Search

The mechanism of miR-30a in myocardial fibrosis in rats with myocardial infarction (MI) was investigated. rAAV9-miR-30a was constructed and transfected to heart via injecting into the left ventricular cavity of MI rats. The sham operation group, control group, miR-30a group and miR-30a-NC group were established. Besides, the 3′-UTR of CTGF was inserted into luciferase expression plasmid (pMir-report), then transfected into COS1 cells. miR-30a and control miRNA were, respectively, cotransfected into COS1 cells. The expression of luciferase was detected before and after knockdown of the binding site of miR-30a and the 3′-UTR of CTGF. Four weeks after MI surgery, cardiac function was measured by color Doppler echocardiography, including short axis shortening (FS) and left ventricular ejection fraction (LVEF); the myocardial collagen volume fraction (CVF) was observed by Masson's staining; deposition of collagen I and collagen III were evaluated by immunohistochemical stain; using real-time PCR to detect expression levels of miR-30a and CTGF; the expression of CTGF was observed by western blotting. In MI group, cardiac function was significantly improved, while the expression levels of CVF, collagen I and III, the ratio of type I/III collagen, CTGF were significantly reduced. After knockdown the binding site of miR-30a and the 3′-UTR of CTGF, luciferase expression in COS1 cells decreased significantly. miR-30a might inhibit the expression of CTGF by directly combining with the 3′-UTR site of CTGF after MI, thereby reduce the production of collagen in myocardia, inhibit myocardial fibrosis, then improve cardiac function. [ABSTRACT FROM AUTHOR]

The aim of this study was to determine the relationship between glucose fluctuation and global registry of acute coronary events (GRACE) risk score in patients with acute coronary syndrome (ACS) and abnormal glucose metabolism using continuous glucose monitoring system (CGMS). A total of 76 patients with ACS admitted into coronary care unit (CCU) were divided into two groups based on their blood glucose level and were further divided into subgroups based on GRACE risk score. A CGMS was used to real-time monitor blood glucose for 72 h in all patients after admitted into CCU. Twenty-four-hour mean blood glucose (24-h MBG) and 24-h mean amplitude of glycemic excursion (24-h MAGE) were calculated. Among the 76 patients, 52 patients had abnormal glucose metabolism. Among the 52 patients, there were 8 patients in low-risk group, 19 patients in moderate-risk group, and 25 in high-risk group. Among the 24 patients with normal glucose metabolism, there were 6 patients in the low-risk group, 6 patients in the moderate-risk group, and 12 in the high-risk group based on GRACE score. For patients with abnormal glucose metabolism, the 24-h MBG and 24-h MAGE of moderate- and high-risk groups were significantly higher than that of the low-risk group, which were not found in patients with ACS and normal glucose metabolism. High prevalence of abnormal glucose metabolism was found in ACS patients admitted into CCU and larger blood glucose fluctuation is associated with moderate and high GRACE risk scores in patients with ACS and abnormal glucose metabolism. [ABSTRACT FROM AUTHOR]

Background: Reports showed no change of 7‐day mortality after primary percutaneous coronary intervention (PCI) for ST‐elevation myocardial infarction (STEMI) between 2001 and 2011 in China. National rolling one‐year interventional standardized training programme began in September 2009. However, the improvement in clinical outcome following STEMI PCI after 2011 remains unclear. Methods and Results: This multicentre MOODY registry study aimed to analyse the clinical improvement after STEMI PCI. Of a total of 9265 acute MI patients registered from 24 centres, 3142 STEMIs having a first medical contact time ≤12 hours and undergoing primary PCI were assigned to the Pre Group (n = 1014, between March 1999 and October 2010) or the Post Group (n = 2128, between 2010 November and 2016 October). The primary endpoint was in‐hospital cardiac death. Study endpoints were also compared between trained and untrained operators and between experienced (≥50 primary PCIs/year) and inexperienced personnel. In‐hospital death after PCI was 3.0% in the Pre Group, significantly higher than 1.6% in the Post Group (P =.035). The improvements in clinical outcome after PCI between the 2016 and Pre Groups were stably sustained through one‐year follow‐up. The significant reduction for in‐hospital death was noted when primary PCI was performed by trained (1.4% vs 5.4%, P <.001) or experienced (2.7% vs 4.8%, P =.001) operators, compared to untrained or inexperienced operators, respectively. Inclusion of the untrained operator into the conventional risk model strongly enhanced the prediction for endpoints. Age, Killip Class 3, diabetes, trans‐radial approach and system delay were five predictors of in‐hospital death after primary PCI. Conclusion: PCI for STEMI by a trained and experienced operator was associated with significant reduction of in‐hospital death. Our results strongly warrant the need for promoting the current system response and patient education. [ABSTRACT FROM AUTHOR]