الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Acute myocardial infarction (AMI) remains the leading cause of morbidity and mortality worldwide. MI is an acute event accompanied by irreversible myocardial tissue injury with increased inflammation that replaces necrotic tissue with a fibrotic scar. Hypertension, smoking, dyslipidemia, diabetes mellitus are considered the most common and important risk factors that contribute in pathogenesis of MI. AMI usually results from rupture or erosion of a vulnerable, lipid-laden, atherosclerotic coronary plaque where a totally occluding thrombus leads to STEMI and partial occlusion, or occlusion in the presence of collateral circulation, results in non-STEMI or unstable angina.
Diagnosis of MI is based on simple principles of good history, physical examination, ECG, echocardiography and series of cardiac biomarkers which differ in their mechanism and time of secretion and action. CK-MB and troponin are the most commonly used biomarkers to diagnose MI, although there are varieties of biomarkers that may have a diagnostic role in MI and may even contribute to the disease pathogenesis as MMPs.
MMPs are family of 24 zinc-dependent endopeptidases that share a common structural framework, with a signal peptide, N-terminal propeptides, catalytic domain, and hemopexin-like C-terminal domain, which is linked to the catalytic domain by a flexible hinge region.
The catalytic activity of MMPs is strongly controlled at four different levels: Gene expression with transcriptional and post-transcriptional regulation, compartmentalization, pro-enzyme activation by removal of the pro-domain and Inhibition by specific inhibitors (TIMPs).
MMPs are important in many biological processes including cell proliferation, migration and differentiation, remodeling of ECM and vascularization, on the other hand, if not properly balanced, MMPs could also contribute to harmful pathological conditions such as arthritis, pulmonary emphysema, endometriosis, neurological diseases, tumors and their metastasis and cardiovascular diseases.
MMP-9 is considered one of the MMPs that have been evaluated in the setting of CVDs where it plays a pivotal role in atherosclerosis, hypertension, MI and heart failure.
MMP-9 has an indirect pre-STEMI role as it contributes in the pathogenesis of many risk factors that leads to MI as hypertension, dyslipidemia and atherosclerosis.
Following MI, both the infarcted region as well as the remote non-infarcted zone undergoes cardiac remodeling as a part of the wound healing response that can be divided into three distinct, but overlapping phases: inflammatory phase, proliferative phase and maturation phase.
MMP-9 role as a marker of cardiac remodeling mainly depends on the timing, cellular source and substrate specificity of it, where it directs many aspects of the inflammatory and proliferative stages of cardiac remodeling in acute STEMI by directly degrading ECM and activating cytokines and chemokines. The combined actions of MMP-9 determine scar formation and quality that is directly contributes to regional and global LV function.