MiR-219a-5p exerts a protective function in a mouse model of myocardial infarction

Background:Myocardial infarction(MI)is known worldwide for its important disabling features,including myocarditis and cardiomyocyte apoptosis.It is believed that microRNA(miRNA)has a role in the cellular processes of apoptosis and myocarditis,and miR-219a-5p has been found to suppress the inflammatory response.However,unknown is the precise mechanism by which miR-219a-5p contributes to MI.Methods:We measured the expression of miR-219a-5p and evaluated its effects on target proteins,inflammatory factors,and apoptosis in a mouse model of MI.Echocardiography was utilized to examine the MI clinical index,and triphenyl tetrazolium chloride staining was employed to analyze the infarcted region.Enzyme-linked immunosorbent assay and Western blotting measured serum and molecular markers in heart tissues.To quantify the association with miR-219a-5p and ATPase sarcoplasmic/endoplasmic reticulum Ca^(2+)transporting 2(ATP2A2),the luciferase activity assay and Pearson’s correlation analysis were employed.Results:MiR-219a-5p exhibited low expression in a mouse model of MI,and its amplification prevented both apoptotic and inflammatory reactions.Specifically,miR-219a-5p targeted ATP2A2.Conclusion:In a mouse model of MI,miR-219a-5p exerted a potent protective effect via direct targeting of ATP2A2.

Usefulness of myocardial performance index for assessing right ventricular function after percutaneous closure of atrial septal defect

Objective Assessment of right ventricular function in patients with atrial septal defect(ASD)is difficult.The Doppler myocardial performance index(MPI)may provide a method of assessing function in these patients.The purposes of this study were to evaluate the right ventricular function and its changes in patients with ASD after transcatheter closure of ASD.Methods MPI,defined as the sum of isovolumic relaxation time and isovolumic contraction time derived by ejection time,was measured from tricuspid inflow and right ventricular outflow;Doppler velocity profiles recorded during routine echocardiography.Twenty nine patients(13 men,16 women;mean age 25.28±12.69,range 6 to 57 years)were diagnosed to secundum ASD[the stretched diameters of ASD were from 9 To 36(24.91±7.98)mm],and had a successfully placed Amplatzer septal occluder(ASO)(the sizes of ASO were from 11 to 40 mm);there were 81 sex-matched,age-matched healthy people(control group 41men,40 women;mean age 29.02±14.22,range 4 to 45 years).MPI was measured again on 3 days and 1 month after closure of ASD.Change in the study group was assessed and compared to the control subjects with structurally normal hearts.A complete 2-dimensional and Doppler echocardiographic examination was performed in all study groups.Results 1)The isovolumic relaxation and isovolumic contraction times[respectively(77.59±14.39)ms vs(60.93±12.94)ms,P<0.0001;(28.28±10.88)ms vs(23.64±9.01)ms,P=0.027]were prolonged,and ejection time[(260.65±21.86)ms vs(271.85±21.92)ms,P=0.033]was shortened in patients with ASD compared with that in control subjects,resulting in a marked increase in the MPI(0.40±0.07 vs 0.31±0.05,P<0.0001)from normal values;2)by Pearson's correlations,the MPI had no correlation with heart rate and blood pressure in control subjects and patients with ASD,but it correlated positively with age in patients with ASD;3)by Pearson's correlations,the MPI correlated positively with the diameter of ASD and pulmonary artery pressure;4)after transcatheter closure of ASD,the MPI decreased markedly.Conclusions 1)MPI is a conceptually new,simple,and reproducible Doppler index in patients with ASD;2)MPI is free from the effect of age,heart rate and blood pressure;(3)MPI appears to be relatively dependent on changes in the diameter of ASD and pulmonary artery pressure;4)the right ventricular function was improved after transcatheter closure of ASD.

Clinical follow up of patients with premature coronary artery disease (PCAD) implanted with drug-eluting stents

Background: Drug-eluting stents (DESs) are associated with lower restenosis rates. However, minimal data on the follow up results of premature coronary artery disease (PCAD) treated with DESs exist. This study was to evaluate clinical characteristics and one- year prognosis of PCAD implanted with DESs in a Chinese population. Methods: 282 patients with PCAD, of which 177 implanted with DESs and 105 prescribed medicine alone were enrolled and analyzed. Major adverse cardiovascular events (MACEs) and the use of medications for secondary prevention were collected and analyzed. Results: Compared with those receiving medicine alone, patients implanted with DESs had higher ratios of males than females, they also had acute coronary syndromes, multi-vessel disease, higher values of cardiac troponin I, longer hospital stays, higher aspirin and clopidogrel use (all P β-blockers and statins use during follow-up, they had higher ratios of recurrent angina and composite MACEs during one-year follow- up (all P y syndrome (OR 1.716, 95% CI: 1.011 - 2.913) and reduced left ventricular ejection fraction (OR 2.539, 95% CI: 1.180 - 5.463) predict MACEs in a one-year follow-up among patients with PCAD. Conclusions: PCAD patients implanted with DESs have more unstable clinical phenotypes and higher MACEs during a one-year follow-up period, though they were prescribed higher ratios of optimal therapeutic medicine. Further enhanced strategies should be made for secondary prevention.

Expression of Circulating Plasma Long Non-Coding RNA uc063iod.1 and Its Relationship with Coronary Artery Disease

Objective: To investigate the expression of LncRNA uc063iod.1 in patients with different diseases and to explore the correlation between expression level of LncRNA uc063iod.1 and Coronary Artery Disease (CAD). Method: Plasma samples were prepared using the blood extracted from total 101 patients undergoing coronary artery angiogram (63 CAD patients and 38 non CAD patients). The expression level of LncRNA uc063iod.1 was detected using quantitative real time polymerase chain reaction (qRT-PCR) and the relationship between expression level of LncRNA uc063iod.1 and CAD was explored. The clinicopathological features of patients with CAD were also discussed in our study. Results: The expression of LncRNA uc063iod.1 was significantly increased in the plasma of patients with CAD (p Conclusion: Upregulation of LncRNA uc063iod.1 in plasma can be used as a biomarker for the diagnosis of CAD.

Impact of Baseline LDL-C and Lp(a) Elevation on Coronary Revascularization in Patients with Acute Coronary Syndrome One-Year after First Percutaneous Coronary Intervention

Objective: The aim of this study was to investigate the effect of Lipoprotein-a [Lp(a)] on Coronary Revascularizaton (CR) on one year follow up in patients with Acute Coronary Syndrome (ACS) after the first Percutaneous Coronary Intervention (PCI). Method: A retrospective study was designed. A total of 475 patients that underwent their first PCI treatment due to ACS between January 2016 and December 2017 were recruited and followed for one year at the Zhongda Hospital, China. The clinical end point after first PCI was prevalence of Major Adverse Cardiovascular Events (MACE) including nonfatal Myocardial Infarction (MI), cardiovascular death, ischemic stroke and Coronary Revascularization (CR). According to the cut point of Lp(a), participants were divided into low Lp(a) subgroup (Lp(a) mg/L) and high Lp(a) subgroup (Lp(a) ≥ 300 mg/L). Furthermore, based on baseline Low Density Lipoprotein Cholesterol (LDL-C) level, participants were divided into low LDL-C (LDL-C mmol/L) and high LDL-C (LDL-C ≥ 1.8 mmol/L) subgroups. Results: The number of prevalence of CR was higher with elevated serum Lp(a) in both low LDL-C subgroup and high LDL-C subgroup, and was significantly different in both the low LDL-C subgroup and high LDL-C subgroup (p = 0.009 and p = 0.006, respectively). Multivariate Cox-hazard regression analysis for CR showed increase in serum LDL-C and Lp(a) increased prevalence of CR by 1.514 and 1.002 folds respectively. Furthermore, Kaplan-Meier cumulative survival curves showed that increased prevalence of CR within one year after first PCI in patients with high Lp(a) [log rank p = 0.000]. Conclusion: Baseline increase of serum LDL-C and Lp(a) significantly increases the prevalence of CR after first PCI within one year. It indicates that after PCI treatment, in patient with serum LDL-C and Lp(a) elevation, treatment with high-dose statin therapy or PCSK9 inhibitors may alleviate the adverse effects imposed by Lp(a) elevation.