Background. When the coronary atherosclerotic plaque becomes vulnerable, a thrombus develops on that ruptured plaque and then occludes the coronary artery, which causes an acute blood defi ciency in the downstream myocardium. Furthermore oxLDL (oxidized Low Density Lipoprotein) is involved in the coronary atherosclerotic plaque pathogenesis, MMP-9 (Matrix Metalloproteinase-9) enzymes plays role during the plaque rupture and CPR (C Reactive Protein) has a prognostic value in myocardial infarction. Objective. To determine the involvement of oxLDL, MMP-9, CRP markers in the pathogenesis of myocardial infarction, to study their involvement in the injury of the myocardium and to evaluate the complications. Material and Methods. The study was conducted using case-control design. The main inclusion criteria of the 40 case groups are that the patient should have a ruptured coronary atherosclerotic plaque, confi rmed by clinical symptom, ECG, serum troponin I, and coronary angiography. Also 40 patients with coronary stenosis or chronic occlusion without ruptured plague were included in the control group. Serum MMP-9 enzyme and oxLDL titers were determined by ELISA according to the manufacturer’s recommended protocol. Additionally CRP was measured by full-automated analyzater. We used CIIS (cardiac infarction injury score) by ECG and Gensini score system (Coronary Angiographic Scoring System) for assessing the severity of coronary heart disease. Results. Serum MMP-9, oxLDL levels (p<0.001) in the case group (ÌÌÐ-9 0.396±0.155 ng/ml; oxLDL 1.411±0.099 μg/ml) were more than in the control group (ÌÌÐ-9 0.223±0.087 ng/ml; oxLDL 1.332±0.163 μg/ml). The logistic analysis shows that ÌÌÐ-9, oxLDL, CRP (MMP-9 OR=0.985, p<0.001; oxLDLOR=0.011, p<0.05; CRP OR=0.041, p<0.005) may play a role in the pathogenesis of the plaque rupture. Serum MMP-9 enzyme level was directly correlated with Gensini score (r=0.552, p<0.01), CIIS (r=0.340, p<0.01) and CRP (r=0.321, p<0.01) titers. Furthermore, serum MMP-9 enzyme increases with accordance of severity of the myocardium injury with the statistical signifi cance (p<0.01): the borderline abnormality group (CIIS<10, 0.227±0.099 ng/ ml), possible injury (CIIS 10-15, 0.317±0.132 ng/ml), probable injury (CIIS >15, 0.376±0.132 ng/ ml) groups. MMP-9 levels were signifi cantly higher in the probable injury group patients (CIIS >15) compared to the possible injury group patients (CIIS 10-15) (p<0.001). ROC Curve analysis shows that MMP-9 enzyme levels variance (area=0.87, p<0.001) are more than other biomarkers making it a diagnostically benefi cial for the coronary atherosclerotic plaque rupture (CRP area=0,733, p<0.001, oxLDL area=0.635, p<0.05). Conclusion: Serum MMP-9, oxLDL and CRP are signifi cantly involved in the pathogenesis of coronary atherosclerotic plaque rupture in the myocardial infarction.

Cardiovascular diseases (CVD) are the leading cause of death in the World (31% of all deaths)and Mongolia as well. CVD has been the leading cause of death in Mongolia for the last 20 years and consists one of 3 death cases. In its turn 59.6% of CVD mortality caused by Ischemic heart diseases. When the coronary atherosclerotic plaque becomes vulnerable, it will a thrombus develops on that ruptured plaque and then occludes the coronary artery, which causes acute blood deficiency in the downstream myocardium. Some studies indicate that matrix metalloproteinase-9 (MMP-9) plays a key role on pathogenesis of plaque rupture. Aim:To study the involvement of serum MMP-9 enzyme in the pathogenesis during the rupture of the coronary atherosclerosis plaque.The study was conducted using case-control design. The main inclusion criteria of the case group is that the patient should have a ruptured coronary atherosclerotic plaque, confirmed by angiography. The total number of patients is 80, half of them belongs to the case group. MMP-9 was determined in serum by ELISA. We used CIIS (cardiac infarction injury score) by ECG and Gensini score system (Coronary Angiographic Scoring System) for assessing the severity of coronary heart disease.The average level of MMP-9 in case and control groups are 0.396±0.155 ng/ml, 0.223±0.087 ng/ ml respectively with p<0.001 significance which shows MMP-9 (OR=0.001, p<0.001) may plays a role in the pathogenesis of plaque rupture. MMP-9 is correlated with Gensini score and CIIS score, respectively (r=0.552, p<0.01; r=0.340, p<0.01) which shows MMP-9 is being elevated with the increase of the severity of coronary heart disease and the cardiac infarction injury. Serum MMP- 9 increases statistically significantly (p<0.001) with the increase of the severity of the stenosis and the number of the affected arteries: no severe stenosis (<75% stenosis) (0.245±0.086 ng/ ml); 1 vessel severe (>75%) stenosis (0.317±0.132 ng/ml), 2 vessel severe stenosis (0.348±0.157 ng/ml), 3 vessel severe stenosis (0.422±0.112 ng/ml). Furthermore, serum MMP-9 enzyme increases with accordance of severity of the myocardium injury with the statistical significance (p<0.01): the borderline abnormality group (CIIS<10, 0.227±0.099 ng/ml), possible injury (CIIS 10-15, 0.317±0.132 ng/ml), probableinjury (CIIS >15, 0.376±0.132 ng/ml) group. MMP-9 levels were significantly higher in the probable injury (CIIS >15) patients compared to the possible injury (CIIS 10-15) patients (p < 0.001). An increase in serum MMP-9 enzyme levels is a risk factor of the coronary atherosclerotic plaque rupture (OR=0.001, p<0.001). MMP-9 enzyme may be a possible marker of atheromatous plaque rupture in coronary heart disease.

Coronary heart disease is a leading cause of mortality in many countries. Acute coronary syndrome is the basis pathophysiology of coronary heart disease. Complication of coronary atherosclerosis composes rupture of plaque and erosion of vulnerable plaque. Endothelial dysfunction is main influence of coronary plaque erosion. But then recently research oxidative stress and reaction of immunocomplex is leading cause of coronary plaque rupture. So the research background will study markers of endothelial dysfunction, oxidative stress, immune reaction in the complication of coronaryatherosclerosis. Aim: Determine the effect of some marker for causing complication of the coronary atherosclerosis. The research has been conducted using case-control study method. In the case group, patients with complication of the coronary atherosclerosis as determined by coronary angiography (stenosis >85%) as in the control group healthy people with carotid artery stenosis (<0.7mm) has been involved. In the study we defined Anti-oxLDL (anti-oxidized low density lipoprotein) using ELISA Kit (Eucardio Lab, USA) and oxLDL (oxidized low density lipoprotein) titer by ELISA Kit (Mercadio, USA), ADMA (Asymmetric dimethylarginine) titer by ELISA kit (Eucardio Lab, USA) reagents in the enzyme binding reaction. Total antioxidant capacity (TAC) was determined by using spectrophotometer method. The average age of people involved in the research is 57.2±9.72 and for the average age is case group 28 (32%) and 50 (68%) for the control group. ADMA titer level for complication of coronary atherosclerosis or case group is (30.1±1.98 ng/ml) which is (13.2±0.57 ng/ml) greater than the control group. It was statistically significant result (p<0.001). Also titer level for case group is oxLDL (72±2.75 mU/l), anti-oxLDL antibody (766±29.8 mU/ml), which is oxLDL (45.1±2.28 mU/l), anti-oxLDL antibody(603±17.74 mU/ml) greater than the control group. It was statistically significant result (p<0.001). But TAC titer level for control group is (116±2.47 nmol/l) which is (108.3±5.43 nmol/l) greater than the case group. It was not statistically significant result (p=0.098). According to the Binary Logistic Regression test the anti-oxLDL (OR=0.992, p<0.001), ADMA (OR=0.681, p<0.001), TAC (OR=1.017, p=0.105), oxLDL (OR=0.900, p<0.001) levels significantly influence the complication of coronary atherosclerosis. Therefore according to the Binary Logistic Regression test the anti-oxLDL level high significantly influence the complication of coronary atherosclerosis. Anti-oxLDL antibody titer are correlated directly with oxLDL (r=0.413, p<0.01), ADMA (r=0.42, p<0.001) levels. However, correlated negative directly with TAC (r=-0.233, p<0.01) level. Markers of endothelial dysfunction (ADMA OR=0.681, p<0.001) and oxidative stress (oxLDL, OR=0.900, p<0.001), (anti-oxLDL antibody, OR=0.992, p<0.001) high influence causing of complication of coronary atherosclerosis.

Cardiovascular diseases (CVD) are the leading cause of death in the World (31% of all deaths)and Mongolia as well. CVD has been the leading cause of death in Mongolia for the last 20 years and consists one of 3 death cases. In its turn 59.6% of CVD mortality caused by Ischemicheart diseases. When the coronary atherosclerotic plaque becomes vulnerable, it will a thrombus develops on that ruptured plaque and then occludes the coronary artery, which causes acute blood deficiency in the downstream myocardium. Some studies indicate thatmatrix metalloproteinase-9 (MMP-9) plays a key role on pathogenesis of plaque rupture. Aim:To study the involvement of serum MMP-9 enzyme in the pathogenesis during the rupture of the coronary atherosclerosis plaque.The study was conducted using case-control design. The main inclusion criteria of the case group is that the patient should have a ruptured coronary atherosclerotic plaque, confirmed by angiography. The total number of patients is 80, half of them belongs to the case group. MMP-9 was determined in serum by ELISA. We used CIIS (cardiac infarction injury score) by ECG and Gensini score system (Coronary Angiographic Scoring System) for assessing the severity of coronary heart disease.The average level of MMP-9 in case and control groups are 0.396±0.155 ng/ml, 0.223±0.087 ng/ ml respectively with p<0.001 significance which shows MMP-9 (OR=0.001, p<0.001) may plays a role in the pathogenesis of plaque rupture. MMP-9 is correlated with Gensini score and CIIS score, respectively (r=0.552, p<0.01; r=0.340, p<0.01) which shows MMP-9 is being elevated with the increase of the severity of coronary heart disease and the cardiac infarction injury. Serum MMP- 9 increases statistically significantly (p<0.001) with the increase of the severity of the stenosis and the number of the affected arteries: no severe stenosis (<75% stenosis) (0.245±0.086 ng/ ml); 1 vessel severe (>75%) stenosis (0.317±0.132 ng/ml), 2 vessel severe stenosis (0.348±0.157 ng/ml), 3 vessel severe stenosis (0.422±0.112 ng/ml). Furthermore, serum MMP-9 enzyme increases with accordance of severity of the myocardium injury with the statistical significance (p<0.01): the borderline abnormality group (CIIS<10, 0.227±0.099 ng/ml), possible injury (CIIS 10-15, 0.317±0.132 ng/ml), probableinjury (CIIS >15, 0.376±0.132 ng/ml) group. MMP-9 levels were significantly higher in the probable injury (CIIS >15) patients compared to the possible injury (CIIS 10-15) patients (p < 0.001). An increase in serum MMP-9 enzyme levels is a risk factor of the coronary atherosclerotic plaque rupture (OR=0.001, p<0.001). MMP-9 enzyme may be a possible marker of atheromatous plaque rupture in coronary heart disease.

Coronary heart disease is a leading cause of mortality in many countries. Acute coronary syndrome is the basis pathophysiology of coronary heart disease. Complication of coronary atherosclerosis composes rupture of plaque and erosion of vulnerable plaque. Endothelial dysfunction is main influence of coronary plaque erosion. But then recently research oxidative stress and reaction ofimmunocomplex is leading cause of coronary plaque rupture. So the research background will study markers of endothelial dysfunction, oxidative stress, immune reaction in the complication of coronaryatherosclerosis. Aim: Determine the effect of some marker for causing complication of the coronary atherosclerosis.The research has been conducted using case-control study method. In the case group, patients with complication of the coronary atherosclerosis as determined by coronary angiography (stenosis >85%) as in the control group healthy people with carotid artery stenosis (<0.7mm) has been involved. In the study we defined Anti-oxLDL (anti-oxidized low density lipoprotein) using ELISA Kit (Eucardio Lab, USA) and oxLDL (oxidized low density lipoprotein) titer by ELISA Kit (Mercadio, USA), ADMA (Asymmetric dimethylarginine) titer by ELISA kit (Eucardio Lab, USA) reagents in the enzyme binding reaction. Totalantioxidant capacity (TAC) was determined by using spectrophotometer method. The average age of people involved in the research is 57.2±9.72 and for the average age is case group 28 (32%) and 50 (68%) for the control group. ADMA titer level for complication of coronaryatherosclerosis or case group is (30.1±1.98 ng/ml) which is (13.2±0.57 ng/ml) greater than the control group. It was statistically significant result (p<0.001). Also titer level for case group is oxLDL (72±2.75 mU/l), anti-oxLDL antibody (766±29.8 mU/ml), which is oxLDL (45.1±2.28 mU/l), anti-oxLDL antibody(603±17.74 mU/ml) greater than the control group. It was statistically significant result (p<0.001). But TAC titer level for control group is (116±2.47 nmol/l) which is (108.3±5.43 nmol/l) greater thanthe case group. It was not statistically significant result (p=0.098). According to the Binary LogisticRegression test the anti-oxLDL (OR=0.992, p<0.001), ADMA (OR=0.681, p<0.001), TAC (OR=1.017, p=0.105), oxLDL (OR=0.900, p<0.001) levels significantly influence the complication of coronary atherosclerosis. Therefore according to the Binary Logistic Regression test the anti-oxLDL level high significantly influence the complication of coronary atherosclerosis. Anti-oxLDL antibody titer arecorrelated directly with oxLDL (r=0.413, p<0.01), ADMA (r=0.42, p<0.001) levels. However, correlated negative directly with TAC (r=-0.233, p<0.01) level.Markers of endothelial dysfunction (ADMA OR=0.681, p<0.001) and oxidative stress (oxLDL, OR=0.900, p<0.001), (anti-oxLDL antibody, OR=0.992, p<0.001) high influence causing of complication of coronary atherosclerosis.