ABSTRACT
The present results demonstrated that high glucose (G), salt (S), and cholesterol C (either alone or in combination), as mimicking extracellular changes in metabolic syndrome, damage cardiomyocyte-like H9c2 cells and reduce their viability in a time-dependent manner. However, the effects were greatest when cells were exposed to all three agents (GSC). The mRNA of glycoprotein (gp) 130 and WSX-1, both components of the interleukin (IL)-27 receptor, were present in H9c2 cells. Although mRNA expression was not affected by exogenous treatment with IL-27, the expression of gp130 mRNA (but not that of WSX-1 mRNA) was attenuated by GSC. Treatment of IL-27 to H9c2 cells increased activation of signal transducer and activator of transcription 3 (STAT3) and protected cells from GSC-induced cytochrome c release and cell damage. The protective effects of IL-27 were abrogated by the STAT3 inhibitor, stattic. The results of the present study clearly demonstrate that the STAT3 pathway triggered by anti-inflammatory IL-27 plays a role in protecting cardiomyocytes against GSC-mediated damage.
Subject(s)
Inflammation/genetics , Interleukins/pharmacology , Metabolic Syndrome/genetics , Myocytes, Cardiac/drug effects , STAT3 Transcription Factor/biosynthesis , Cell Survival/drug effects , Cholesterol/pharmacology , Cytochromes c/metabolism , Gene Expression Regulation/drug effects , Glucose/pharmacology , Glycoproteins/biosynthesis , Glycoproteins/metabolism , Humans , Inflammation/drug therapy , Inflammation/pathology , Interleukins/metabolism , Metabolic Syndrome/drug therapy , Metabolic Syndrome/pathology , Myocytes, Cardiac/metabolism , Myocytes, Cardiac/pathology , RNA, Messenger/biosynthesis , Receptors, Interleukin/biosynthesis , Receptors, Interleukin/metabolism , STAT3 Transcription Factor/genetics , Signal Transduction/drug effectsABSTRACT
BACKGROUND/PURPOSE: People receive electrocardiogram (ECG) examination for various reasons in a hospital setting. An important clinical practice issue may be that cardiologists need to be consulted for Brugada-type ECGs identified through routine screening. We investigated the prevalence and prognosis of patients with Brugada-type ECG in a hospital-based population in an attempt to improve the management of these patients. METHODS: In 20,562 patients seeking medical care for non-cardiovascular reasons, 74,955 ECGs were performed from December 1999 to February 2001. The diagnostic criteria for Brugada-like ECG from the European Society of Cardiology were used. International Statistical Classification of Diseases codes and city residents' records were documented to indicate the reasons for visiting clinics or hospitalization and mortality outcome. Medical records were reviewed and telephone interviews were conducted. RESULTS: Twenty-six (0.13%) of the 20,562 patients were confirmed to have Brugada-type ECGs. None of these patients had ever experienced syncope, near syncope or sudden cardiac death. After 57.1 ± 15.8 months of follow-up, there were four deaths out of the 26 patients with Brugada-type ECG (15.4%, 95% CI: 1.53-2.9%) compared with 2899 of those without (14.1%, 95% CI: 13.6-14.5%; p=0.89, log-rank test). Neither sudden cardiac death (p=0.61) nor hospitalized death (p=0.55) was different between patients with and without Brugada-type ECG. CONCLUSION: Patients with Brugada-type ECGs are not rare in a hospital-based population. The presence of Brugada-type ECGs in patients without syncope or sudden cardiac death was not associated with hospitalized mortality.
