Acute coronary syndrome is considered as a severe subtype of coronary heart diseases. It is due to progressive inflammation of the vascular wall, and it is considered as the most common cause of mortality worldwide . The key mechanism of ACS is the rupture of atherosclerotic plaques. MMPs play the main role in the rupture of the vulnerable plaques by degrading the fibrous tissue of the plaques [4, 5].
CD147, a member of the immunoglobulin superfamily, is a potent inducer of extracellular MMP, lymphocyte development, and immune response . Higher levels of CD147 expression were detected in CAD patients. These high levels were not only detected in the plasma but also on platelets, monocytes, and granulocytes in the circulation. The severe situation of CAD is highly correlated with the level of CD147 on platelets . The CD147 level was very high in ACS when compared with SA patients and the control group. Also, the higher levels of CD147 in the plasma were found in culprit vessels. These findings were strong evidence that CD147 was more relevant to unstable plaques and acute vascular diseases .
In our research, we found that the mean value of CD147 gene expression in the ACS group was significantly highly increased when compared to the control group. This finding could be explained on the basis of the identification of CD147 as a potent activator of MMP in adjacent fibroblasts through the homotypic CD147–CD147 interaction [24, 25]. Moreover, CD147 has recently been recognized as a potent marker of inflammation . It has also a vital role in the complex process of atherogenesis, atheroprogression, acute atherosclerothrombosis, and angiogenesis, which play a critical role in advanced atherosclerotic plaques. Furthermore, it is believed to promote plaque destabilization . All the previous factors may support many impaired pathways of atherosclerotic plaques leading to possible rupture of the vulnerable ones .
MMPs become activated by complex activation cascade: the pro-MMPs become activated by plasmin or by binding to membrane-anchored MMPs [27, 28]. So membrane type 1 MMP (MT1-MMP) facilitates all associated proteolysis and enhances monocyte migration and transmigration through activated endothelial cells . MMP9 is highly found in the plasma of MI patients .
In a study by Schmit et al. , they discovered that in vitro EMMPRIN induce MMPs in SMCs (MMP-2) and monocytes (MMP-9). This assumes that the expression of EMMPRIN is greatly involved in MT1MMP expression and secretion of MMP9 in acute MI. They also approved that EMMPRIN-hindering will abrogate the activity of MMP-9. These findings suggest that EMMPRIN may not only induce MMPs directly but also play an important role as a key element in MMP induction.
In 2015, Sturhan et al.  proved that there is a significant difference in monocyte subtype distribution between healthy subjects and patients with stable CAD and no significant difference between acute MI patients and stable CAD one. This finding proves that the upregulation of EMMPRIN is associated with the rupture of the plaques by MMP-9 and followed by MI. EMMPRIN can function as an adhesion receptor. Platelets induce a pro-inflammatory phenotype in monocytes via CD147. The upregulation of CD147 gene expression in ACS affects monocyte differentiation and upregulates EMMPRIN in unstable patients as rupture plaques in acute MI are associated with a high expression level of CD147 gene. All these results go hand in hand with our findings.
SOD activity in this study showed a highly significant increase in the mean value in the diseased group when compared to the control one (p < 0.001). Increased SOD activity can predict a worse outcome in CAD patients . In CAD, increased activity of SOD is not good, as it leads to peroxidation of lipids and hypersensitivity to oxidative stresses . The main function of SOD is the conversion of superoxide anion to H2O2  but increased SOD activity will shift the equilibrium equation, and this will lead to decreased H2O2 concentration .
Alongside with these findings, Vichova and Motovska in 2013  reported that interruption of blood flow in the coronary arteries causes ischemia of the supplied tissues leading to their injury, necrosis, and apoptosis. During ischemia, cellular defense against oxidative injury is impaired with lower activities of SOD, glutathione peroxidase, and huge amount of ROS produced. A second explanation is that SOD is essential for radical disposal so that the low radical concentration is important to stop lipid peroxidation. If these chain of reactions are scavenged by decreased superoxide radical, this will lead to the whole reaction to be stopped or terminated . A third explanation is that increasing SOD activity results in an increase of H2O2 concentration .
Brown and Griendling  reported that the presence of ROS is responsible for the increased activity of SOD as a result of inflammation and neutrophil migration. Also, Buettner et al.  suggested that SOD is not like GPX-1 as the increase in SOD activity has no protective effect but is associated with the deregulation of oxidative processes leading to severe tissue damage and an adverse outcome.
MDA is the result of lipid peroxidation. It is an undependable marker of oxidative damage, so the measurement of the MDA level is considered as a useful indicator and marker for the identification and assessment of ACS patients . During myocardial ischemia or ongoing MI, high levels of free radicals may be generated. MDA that is generated from breakdown of lipids during peroxidation processes is considered as a reliable marker of oxidative damage .
Furthermore, Sharma et al. in 2008  reported that the serum MDA level is increased in CAD patients significantly when compared to the control group. Also, Yaghoub et al.  proved that the serum level of MDA is considered as a potent marker of lipid peroxidation in CAD patients when compared to the control group, and this increase is correlated with the disease severity. In agreement with the previous authors, we found a significant increase in MDA in the ACS group when compared to the control one (p < 0.001).
High sensitive cardiac troponin I assay enables accurate quantification of troponin in most of healthy people. Moreover, these assays can help the assessment of patients with chest pain through the development of safe strategies to exclude myocardial infarction [43, 44]. Coven et al.  also demonstrated that the current definition of NSTEMI requires a typical clinical syndrome plus elevated troponin or CK-MB. They also found that cardiac-specific troponins are not detectable in the blood of healthy individuals. Therefore, they provide high specificity for detecting injury of cardiac myocytes. These molecules are also more sensitive than CK-MB for myocardial necrosis and consequently improve early detection of small myocardial infarctions.
Alvin et al. , on the contrary, found that CK-MB-testing provides no incremental value to patient care and its elimination can lead to millions of health care dollars saved without adversely affecting patient care. In our work, we found a highly significant positive correlation between the levels of CD147 gene expression, CK-MB and high sensitive troponin I in both studied groups.
These results agree completely with the findings reported by Sturhan et al. . The explanation of our findings simply depends on the following facts: interaction of monocytes and platelets via CD147 leads to inflammation and differentiation . There is no doubt that platelets induce pro-inflammatory phenotype in monocytes by CD147 as platelets play an important role in coronary heart disease, and this will speculate that the upregulation of CD147 in ACS must affect monocyte differentiation in their inflammatory activity . The expression levels of healthy subjects were similar to patients with stable CAD. This means that the upregulation of CD147 on monocytes must be associated with unstable patients such as plaque rupture in acute MI .
Current care pathways are unable to exclude out MI presentation that is requiring admission to hospital in most patients, although most of them have no myocardial infarction and must be discharged from the hospital. High sensitive troponin I assay is a helpful and effective strategy to exclude MI .