الفهرس 
ACKNOWLEDGMENTS
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Abstract
This study was performed on seventy CAD patients that were scheduled for an elective diagnostic coronary angiography, in the Cardiac Catheterization Unit of Assiut University Hospital, and twenty apparently healthy persons as controls.
The studied participants were classified into:
1) Group (I): Twenty apparently healthy individuals as a control group.
2) Group (II): Seventy patients, as the main patient group, scheduled for an elective coronary angiography, they were further subdivided into:
• Group (IIa): Twenty-five CAD patients with normal coronary angiography.
• Group (IIb): forty-five patients with documented atherosclerotic CAD by coronary angiography.
CAD severity was assessed using a six-level score (Garcia et al., 2004):
(1) Normal coronary angiogram.
(2) Non-significant CAD (<70% stenosis in ≥1 epicardial vesselor <50%
stenosis of left main coronary artery).
(3) Significant 1-vessel disease (≥70% stenosis in one major epicardial
vessel).
(4) Significant 2-vessel disease (≥70% stenosis in two major epicardial
vessels).
(5) Significant 3-vessel disease (≥70% stenosis in all three major epicardial vessels).
(6) Significant left main CAD (≥50% stenosis of left main coronary artery).
All groups of the study were subjected to:
(1) Full medical history.
(2) Full clinical examinations.
(3) ECG and echocardiography.
(4) Coronary angiography: only the patients were subjected to it.
(5) Laboratory investigations:
A. Routine investigations:
o Complete blood count.
o Fasting serum glucose.
o Kidney function tests.
o Liver function tests.
o Serum lipid profile.
o TSH, T3 and T4.
B. Special investigations:
o Plasma myeloperoxidase (MPO) level.
o Genotyping of MPO gene -463G>A polymorphism
using PCR-RFLP.
o Plasma oxidized LDL.
o Serum HsCRP.
o Plasma fibrinogen.
o Plasma apolipoproteins A-I and B.
The results of the previous special investigations revealed the following data:
Myeloperoxidase, ox-LDL, hsCRP, fibrinogen, lipid profile, apolipoproteins A-I and B and their ratios in the studied groups:
There were statistically high significant elevation in the mean values of plasma myeloperoxidase in the main patient group (II) and the patients with documented atherosclerotic CAD group (IIb) when compared to the control group (I) (P < 0.001), and significant elevation in group IIa when compared to group I and in group IIb as compared to group IIa (P < 0.05).
Statistically significant elevation of the median values of plasma ox-LDL were detected in group IIb when compared to group I (P < 0.01), and in group II when compared to the control group (I) (P < 0.05). No significant difference could be detected between group IIa and IIb, or in group IIa as compared to the control group (I).
There were statistically high significant elevation of the median values of serum hsCRP in each of group II and IIb when compared to the control group (I) (P < 0.001), and a significant elevation in group IIa when compared to group I (P < 0.01), and in group IIb as compared to group IIa (P < 0.05).
Statistically high significant elevation of plasma fibrinogen mean values were found in the main patient group (II), patients with normal angiography group (IIa), and the patients with documented atherosclerotic CAD group (IIb) when compared to the control group (I) (P < 0.001), and a significant elevation was observed when comparing group IIb to IIa (P < 0.05).
The mean values of LDL-c, apo B, apo B/apo A-I, TC/HDL-c and LDL-c/HDL-c ratios in each of group II, IIa, and IIb were significantly higher and the mean values of HDL-c and apo A-I were significantly lower than those in the control group (I), while significant elevation of total cholesterol was detected in each of group II and IIb as compared to group I. Although the lipid profile was different between the normal angiography (IIa) and stenotic angiography (IIb) patients, these differences were not statistically sig¬nificant except for apo A-I, apo B and apo B/apo A-I ratio. No significant differences were detected in the mean values of triglycerides between all studied groups.
Relation between plasma myeloperoxidase and CAD severity score in the main patient group (II):
A statistically significant elevation of mean plasma MPO levels according to the six level CAD severity score was detected in patients with higher CAD severity score (scores 5 & 6) as compared to those with lower CAD severity score [scores 1 & 2 or scores 3 & 4 (P < 0.05)] and Spearman’s correlation coefficient showed a significant positive association between plasma MPO levels and CAD severity score.
Relation between ox-LDL, hsCRP, fibrinogen, lipid profile, apolipoproteins A-I and B, their ratios and CAD severity according to CAD severity score in the main patient group (II):
There was a statistically significant elevation of serum hsCRP median values, mean values of LDL-c/HDL-c ratio, plasma apo B mean values and mean apo B/apo A-I ratio according to CAD severity score in the patients with scores 5 & 6 as compared to each of scores 1 & 2 and 3 & 4 (P < 0.001, < 0.001 for hsCRP) (P < 0.05, <0.05 for LDL-c/HDL-c ratio) (P < 0.01, <0.05 for apo B) (P < 0.01, < 0.01 for apo B/apo A-I ratio). Moreover a statistically significant elevation of mean plasma apo B/apo A-I ratio in scores 3 & 4 as compared to scores 1 & 2 (P < 0.05) could also be detected. And a significant reduction of mean plasma apo A-I according to CAD severity score could also be found in both scores 3 & 4 and 5 & 6 as compared to scores 1 & 2 (P < 0.05, <0.01 respectively). While, no statistically significant differences in the median values of plasma ox-LDL or in the mean values of plasma fibrinogen according to CAD severity score could be found.
Distribution of MPO genotypes in the studied groups and its relation to CAD severity in the main patient group (II):
In the controls (group I) 9 persons (45%) had homozygous GG genotype, and 11 persons (55%) had heterozygous GA genotype, and in the main patient group (group II) 33 patients (47.14%) had GG genotype, and 37 patients (52.86%) had GA genotype. While, homozygous AA genotype was neither found in the controls (group I) nor in the patients (group II) of this study. In the patients with normal angiography group (group IIa) GG genotype was found in 11 patients (44%) while GA genotype in 14 patients (56%). In the patients with atherosclerotic documented obstructive CAD (stenotic lesion) group (group IIb) 22 patients (48.89%) had GG genotype and 23 (51.11%) had heterozygous GA genotype. In the non-significant CAD (score 2), there were no patients in this group (no GG or GA genotype). In both the significant 1-vessel disease (score 3) and the significant 2-vessel disease (score 4), each of them had 6 patients with GG genotype (40%) and 9 with GA genotype (60%). In the significant 3-vessel disease (score 5), 6 patients had GG genotype (54.55%) and 5 had GA genotype (45.45%), while in the significant left main CAD (score 6) the GG genotype was found in all 4 patients of this group (100%).
According to the dichotomization of the CAD severity score the distribution of genotypes was as follow:
(1) Scores 1 & 2: 11 (44%) patients for GG and 14 (56%) for GA genotype.
(2) Scores 3 & 4: 12 (40%) patients for GG and 18 (60%) for GA genotype.
(3) Scores 5 & 6: 10 patients for GG (66.7%) and 5 for GA genotype (33.3%).
No statistically significant association was found between MPO genotype distribution in the main patient group (II) and CAD severity as assessed by the six level CAD severity score ( (Chi square) test= 5.44, P > 0.05) or by the dichotomization of CAD severity score ( (Chi square) test= 3.008, P > 0.05).
Plasma myeloperoxidase in different MPO genotypes of the studied groups:
In the control group (I), there were significant elevation of the mean values of plasma MPO in carriers of GG genotype compared to carriers of GA genotype (P<0.05). Plasma myeloperoxidase level was significantly elevated in patients with homozygous GG genotype when compared to the GA genotype carriers of the same group in each of the main patient group (II) (P < 0.001), patients with normal angiography (IIa) (P<0.001), patients with documented atherosclerotic CAD (IIb) (P <0.000), CAD severity scores 1 & 2 (P <0.001), scores 3 & 4 (P <0.001) and scores 5 & 6 (P <0.000) groups.
Correlations between ox-LDL, hsCRP, fibrinogen, lipid profile, apolipoproteins A-I and B, their ratios and CAD severity score in the main patient group (II):
There was a statistically high significant positive correlation between serum hsCRP and CAD severity score while no association could be found between CAD severity and each of ox-LDL and fibrinogen.
There were stronger positive significant associations between CAD severity score and apo B (P< 0.01), apo B/apo A-I ratio (P< 0.001), and a stronger negative association between it and apo A-I (P< 0.01) than with total cholesterol and LDL-c (P < 0.05).
There was a significant negative correlation between ejection fraction and CAD severity score, while no significant correlations between CAD severity score and each of BMI, age, WBCs, neutrophils or HDL could be found.