الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 112 |  |  |
| | | from | 112 | | |
Abstract
Inflammation is part of the non-specific immune response that occurs in reaction to any type of bodily injury. Cardinal signs of inflammation are increased blood flow, elevated cellular metabolism, vasodilatation, release of soluble mediators, extravasation of fluids and cellular influx. In some disorders the inflammatory process, which under normal conditions is self-limiting, becomes continuous and chronic, giving rise to inflammatory disease.
Over the last decade inflammatory immune responses have been implicated in several aspects of cardiovascular disease. Current concepts propose that the inflammation is aspectic and is not directly caused by infectious organisms. However, the precise relationship between inflammation, pathogens and cardiovascular disease remains incompletely understood. It is believed that depending on the specific disease different inflammatory pathways are of relevance.
Manifestations of cardiovascular disease, such as hypertension and ischemic heart disease are now considered to be connected to inflammation. Equally important, inflammation is now firmly recognized to participate in the process of atherosclerosis. Clinical consequences of atherosclerosis, such as myocardial infarction (MI) caused by rupture of the atherosclerotic plaque, elicit a complex inflammatory response. Depending on the context and stage of the disease, different inflammatory events are in progress.The current body of evidence support the mechanist and prognostic roles of inflammatory mediators in classic heart diseases like sepsis-induced cardiomyopathy, myocardial infarction, heart failure and cardiogenic shock. Cytokines represent a major mediator of inflammation and therefore are potential drug targets. However, application of these mediators as diagnostic and therapeutic targets in heart disease needs further clarification.