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Proinflammatory Cytokines in Acute Coronary Syndromes.

BACKGROUND
Over the last decades the role of inflammation and immune system activation in the initiation and progression of coronary artery disease (CAD) has been established.


OBJECTIVES
To present the interplay between cytokines and their actions preceding and shortly after ACS.


METHODS
We search in a systemic manner for identification of the most relevant articles to the topic inflammation, cytokines, vulnerable plaque and myocardial infarction in MEDLINE, COCHRANE and EMBASE databases.


RESULTS
Different classes of cytokines (intereleukin [IL]-1 family, Tumor necrosis factor alpha (TNF-α) family, chemokines, adipokines, interferons) are implicated in the entire process leading to destabilization of the atherosclerotic plaque and consequently to the incidence of myocardial infraction. Especially IL-1 and TNF-α family are involved in inflammatory cell accumulation, vulnerable plaque formation, platelet aggregation, cardiomyocyte apoptosis and adverse remodeling following myocardial infraction. Several cytokines such as IL-6, adiponectin, interferon-γ, appear with significant prognostic value in ACS patients. Thus, research interest focuses on the modulation of inflammation in ACS to improve clinical outcomes.


CONCLUSION
Understanding the unique characteristics that accompany each cytokine-cytokine receptor interaction could illuminate the signaling pathways involved in plaque destabilization and indicate future treatment strategies to improve cardiovascular prognosis in ACS patients.