الفهرس 
ACUTE CORONARY SYNDROME (ACS)Only 14 pages are availabe for public view
 |  | from | 177 |  |  |
| | | from | 177 | | |
Abstract
C
HD is the leading cause of death and disability. Its presentation varies from chronic CHD to ACS that includes UA and MI.
Understanding the pathophysiology that leads to ACS and identifying its risk factors are crucial steps for efforts to prevent this disease. Many CHD risk factors are modifiable. On the other hand there are risk factors that cannot be modified.
Blood flow is maintained by the proper balance of hemostasis and fibrinolysis. The process of blood coagulation is controlled by a series of negative feedback steps that include Serpins. One of the recently identified serpins is ZPI. It forms a complex with its cofactor PZ to inhibit activated factors X, XI and IX by different mechanisms.
The physiological function of PZ still remains unclear. However, many disease states have been reported in relation to PZ deficiency. The pathological consequences of decreased levels of PZ are still uncertain, but increasing evidence supports the opposing role, i.e. deficiency of PZ might increase thrombotic risk.
The possible role of PZ deficiency in the occurrence of cardiovascular diseases has been evaluated with conflicting findings. Thus, this work aimed to detect PZ level in patients with ACS and to investigate the role of PZ as an independent risk factor for ACS.
The material of this study entailed 55 patients with ACS. Thirty healthy subjects, age and sex matched, were included as a control group. All enrolled patients were subjected to E.C.G, measurement of cardiac biomarkers, lipid profile, liver function tests, kidney function tests, fasting and postprandial blood glucose, PT and PTT as well as plasma level of PZ.
Plasma PZ showed significantly lower level in ACS patients and subgroups as compared to controls. There was no statistically significant difference of PZ level among the different subgroups of ACS.
Correlation studies revealed a highly significant negative correlation between the age and PZ level, which may explain the high incidence of ACS in old ages. Plasma PZ showed significantly lower levels of PZ in female versus male patients.
Plasma PZ showed significantly lower level in patient’s age subgroup > 55 years than the < 55 years.
Plasma PZ showed significantly lower levels in hypertensive, smokers and patients with positive family history of ACS who are < 55years. As regards sex, diabetes mellitus, and dyslipidemia, there was no statistically significant difference of PZ level in those patients.
Plasma PZ showed significantly lower levels in diabetic and hypertensive patients who are > 55years. On the other hand, no statistically significant differences in PZ levels were detected as regards sex, dyslipidemia, smoking and family history of ACS.
Plasma PZ showed significantly lower levels in ACS patients group whose age < 55years with the increase in number of associated risk factors. On the other hand, Plasma PZ showed no statistically significant difference in ACS patients group whose age > 55 years as regards number of positive risk factors. Therefore, the level of PZ was shown to decrease with age either with or without positive risk factors.
The results obtained by the ROC curve and by interactive dot diagram indicate the predictive cutoff value of PZ in ACS group and subgroups. Thus, PZ may provide a valuable tool for diagnosis ACS.
The results obtained by Uni-variate logistic regression analysis showed an increased risk of ACS with reduced PZ levels and thus PZ is proved as an established risk factor for ACS.
Finally, the results obtained by Multi-variate logistic regression analysis showed an increased susceptibility to ACS with low levels of PZ and thus denoted PZ as an independent risk factor for ACS.