الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Coronary artery disease (CAD) is today the leading cause of mortality worldwide, and it continues to be a major burden upon public health,(10) CAD is expected to remain the world’s leading cause of disease burden (which represents aggregate mortality and morbidity) in 2020, despite considerable progress in prevention and treatment over the past 20 years. (9)
Acute coronary syndrome describes a spectrum of clinical syndromes ranging from unstable angina to NSTEMI and STEMI. Patients presenting with ACS are divided into those with ST elevation (lasting more than 20 minutes) or new left bundle branch block, and those with NSTEACS which includes unstable angina, and NSTEMI.(1)
Fibrinogen (clotting factor I), precursor of fibrin is a glycoprotein synthesized by the liver and maintained in plasma at concentration ranging from 2-4 g/L, the fibrinogen molecule consists of two sets of three non identical polypeptide chains which encoded by fibrinogen gamma, fibrinogen alpha and fibrinogen beta genes clustered chromosome 4. (121)
Early evidence from previous decades pointed to a strong association between fibrinogen levels and CAD manifestation The Gothenburg Study(139) reported that plasma fibrinogen levels represent an independent risk factor for myocardial infarction (MI).
Fibrinogen association with coronary heart disease is similar to those of classic risk factors, such as blood pressure and serum cholesterol, and to the circulating concentration of C-reactive protein (CRP), which, like fibrinogen, is a marker of the inflammatory response, including low-grade inflammation in healthy persons.(197)
The current study aimed to clarify whether fibrinogen release is a factor initiating the inflammatory process in MI or is predominantly a response to that clinical condition.
The current study included seventy patients of both sexes who met the American Heart association (AHA) recommendations for diagnosis of ACS (51) from those attending the intensive care unit’s critical care medicine department, faculty of medicine, Alexandria University. Approval of the study from ethical committee was obtained & an informed consent was taken from each patient included in the study.
Patients were divided into the following groups:
• Group A: Included 20 patients with unstable angina.
• Group B: Included 40 patients with ST segment elevation MI:
They were divided into two equal sub-groups:
- Group B 1: with successful thrombolytic therapy.
- Group B 2: with failed thrombolytic therapy.
• Group C: included 10 healthy control persons as a control group of same age and sex.
Patients were diagnosed and treated according to AHA recommendations (51) also complete clinical examination including chest and heart auscultation. Serial ECG was done. Fibrinogen (mg/dl), Creatinine Kinase-Myocardial Band (CK-MB (ng/ml)), Troponin I( ng/ml) and C-reactive protein (mg/l) were withdrawn on admission of all patients except plasma fibrinogen level (mg/dl) in group B of patients which was withdrawn 24 hours after admission.
The four groups were matching as regards the patients’ age, gender but according to risk factors HTN and IHD history were significantly higher in unstable angina group than control group and smoking was significantly higher in failed thrombolytic group than control .there was no significant difference between the four groups according to time of presentation. Complications were more found in group B1and B2 but it wasn’t statistically different from the other two groups. Although the anterior raising was more common than the inferior and lateral raising in patients with STEMI there was no significant difference between group B1and B2 regarding the site of ST segment rising. There was significantly higher ICU stay in group B1and B2 than patients of group A and there was significantly high ICU stay in group B2 than group B1.
It was found that CKMB level and Troponin I were significantly higher in STEMI groups (group B1and B2) than unstable angina and control groups both on admission and after 6 hours, also it was found the values of CKMB and Troponin I after 6 hours were significantly higher than values of admission in group B1and B2. As regard the CRP, it was found that values of group B1 and B2 were significantly higher than the values of group A and C.
It was found that fibrinogen in patients of group B1and B2 (patients with STEMI after receiving thrombolytic) had no significant difference but it significantly lower than fibrinogen in group A and group C, while there was no significant difference between group A and group C as regard fibrinogen. On correlating the results of Fibrinogen level with different risk factors it was found that fibrinogen level was higher in patients with history of IHD where as there was no significant difference in correlation fibrinogen level with the other risk factors.
It was concluded that:
There is a strong direct relationship between the risk factors for ischemic heart disease and developing acute myocardial infarction.
The significant high level of CRP in ACS patients in the present study clarified that inflammation plays a major role in the pathogenesis of myocardial infarction.
Failed thrombolytic therapy associated with more complications and ICU stay.
Fibrinogen was higher in patients with history of IHD so fibrinogen level is associated with increased risk of development IHD.
Both increase of fibrinogen and CRP on admission in UA patients indicates that fibrinogen is one of the factors initiating the inflammatory process in ACS.
The significant decrease of fibrinogen after receiving thrombolytic therapy shows that fibrinogen is directly related to the coagulation process of the AMI.
It is recommended that:
• A study on a larger group of patients should be conducted to provide more accurate data.
• Evaluation of the fibrinogen level in patients with NSTEMI patients with STEMI who didn’t receive any reperfusion therapy or had PCI as reperfusion therapy as fibrinogen in the current study was only tested in patients with UA and STEMI after thrombolytic therapy.
• Serial fibrinogen level from admission to discharge of patients to follow up the course of fibrinogen during their hospital stay before and after receiving thrombolytic as fibrinogen in the current study in patients with STEMI was only withdrawn after 24.
• Follow up the patients after discharge and correlate the fibrinogen level with post discharge complications and mortality to evaluate the prognostic value of fibrinogen.