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

Meisel, Simcha; Shapiro, Hava; Radnay, Judith; Neuman, Yoram; Khaskia, Abdul-Rahim; Gruener, Nachman; Pauzner, Hana; David, Daniel

doi:10.1016/s0735-1097(97)00424-5

Cited by 140 publications

(84 citation statements)

References 21 publications

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“…7 Meisel et al 10 recently described a 30% increased density of CD14 receptors in patients in the acute phase of MI. Our data in healthy volunteers without acute illness showed that the C(Ϫ260)3 T change affects the level of CD14 gene expression, and thus we suppose that this increased density is permanent and genetically determined.…”

Section: Discussionmentioning

confidence: 98%

C(−260)→T Polymorphism in the Promoter of the CD14 Monocyte Receptor Gene as a Risk Factor for Myocardial Infarction

et al. 1999

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Background-The CD14 receptor of monocytes is an important mediator for the activation of monocytes/macrophages by endotoxins from the envelope of Gram-negative bacteria (lipopolysaccharides). We identified a polymorphism in the CD14 receptor and examined whether this genetic marker influenced the expression of the CD14 receptor on monocytes and affected the predisposition to myocardial infarction. Methods and Results-We identified a C(Ϫ260)3 T nucleotide change, creating a HaeIII polymorphism in the promoter of the CD14 gene. The polymorphism was determined in 178 male patients Ͻ65 years old (cases; average age, 55.9Ϯ6.3 years) at the time of their first myocardial infarction and in 135 representative selected male control subjects (controls; average age, 55.2Ϯ11.5 years). The frequency of the T allele (absence of the cutting site) was 0.49 in cases and 0.35 in controls (Pϭ0.0005; OR, 1.781; 95% CI, 1.286 to 2.465). Subsequently, we measured the expression of monocyte CD14 by flow cytometry in 18 volunteers with different CD14 genotypes. A significantly higher density of the CD14 receptor was shown in the T/T homozygotes than in the others (Pϭ0.0028). Conclusions-A higher frequency of allele T(Ϫ260) in the promoter of the CD14 receptor gene was found in myocardial infarction survivors than in controls. At the same time, this variation was associated with a higher density of CD14 receptors in healthy volunteers. Therefore, we can conclude that in addition to the well-established risk factors, a genetically determined reaction of monocytes/macrophages to infectious stimuli could play an important role in the process of atherosclerosis. (Circulation. 1999;99:3218-3220.)

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Section: Discussionmentioning

confidence: 98%

C(−260)→T Polymorphism in the Promoter of the CD14 Monocyte Receptor Gene as a Risk Factor for Myocardial Infarction

et al. 1999

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“…22) Peripheral blood monocytes isolated from AMI patients also expressed significantly higher amounts of lymphocyte function associated antigen-1 (LFA-1), CD11b / CD18, very late activating antigen-4 (VLA-4), and intercellular adhesion molecule-1 (ICAM-1) than control subjects. 6) Since a rapid increase in leukocyte adhesion to endothelial cells is one of the first events of an acute inflammatory response and part of the pathogenesis of vascular diseases, the increase in adhesion molecules in the peripheral as well as the coronary tree in ACS patients provides clear evidence for monocytes having an important role in the acute phase of CAD.…”

Section: Discussionmentioning

confidence: 99%

“…In monocytes, the expression level of adhesion molecules was shown to be elevated in ACS patients. 6,7) Furthermore, monocytes isolated from UA patients were shown to be in an activated state with respect to the expression of a tissue factor (TF) which has a pro-coagulating activity. 8,9) T-lymphocytes expressing activation markers such as very late activation antigen-1 (VLA-1) and HLA-DR have been reportedly found in atherosclerotic plaques.…”

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confidence: 99%

Correlation between Monocyte and T-lymphocyte Activation Markers in Patients with Acute Coronary Syndrome.

Choi

Lee

et al. 2000

Jpn Heart J

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SUMMARYEvidence suggesting the involvement of activated monocytes and T-lymphocytes in the acute phase of coronary artery disease (CAD) has been increasing. But a detailed analysis of a correlation between monocyte and T-lymphocyte activation markers in CAD has not yet been done. We analyzed plasma C-reactive protein (CRP) levels and the expression levels of CD14 and CD11b on monocytes and the percentage of HLA-DR + T-lymphocytes in 25 patients with acute coronary syndrome (ACS), 12 stable angina (SA) patients, and 23 control subjects using flow-cytometry. The expression of CD14 by monocytes was increased significantly in ACS patients (activation index = 38.7 ± 2.5, mean ± SEM) in comparison to the control subjects (8.0 ± 1.9) and the SA patients (16.9 ± 3.9) (p < 0.001 and p < 0.01, respectively). The expression of CD11b by monocytes of ACS patients (4.6 ± 0.6) was also increased significantly in comparison to control subjects (2.2 ± 0.1) and the SA patients (2.2 ± 0.3) (p < 0.001 for both). Also, a significantly higher percentage of HLA-DR positive T-lymphocytes (19.2 ± 1.8 vs 13.5 ± 1.2%, p < 0.05) was observed among ACS patients in comparison to control subjects. Significant increases in plasma CRP levels were also detected in ACS patients. Furthermore, there were statistically significant correlations among these activation markers. These results indicate that activation of inflammatory cells may play a role in the pathogenesis of ACS. The correlation between the activation status of monocytes and T-lymphocytes indicates that the activation of these immune cells is linked in such a way that activation of one type of cell may lead to the activation of another type of cell. (Jpn Heart J 2000; 41: 605-615) Key words: CD14, CD11b, HLA-DR, Unstable angina, Stable angina, Inflammation, Flow cytometry INCREASING evidence suggests that inflammatory changes and activation of immune cells are involved in the acute phase of atherosclerosis.1) The atherosclerotic plaques of AMI and UA patients are considered active plaques and vulneraFrom the Cardiology Division, Cardiovascular Institute,

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“…There may be some patients in whom the CFV pattern has already been determined by the size of the myocardial infarct before reperfusion therapy. However, it was reported that reperfusion therapy resulted in insufficient coronary microcirculation attributable to reperfusion injury, such as oxygen-free radical injury, 28,29 calcium overload, microvascular spasm, 10 neutrophil plugging of the microvessels, 30 and tissue edema 8 or embolization of the coronary microvasculature attributable to dissemination of thrombi and the contents of the disintegrated atheroma in the lesion to distal parts of the coronary vasculature. 31,32 In the present study, in 75% of the patients with severe microvascular injury, an ST-segment reelevation was observed in the absence of epicardial mechanical obstruction immediately after PCI.…”

Section: Microvascular Injury and Coronary Flow Velocity Patternmentioning

confidence: 99%

Coronary Flow Velocity Pattern Immediately After Percutaneous Coronary Intervention as a Predictor of Complications and In-Hospital Survival After Acute Myocardial Infarction

et al. 2002

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Background— Recently, it was reported that the degree of microvascular injury and left ventricular functional recovery during the chronic period can be predicted after treatment of the infarct-related artery based on the coronary flow velocity (CFV) pattern assessed using a Doppler guidewire. The aim of this prospective study was to examine whether the CFV pattern may predict complications and in-hospital survival after acute myocardial infarction (AMI). Methods and Results— The study population consisted of 169 consecutive patients with a first anterior AMI successfully treated with percutaneous coronary intervention (PCI). We examined the CFV pattern immediately after PCI using a Doppler guidewire. In accordance with previous findings, we defined severe microvascular injury as a diastolic deceleration time ≤600 ms and the presence of systolic flow reversal. Patients were divided into two groups: those without severe microvascular injury (n=118; group 1) and those with severe microvascular injury (n=51; group 2). All of the patients who had cardiac rupture were in group 2. Congestive heart failure (CHF) was observed more frequently in group 2 than in group 1 (53% versus 8%, P <0.001). The in-hospital cardiac mortality rate was significantly higher in group 2 than in group 1 (18% versus 0%, P <0.001). Nine patients in group 2 died, 5 patients because of CHF and 4 patients because of cardiac rupture. Conclusions— These findings suggest that the CFV pattern is an accurate predictor of the presence or absence of complications and of in-hospital survival after AMI.

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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

Cited by 140 publications

References 21 publications

C(−260)→T Polymorphism in the Promoter of the CD14 Monocyte Receptor Gene as a Risk Factor for Myocardial Infarction

C(−260)→T Polymorphism in the Promoter of the CD14 Monocyte Receptor Gene as a Risk Factor for Myocardial Infarction

Correlation between Monocyte and T-lymphocyte Activation Markers in Patients with Acute Coronary Syndrome.

Coronary Flow Velocity Pattern Immediately After Percutaneous Coronary Intervention as a Predictor of Complications and In-Hospital Survival After Acute Myocardial Infarction

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