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Abstract
Coronary artery disease is a major problem and a growing cause of both morbidity and mortality .The severity of coronary artery disease determines the clinical presentation and the pathogenesis of the disease. In addition, the strategy of the therapy will differ according to the underlying disease severity.
Atherosclerosis was considered a blind lipid storage disease. Recent advances in basic science have established a fundamental role for inflammation in mediating all stages of this disease from initiation through progression and, ultimately, the thrombotic complications of atherosclerosis .These new findings provide important links between risk factors and the mechanisms of atherogenesis. Elevation in markers of inflammation predicts outcomes of patients with acute coronary syndromes, independently of myocardial damage. In addition, low-grade chronic inflammation, as indicated by levels of the inflammatory marker such as C-reactive protein, prospectively defines risk of atherosclerotic complications, thus adding to prognostic information provided by traditional risk factors .These new insights into inflammation in atherosclerosis not only increase our understanding of this disease, but also have practical clinical applications in risk stratification and targeting of therapy for this scourge of growing worldwide importance.
The traditional biomarkers of myocardial necrosis were not cardio specific and also reflect myocyte injury but do not pinpoint the specific mechanism of injury and are not active contributors to pathophysiology of CAD. There is still a need of development of earlier markers that can reliably rule out myocardial damage from the emergency room at patient presentation and , hopefully, detect myocardial ischemia both with and without the presence of irreversible myocyte injury.