الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
The adipose tissue is an endocrine organ producing substances called adipocytokines that have different effects on lipid metabolism, metabolic syndrome, and cardiovascular risk.Visfatin is a new adipocytokine which is largely secreted by visceral adipose tissue and its effects in the development of diabetes and inflammatory reactions are similar to insulin. IL-8 is also an adipocytokine mainly produced by macrophages, has important chemoattractant properties. Circulating levels are increased by hyperinsulinemia and hyperglycemia.
Aim of the work : Assessment of the following parameters:
• Serum concentration of visfatin.
• Serum concentration of interleukin-8.
In the following groups.
• Patients of Myocardial Infarction only.
• Patients with type 2 diabetes mellitus.
• Patients with both type 2 diabetes mellitus and myocardial Infarction.
• and compare these levels with control subjects.
Patients &Methods: 80 subjects were enrolled in the study and divided into three groups 20 Myocardial infarction patients (MI) ,20 type 2diabetes mellitus (T2DM ) and 20 diabetic patients omplicated with myocardial infarction (DM+MI) with duration of diabetes higher then 5 years and were matched with 20 control. visfatin and interleukin-8 were measured by ELIZA kits.Results: Serum visfatin levels were found significantly higher in the three groups of patients (myocardial infarction patients, diabetic patients, and diabetic patients complicated with Myocardial infarction) compared to the controls (p < 0.001). However, it was more elevated in diabetic with MI (p < 0.01) than in diabetic patients alone and myocardial infarction patients alone. AS regard Interleukin-8, it was also significantly higher in the three groups than in the controls (p < 0.001), and more elevated in diabetic with MI (p < 0.01) than in diabetic patients and myocardial infarction patients.Recommendations & conclusions : The biological mechanisms linking serum visfatin and Interleukin-8 to diabetes are obscure and remain to be fully elucidated in future studies. Further investigations are needed to determine whether visfatin measurement influences the approach of clinicians toward myocardial infarction and diabetes.
In conclusion, this study shows that visfatin and Interleukin-8 are elevated in myocardial infarction,type 2 diabetic patients but more elevated in in patients having both. Fasting glucose and peak troponin-I levels are the most prominent predictors of visfatin. The biological mechanisms linking serum visfatin todiabetes are obscure and remain to be fully elucidated in future studies. Further investigations are needed to determine whether visfatin measurement influences the approach of clinicians toward myocardial infarction and diabetes.
The plasma visfatin level on admission is a strong and independent predictive factor acute STEMI.The visfatin levels were positively associated with cardiac enzymes; thus, visfatin level may be closely associated with the myocardial damage, which could provide prognostic information.
Could visfatin also have anti-inflammatory properties? Even though the role of visfatin in the diabetes mellitus pathogeny is far from being revealed, there are studies that indicate the fact that the visfatin values are independent and significantly associated with type 2 diabetes, plasma visfatin being increased in type 2 diabetes patients.
The data show that in all studied groups,the serum IL-8 concentration is elevated and that the inflammatory process and PMN probably play an important role in the development of late vascular complications of diabetes. There is sufficient evidence in the scientific literature to support beyond any doubt the involvement of IL-8 in the establishment and preservation of the inflammatory microenvironment of the insulted vascular wall. However, how the information derived from in vitro studies and animal models can be applied in a clinical setting remains to be determined. The management of atherosclerotic cardiovascular disease consists of primary prevention, secondary prevention, and treatment of acute complications of atherosclerosis. Primary prevention requires overall cardiovascular risk estimation and risk factor modification. In cardiovascular risk estimation, several reports have indicated that increased serum levels of IL-8 are correlated with an increased risk of cardiovascular disease or acute cardiovascular events. However, these data are primarily the results of single-centre small-scale observational studies. There is limited data available derived from large-scale clinical trials illustrating the additive value of IL-8 on traditional risk factors as prognostic markers of short- or long-term outcome after acute cardiovascular events or in a primary prevention setting. Of note, the largest available cohort, including 381 CAD patients and 1977 controls, revealed that elevated systemic levels of IL-8 do not represent independent risk factors for coronary events. Another issue is whether additional markers for CAD are required in either a primary or a secondary setting. Inflammatory markers have to demonstrate high specificity and sensitivity and increase predictive value positively or negatively, especially if we take into account cost-efficiency parameters and the fact that most traditional risk factors are highly modifiable.
Recommendations
Regarding the therapeutic potential of IL-8, only limited data are available. As in any immune-modulating therapeutic approach, there are several drawbacks that need to be considered. First of all, atherosclerosis is a chronic condition; thus, long-term therapy must be applied. This raises tolerability and safety issues for a potential therapeutic agent that blocks a non-specific chemotactic pathway. Secondly, IL-8 is an important mediator of several aspects of immune response. Therefore, the complete blockade of IL-8 signalling pathways may not be desirable. Thus, techniques need to be applied to ensure that IL-8 signal blocking takes place in specific areas and tissues. An appealing area of investigation for immunesuppressive therapies is restenosis after PCI, in which IL-signalling blockers may be tested as potential agents for stent eluting.However, a specific IL-8 gene haplotype has been associated with reduced risk for ISR,providing indirect evidence that the IL-8-mediated pathways are involved in the process of ISR.57 Thus, targeting IL-8 pathways in an effort to reduce the rate of ISR could be a challenging field of investigation.
Nonetheless, it is necessary to take into account that alltherapeutic approaches to cardiovascular disease have been evaluated in large-scale clinical trials with specific endpoints. Therefore, despite its promising in vivo and in vitro indications, any IL-8 modulating therapy must be proven to exhibit the ability to reduce cardiovascular morbidity and mortality. To the best of our knowledge, no large-scale clinical trials are currently evaluating the effectiveness of IL-8-based treatments in cardiovascular disease. It will be therefore a long wait before IL-8-based therapeutic approaches find their way into clinical practice.