ABSTRACT
This study aimed to explore the relationship between plasma interleukin 6 (IL-6) levels, adverse cardiovascular events, and the severity of acute coronary syndrome (ACS). A literature review was performed of studies regarding IL-6 and ACS extracted from databases including EMBASE, Cqvip, MEDLINE, Web of Knowledge, PubMed, Cochrane Library, China National Knowledge Infrastructure, and Wanfang data. The Newcastle-Ottawa scale (NOS) was used to evaluate the quality of the literature. The literature was screened, its quality was evaluated, and relevant data were extracted for performing meta-analysis using RevMan software (version 5.3). A total of 524 studies were included in the initial survey. After several rounds of screening and analysis, six studies met the inclusion criteria and underwent meta-analysis using a fixed-effect model. Patients were divided into non-severe and severe groups based on the concentration of high-sensitivity C-reactive protein. Meta-analysis of the relationship between IL-6 and the severity of ACS showed that the plasma IL-6 level of patients in the severe group was significantly higher than that of patients in the non-severe group (p<0.00001). Additionally, patients with experience of major adverse cardiovascular events had significantly higher plasma IL-6 levels than did patients without experience of such events (p<0.00001). In summary, patients with ACS and high IL-6 levels tended to be in a critical condition, with a higher risk of adverse cardiovascular events and worse prognosis. Thus, IL-6 levels could indicate whether patients with ACS may have adverse cardiovascular events and determine the severity of ACS.
Subject(s)
Humans , Interleukin-6 , Acute Coronary Syndrome , Prognosis , C-Reactive Protein , ChinaABSTRACT
In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release (CICR) in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6weeks after myocardial infarction (MI). In the post-MI cardiomyocytes, the amplitude of ICaL decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alphalc, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant.It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes,which leads to the decreased CICR in the cell and contractile dysfunction of myocardium.