Exogenously over-expression of periostin gene in the heart led to impaired cardiac function, including left ventricle dilation, cardiac myocytes decrease and collagen deposition increase, which suggested a correlation between elevated periostin with deteriorated cardiac function. Furthermore, inhibition the expression of periostin was able to improve cardiac systolic ejection function and animal survival rate. These researches demonstrated a detrimental Epimedoside-A effect of periostin in cardiovascular system. However, other researches have drawn opposite conclusions about the effect of periostin on myocardium remodeling. Dennis Ladage et al found that delivery of periostin peptide into the pericardial space of MI swine exerted beneficial effects on myocardium repair, reducing infarct myocardium size, attenuating left ventricular systolic function and increasing capillary density post MI. Another research group demonstrated that periostin was able to induce reentry of differentiated mammalian cardiomyocytes into the cell cycle both in vitro and in vivo. Delivery of recombinant periostin into the heart of MI rat improved cardiac systolic function, reduced fibrosis and hypertrophy as well as enhanced myocardium repair. Although the net effect of periostin on ventricular remodeling after acute myocardial infarction has not reached a consensus, there is no doubt that this molecule acts as an important regulator in this process. Myocardial periostin was significantly up-regulated after AMI and participated actively in cardiac remodeling. However, few researches focused on the change in circulating periostin after AMI. This study was designed to investigate the association of serum periostin level with cardiac function and short term disease prognosis in acute myocardial infarction patients. Our study found that serum periostin was in negative association with left ventricular ejection fraction and left atrium diameter as well as in positive association with Killip class in acute myocardial infarction patients. Higher serum periostin level was related to increased composite cardiovascular events after six months follow up post AMI. Acute myocardial infarction is one of the lethal diseases in the world, with an increasing morbidity and threatens the public health. The local ischemia and hypoxia conditions after AMI caused irreversible cardiomyocytes death or apoptosis and these cardiomyotes were gradually replaced by interstitial fibrosis Tubeimoside-I Through ventricular remodeling process. As scar and fibrosis structure lacked the ability of contractility and electric activity, systolic function and electric coupling of the heart were impaired and these finally led to deteriorated cardiac function. Activated fibroblasts in the extra-cellular matrix secreted various ECM proteins that contributed to ventricular remodeling after AMI. Through binding to targeted receptors and conducting cell signaling, these proteins played an important role in regulation of cardiomyoctes kinetics such as proliferation, migration and apoptosis. Periostin is an extra-cellular protein proved to play an important role in cardiovascular development and disease.