01 vs. placebo.

 
The free TFPI levels in either the enalapril or placebo group did not significantly change during the study period (Fig. 3).



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  		Figure 3 Serial changes in the plasma levels of free tissue factor pathway inhibitor (TFPI) antigen in patients treated with enalapril and placebo (mean ± SEM). Solid circle = enalapril; open circle = placebo.

 
The MCP-1 levels (pg/ml) in the enalapril group significantly decreased from 919 ± 173 before the administration to 789 ± 128 on day 3 (Fig. 4). The levels on days 7 and 28 were also significantly lower. The MCP-1 levels in the placebo group did not significantly change during the study period. The MCP-1 levels on days 3, 7 and 28 in the enalapril group were significantly lower than those in the placebo group.



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  		Figure 4 Serial changes in the plasma levels of monocyte chemoattractant protein-1 (MCP-1) antigen in patients treated with enalapril and placebo (mean ± SEM). Solid circle = enalapril; open circle = placebo. *p < 0.05 vs. before administration; {dagger}{dagger}p < 0.01 vs. placebo; {dagger}p < 0.05 vs. placebo.

 
The correlation between two variables.   The correlation coefficient among the ACE activity, TF, free TFPI and MCP-1 levels before the administration was calculated in all patients. There was a good correlation (r = 0.734, p < 0.0001) between the ACE activity and the MCP-1 levels (Fig. 5A). The ACE activity was positively correlated with the TF levels (r = 0.553, p = 0.0010, Fig. 5B). Furthermore, MCP-1 levels were also positively correlated with TF levels (r = 0.746, p < 0.0001, Fig. 5C). There were no correlations between the free TFPI levels and the other variables.



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  		Figure 5 The correlations between the serum angiotensin-converting enzyme (ACE) activity and plasma monocyte chemoattractant protein-1 (MCP-1) levels (A), the serum ACE activity and plasma tissue factor (TF) levels (B) and the MCP-1 and TF levels (C).

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
The use of ACE inhibitors in patients with myocardial infarction is known to reduce the morbidity and mortality by major cardiovascular events (1–3). Vaughan et al. (21) recently demonstrated that administration of ACE inhibitor decreases plasma PAI-1 levels in patients with myocardial infarction. We also showed the effects of ACE inhibitor on endogenous fibrinolysis in patients with recent myocardial infarction (22). In contrast, we have demonstrated that plasma TF levels are elevated in patients with myocardial infarction and unstable angina in the previous studies (8–10). These results show that there is an abnormal activation of the procoagulant system in patients with myocardial infarction.

Recently, it was revealed that plaques from patients with unstable angina or myocardial infarction had significantly high concentrations of TF antigen and activity, and that heightened TF levels contribute to the high procoagulant activity of atherosclerotic lesions in the coronary artery (23–25). The plasma TF levels decreased after administration of enalapril in the present study. This fact is consistent with the data that exposure of vascular smooth muscle cells and aortic endothelial cells to angiotensin II induced expression of TF mRNA (26,27).

In the present study, plasma TF levels decreased along with ACE activity, and there was a positive correlation between the TF levels and the ACE activity. These data may indicate that the inhibition of ACE decreases the over-expression of TF in patients with myocardial infarction. In plasma there are two types of TF: One is a membrane-bound form with potent procoagulant activity, and the other is a soluble form with a faint procoagulant activity. We reported that there is good correlation between procoagulant activity and plasma membrane-bound TF levels in patients without renal dysfunction.

Furthermore, we observed a highly positive correlation between plasma TF levels and membrane-bound TF levels in another study on myocardial infarction without renal dysfunction (28). None of the patients in the present study had renal dysfunction. Therefore, in the current study it is suggested that the elevation of plasma TF level reflects the heightened TF activity—that is, heightened procoagulant activity—and that it also reflects the increase of membrane-bound TF from atherosclerotic lesions of myocardial infarction.

Most TFPI is synthesized in endothelial cells (29,30) and binds with proteoglycans on the endothelial cell surface (31–33). The TFPI can be separated into free TFPI, lipoprotein-associated TFPI and endothelial cell-associated TFPI. Total TFPI consists of free TFPI and lipoprotein-associated TFPI. It is reported that anticoagulant activity of lipoprotein-associated TFPI is markedly lower than that of free TFPI (34) and that free TFPI reflects the changes in endothelial cell-associated TFPI (35). In the present study, the free TFPI levels did not change after administration of enalapril, and the levels were not correlated with the ACE activity or TF levels. These data are supported by the report that exposure of aortic endothelial cells to angiotensin II did not affect the expression of TFPI mRNA (27).

Recently, it has been reported that the presence of TFPI in human atherosclerotic plaques is associated with reduced TF activity (36). The present study showed that not only the plasma TF levels but also the free TFPI levels were examined after administration of enalapril. It was also reported that administration of recombinant TFPI attenuates stenosis after balloon-induced arterial injury (37). Falciani et al. (38) concluded that blood clotting activation observed in patients with ischemic heart disease was related to elevated TF circulating levels not sufficiently inhibited by the elevated TFPI levels present. It may be an important finding that administration of enalapril diminished TF levels but did not affect TFPI levels.

Monocyte chemoattractant protein-1 is expressed by vascular smooth muscle cells, endothelial cells and monocytes (39–41). In the present study, plasma MCP-1 levels were higher in the patients with myocardial infarction than in normal patients, and were positively correlated with plasma TF levels. Furthermore, plasma TF level decreased along with a decrease in MCP-1 level. These results are inferred by the report that MCP-1 induces the expression of TF in human monocytes (42). Matsumori et al. (43) recently reported that plasma MCP-1 levels are elevated in patients with acute myocardial infarction. Hernàndez-Presa et al. (44) have recently shown that angiotensin II increases MCP-1 mRNA expression, nuclear factor-{kappa}B activation and macrophage accumulation in the artery wall in vitro and these changes are diminished by an ACE inhibitor. In our study, heightened plasma MCP-1 levels decreased by administration of enalapril in patients with myocardial infarction. We thus demonstrated that administration of ACE inhibitor suppresses the increased MCP-1 and TF expression in patients with myocardial infarction.

Conclusions.   This study demonstrates that administration of enalapril reduces the increased procoagulant activity in patients with myocardial infarction associated with inhibition of the activation and accumulation of macrophages and monocytes. It also suggests one mechanism of an improvement in survival in patients with myocardial infarction after administration of ACE inhibitors.


   Footnotes
 
This study was supported in part by a Research Grant from the Smoking Foundation, and a Research Grant for Cardiovascular Diseases (9A-3 and 10C-5) from the Ministry of Health and Welfare, Tokyo, Japan.


   References
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 Abstract
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 Results
 Discussion
 References
 

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H. Zhou, A. S. Wolberg, and R. A. S. Roubey
Characterization of monocyte tissue factor activity induced by IgG antiphospholipid antibodies and inhibition by dilazep
Blood, October 15, 2004; 104(8): 2353 - 2358.
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 Arterioscler. Thromb. Vasc. Bio.Home page
T. Omura, M. Yoshiyama, S. Kim, R. Matsumoto, Y. Nakamura, Y. Izumi, H. Ichijo, T. Sudo, K. Akioka, H. Iwao, et al.
Involvement of Apoptosis Signal-Regulating Kinase-1 on Angiotensin II-Induced Monocyte Chemoattractant Protein-1 Expression
Arterioscler. Thromb. Vasc. Biol., February 1, 2004; 24(2): 270 - 275.
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 CirculationHome page
D. J. Kereiakes
Adjunctive Pharmacotherapy before Percutaneous Coronary Intervention in Non-ST-Elevation Acute Coronary Syndromes: The Role of Modulating Inflammation
Circulation, October 21, 2003; 108(90161): III-22 - 27.
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 Arch Intern MedHome page
D. S. Jacoby and D. J. Rader
Renin-Angiotensin System and Atherothrombotic Disease: From Genes to Treatment
Arch Intern Med, May 26, 2003; 163(10): 1155 - 1164.
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 Nephrol Dial TransplantHome page
V. Schachinger and A. M. Zeiher
Atherogenesis--recent insights into basic mechanisms and their clinical impact
Nephrol. Dial. Transplant., December 1, 2002; 17(12): 2055 - 2064.
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 Eur Heart J SupplHome page
C. Kluft, R. Kleemann, and M.P.M. de Maat
How best to counteract the enemies? By controlling inflammation in the coronary circulation
Eur. Heart J. Suppl., November 1, 2002; 4(suppl_G): G53 - G65.
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 Cardiovasc ResHome page
B. Jilma and P. Jilma-Stohlawetz
Female gender, menstrual cycle and estradiol affect plasma levels of monocyte chemotactic protein-1 (MCP-1) in humans
Cardiovasc Res, August 1, 2002; 55(2): 416 - 416.
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 Cardiovasc ResHome page
S. Stork, K. Baumann, C. von Schacky, and P. Angerer
The effect of 17{beta}-estradiol on MCP-1 serum levels in postmenopausal women
Cardiovasc Res, February 15, 2002; 53(3): 642 - 649.
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 Cardiovasc ResHome page
A. H.M Moons, M. Levi, and R. J.G Peters
Tissue factor and coronary artery disease
Cardiovasc Res, February 1, 2002; 53(2): 313 - 325.
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 CirculationHome page
K. K. Koh, D. K. Jin, S. H. Yang, S.-K. Lee, H. Y. Hwang, M. H. Kang, W. Kim, D. S. Kim, I. S. Choi, and E. K. Shin
Vascular Effects of Synthetic or Natural Progestagen Combined With Conjugated Equine Estrogen in Healthy Postmenopausal Women
Circulation, April 17, 2001; 103(15): 1961 - 1966.
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 ANN INTERN MEDHome page
U. Rauch, J. I. Osende, V. Fuster, J. J. Badimon, Z. Fayad, and J. H. Chesebro
Thrombus Formation on Atherosclerotic Plaques: Pathogenesis and Clinical Consequences
Ann Intern Med, February 6, 2001; 134(3): 224 - 238.
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 Journal of Renin-Angiotensin-Aldosterone SystemHome page
W. B Strawn, R. H Dean, and C. M Ferrario
Novel mechanisms linking angiotensin II and early atherogenesis
Journal of Renin-Angiotensin-Aldosterone System, March 1, 2000; 1(1): 11 - 17.
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