High cystatin C levels predict long-term mortality in patients with ST-segment elevation myocardial infarction undergoing late percutaneous coronary intervention: A retrospective study.

OBJECTIVES: Late percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI), defined as time of PCI > 7 days from symptom onset, is a common practice with clinical benefits. This study aimed to evaluate the predictive value of admission cystatin C (cys C) level on long-term mortality in STEMI patients receiving late PCI. METHODS: Medical records of STEMI patients who were hospitalized between 2009 and 2011 from eight PCI-capable hospitals in Northwest China were retrospectively analyzed. Cys C level ≥ 1.105 mg/L was considered as the best predictor of long-term mortality based on the receiver-operating characteristic analysis. Patients were followed up by phone or face-to-face interviews, and the long-term mortality was obtained by reviewing medical records. RESULTS: The final analysis included 716 STEMI patients who received late PCI and had available cys C levels prior to PCI, and 524 were assigned into the high cys C group and 192 the low cys C group. Patients were followed up for an average length of 40.37 months. Compared with the low cys C group, the high cys C group had a higher long-term all-cause mortality (10.4% vs 2.9%, P < 0.001) and a higher cardiac mortality (6.8% vs 2.1%, P = 0.004). Multivariate Cox regression analysis showed that high cys C level was an independent predictor for both long-term all-cause mortality and cardiac mortality. CONCLUSIONS: High cys C level at admission is an independent predictor of long-term mortality in STEMI patients undergoing late PCI.

Increased Cystatin C Level in ST-Elevation Myocardial Infarction Predisposes the Prognosis of Angioplasty.

BACKGROUND: The study aimed to evaluate the prognostic value of cystatin C in ST-elevation acute myocardial infarction (STEMI) patients who underwent elective percutaneous coronary intervention (PCI). METHODS: A retrospective study was conducted on 664 STEMI patients from 7 centers who were treated with elective PCI. These patients were divided into 3 groups according their admission cystatin C levels as < 0.84, 0.84-1.03 and ≥1.04mg/L. The all-cause mortalities and the composite endpoints, including mortality, reinfarction, rehospitalization for heart failure and angina or repeat target vessel revascularization were observed for up to 5 years. RESULTS: As cystatin C levels from low to high, all-cause mortalities were progressively increased 0.9%, 3.7% and 9.5% (P < 0.001), as well as the composite endpoints, 11.1%, 21.7% and 40.7%, respectively (P < 0.001). When patients had the level of cystatin C ≥0.84mg/L, their risks of composite endpoints increased 2- to 3-fold of those with <0.84mg/L, with the adjusted hazard ratio of 2.096 (95% CI: 1.047-4.196, P = 0.037) and 3.608 (95% CI: 1.939-6.716, P < 0.001), respectively. CONCLUSIONS: Increased cystatin C levels may be associated with enhanced risks of composite endpoints in patients with STEMI undergoing elective PCI.

Inhibition of PKR protects against H2O2-induced injury on neonatal cardiac myocytes by attenuating apoptosis and inflammation.

Reactive oxygenation species (ROS) generated from reperfusion results in cardiac injury through apoptosis and inflammation, while PKR has the ability to promote apoptosis and inflammation. The aim of the study was to investigate whether PKR is involved in hydrogen peroxide (H2O2) induced neonatal cardiac myocytes (NCM) injury. In our study, NCM, when exposed to H2O2, resulted in persistent activation of PKR due to NCM endogenous RNA. Inhibition of PKR by 2-aminopurine (2-AP) or siRNA protected against H2O2 induced apoptosis and injury. To elucidate the mechanism, we revealed that inhibition of PKR alleviated H2O2 induced apoptosis companied by decreased caspase3/7 activity, BAX and caspase-3 expression. We also revealed that inhibition of PKR suppressed H2O2 induced NFκB pathway and NLRP3 activation. Finally, we found ADAR1 mRNA and protein expression were both induced after H2O2 treatment through STAT-2 dependent pathway. By gain and loss of ADAR1 expression, we confirmed ADAR1 modulated PKR activity. Therefore, we concluded inhibition of PKR protected against H2O2-induced injury by attenuating apoptosis and inflammation. A self-preservation mechanism existed in NCM that ADAR1 expression is induced by H2O2 to limit PKR activation simultaneously. These findings identify a novel role for PKR/ADAR1 in myocardial reperfusion injury.

Short-Term Outcomes and Safety of Computed Tomography-Guided Percutaneous Microwave Ablation of Solitary Adrenal Metastasis from Lung Cancer: A Multi-Center Retrospective Study.

OBJECTIVE: To retrospectively evaluate the short-term outcomes and safety of computed tomography (CT)-guided percutaneous microwave ablation (MWA) of solitary adrenal metastasis from lung cancer. MATERIALS AND METHODS: From May 2010 to April 2014, 31 patients with unilateral adrenal metastasis from lung cancer who were treated with CT-guided percutaneous MWA were enrolled. This study was conducted with approval from local Institutional Review Board. Clinical outcomes and complications of MWA were assessed. RESULTS: Their tumors ranged from 1.5 to 5.4 cm in diameter. After a median follow-up period of 11.1 months, primary efficacy rate was 90.3% (28/31). Local tumor progression was detected in 7 (22.6%) of 31 cases. Their median overall survival time was 12 months. The 1-year overall survival rate was 44.3%. Median local tumor progression-free survival time was 9 months. Local tumor progression-free survival rate was 77.4%. Of 36 MWA sessions, two (5.6%) had major complications (hypertensive crisis). CONCLUSION: CT-guided percutaneous MWA may be fairly safe and effective for treating solitary adrenal metastasis from lung cancer.

Prognostic Value of the Percentage of Neutrophils on Admission in Patients with ST-elevated Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

BACKGROUND AND AIMS: An elevated neutrophil count or neutrophil/lymphocyte ratio on admission has been reported to be an independent predictor of adverse cardiac events in patients with acute coronary syndrome (ACS). The relationship between the percentage of neutrophils (N%) at the time of admission and the long-term outcomes in patients with ST-segment elevated myocardial infarction (STEMI) who have undergone primary percutaneous coronary intervention (PCI) remains unclear. The aim of this study was to investigate the usefulness of the admission N% in predicting long-term mortality in patients with STEMI who were undergoing primary PCI. METHODS: We evaluated 701 consecutive patients admitted to nine medical institutions in northwest China within 24 h after symptom onset from January 1, 2009-December 31, 2011. Using a receiver-operating characteristic analysis, N% ≥82.1% was the best predictor of long-term mortality. Patients were divided into two groups according to this criterion. Mean follow-up time was 39.03 months. RESULTS: The long-term all-cause mortality rate was significantly higher in patients with a high N% level (7.17 vs. 3.11%, p = 0.015) as was the rate of cardiac mortality (6.48 vs. 2.59%, p = 0.013). In a multivariate logistic analysis, a high N% level was an independent predictor of long-term all-cause mortality (odds ratio 2.59, 95% confidence interval 1.21-5.53, p = 0.002) and long-term cardiac mortality (odds ratio 2.79, 95% confidence interval 1.24-6.28, p = 0.013). CONCLUSIONS: A high N% level on admission is an independent predictor of long-term mortality in STEMI patients undergoing primary PCI.

MiR-31 Downregulation Protects Against Cardiac Ischemia/Reperfusion Injury by Targeting Protein Kinase C Epsilon (PKCε) Directly.

BACKGROUND: Various miRNAs have been shown to participate in cardiac ischemia/reperfusion injury (I/R). miR-31 was identified as the most strikingly upregulated miRNA after acute myocardial infarction; therefore, the underlying role and mechanism of miR-31 in cardiac I/R was investigated. METHODS: miR-31 expression was detected after cardiac I/R in mice. The cardioprotective effect of miR-31 downregulation was assessed in vitro and in vivo. The functional target gene and its downstream molecule were determined. RESULTS: miR-31 expression increased after I/R. miR-31 downregulation increased cell viability and SOD activity and decreased LDH activity and MDA content in vitro. Additionally, miR-31 downregulation alleviated myocardial infarct size in vivo. PKCε was identified as the functional target gene of miR-31, and NFκB was identified as its downstream molecule that was involved in the miR-31-mediated cardioprotective effect. CONCLUSION: miR-31 expression increased throughout the cardiac I/R process, and miR-31 downregulation induced a cardioprotective effect via a miR-31/PKCε/NFκB-dependent pathway.