Prognostic Factors for In-Hospital and Long-Term Survival in Patients with Acute ST-Segment Elevation Myocardial Infarction after Percutaneous Coronary Intervention.

Acute ST segment elevation myocardial infarction (STEMI) is one of the causes of death and disability in patients with cardiovascular diseases. This study aimed to investigate the prognostic factors of in-hospital and long-term survival in patients with acute STEMI undergoing percutaneous coronary intervention (PCI). Patients with STEMI undergoing PCI were divided into the death group (n = 54) and the survival group (n = 306) based on the outcomes during hospitalization. The routine blood and biochemistry tests, Killip classes and global registry of acute coronary events (GRACE) risk score were detected. The 1-, 2- and 3-year survival rates after PCI was observed through a 3-year follow-up. The survival factors, survival rates and multivariate analyses were conducted using Logistic regression analysis, Kaplan-Meier survival analysis and Cox proportional hazards regression. The incidence of cardiogenic shock and anterior wall MI (AWMI), the serum levels of γ-glutamyl endopeptidase (γ-GGT) and creatine kinase isoenzyme MB (CK-MB), Killip classes and GRACE risk score were higher in the death group, compared with the survival group. AWMI, cardiogenic shock, high serum levels of γ-GGT and CK-MB, Killip class III-IV and high GRACE risk scores were associated with in-hospital mortality. AWMI, cardiogenic shock, Killip class III-IV and high GRACE risk scores were correlated with a poor long-term survival. Our findings have demonstrated that AWMI, cardiogenic shock, high serum levels of γ-GGT and CK-MB, Killip class III-IV, and high GRACE risk scores are risk factors for in-hospital and long-term prognosis of acute STEMI patients.

Hydrogen gas protects against serum and glucose deprivation­induced myocardial injury in H9c2 cells through activation of the NF­E2­related factor 2/heme oxygenase 1 signaling pathway.

Ischemia or hypoxia­induced myocardial injury is closely associated with oxidative stress. Scavenging free radicals and/or enhancing endogenous antioxidative defense systems may be beneficial for the impediment of myocardial ischemic injury. Hydrogen (H2) gas, as a water­ and lipid­soluble small molecule, is not only able to selectively eliminate hydroxyl (·OH) free radicals, but also to enhance endogenous antioxidative defense systems in rat lungs and arabidopsis plants. However, thus far, it has remained elusive whether H2 gas protects cardiomyocytes through enhancement of endogenous antioxidative defense systems. In the present study, the cardioprotective effect of H2 gas against ischemic or hypoxic injury was investigated, along with the underlying molecular mechanisms. H9c2 cardiomyoblasts (H9c2 cells) were treated in vitro with a chemical hypoxia inducer, cobalt chloride (CoCl2), to imitate hypoxia, or by serum and glucose deprivation (SGD) to imitate ischemia. Cell viability and intracellular ·OH free radicals were assessed. The role of an endogenous antioxidative defense system, the NF­E2­related factor 2 (Nrf2)/heme oxygenase 1 (HO­1) signaling pathway, was evaluated. The findings revealed that treatment with CoCl2 or SGD markedly reduced cell viability in H9c2 cells. H2 gas­rich medium protected against cell injury induced by SGD, but not that induced by CoCl2. When the cells were exposed to SGD, levels of intracellular ·OH free radicals were markedly increased; this was mitigated by H2 gas­rich medium. Exposure of the cells to SGD also resulted in significant increases in HO­1 expression and nuclear Nrf2 levels, and the HO­1 inhibitor ZnPP IX and the Nrf2 inhibitor brusatol aggravated SGD­induced cellular injury. H2 gas­rich medium enhanced SGD­induced upregulation of HO­1 and Nrf2, and the HO­1 or Nrf2 inhibition partially suppressed H2 gas­induced cardioprotection. Furthermore, following genetic silencing of Nrf2 by RNA interference, the effects of H2 gas on the induction of HO­1 and cardioprotection were markedly reduced. In conclusion, H2 gas protected cardiomyocytes from ischemia­induced myocardial injury through elimination of ·OH free radicals and also through activation of the Nrf2/HO­1 signaling pathway.

[Diagnostic value of combining detection of human epididymis protein 4 and CA125 in patients with malignant ovarian carcinoma].

OBJECTIVE: To investigate the clinical value of combination of human epididymis protein 4 (HE4), CA125 and the Risk of Ovarian Malignancy Algorithm (ROMA) in diagnosis of ovarian carcinoma. METHODS: To detect the serum concentration of HE4 using ELISA and CA125 using ECL in patients of ovarian carcinoma group (n = 119), borderline ovarian tumor group (n = 36), benign ovarian neoplasm group (n = 96) and female healthy control group (n = 53). The ROMA based on the serum level of CA125, HE4 and a woman's menopausal status was used to calculate the predicted probability (PP) and diagnostic results of ovarian cancers. RESULTS: The receiver operating characteristic (ROC) analysis showed the cut-off value was 67.3 pmol/L (the AUC was 0.906, the sensitivity was 80.7% and specificity was 94.6%). The serum levels of HE4 and CA125 in the ovarian carcinoma group were significantly higher than that in the borderline ovarian tumor group, benign ovarian neoplasm group and female healthy control group (P < 0.01). The serum levels of CA125 and HE4 showed statistically no significant difference between the borderline ovarian tumor group and benign ovarian neoplasm group (P > 0.05). The levels of HE4 and CA125 were reduced significantly in ovarian patients after surgery therapy (P < 0.01). The sensitivity and specificity of HE4 + CA125 combination was 92.7% and 72.5%. The ROMA that can classify patients into high and low risk groups was established as 9.3% in premenopausal and 27.3% in postmenopausal women. CONCLUSIONS: HE4 is a helpful biomarker for ovarian carcinoma diagnosis. Biomarker combination of HE4 and CA125, and applying of the ROMA are helpful to improve the accuracy in diagnosis of ovarian cancers.

[Significance of CEA, SCC and Cyfra21-1 serum test in esophageal cancer].

OBJECTIVE: To study the clinical significance of serum CEA, SCC and Cyfra21-1 test in the diagnosis, prediction of prognosis and postoperative monitor of recurrence in esophageal cancer. METHODS: The concentration of serum CEA and Cyfra21-1 was measured by electrochemiluminescence immunoassay (ECLIA) using Elecsys 2010, CEA kit and Cyfra21-1 kit. Serum SCC was measured by microparticle enzyme immunoassay (MEIA) using IMx System and SCC kit. Serum of 206 patients with esophageal cancer (203 squamous cell carcinoma, 2 small cell carcinoma and 1 adenosquamous carcinoma) was measured preoperatively, 71 of whom also measued 8 to 12 days after resection. RESULTS: The cut-off value of CEA and Cyfra21-1 was < or = 3.25 ng/ml and < or = 2.61 ng/ml, which were determined by the data of 45 healthy Chinese measured during the same period. The positive ratios of serum CEA and Cyfra21-1 in 206 cases were 29.1% and 45.1%. The combined positive ratio of CEA and Cyfra21-1 was 57.3%. The CEA positive ratios, according to the pathological stage of 165 resectable patients, were 16.6% (stage I), 26.8% (II) and 30.8% (III). For Cyfra21-1, they were 27.8%, 37.5% and 50.5%. For CEA combined with Cyfra21-1, they were 38.9%, 50.0% and 63.7%. The mean value of CEA, SCC and Cyfra21-1 (especially SCC and Cyfra21-1) was found to be well correlated with the tumor volume, TNM stage and depth of tumor invasion. Patient with bulky tumor or advanced tumor (T4) usually had much higher mean value than those with early stage tumors. One week after radical resection, the level of the three tumor markers fell to normal level in 92.9% of 71 patients. The level of serum CEA and Cyfra21-1 varied greatly in a small part of the patients. Extremely elevated serum CEA and Cyfra21-1 usually indicated advanced lesion or tumor metastasis. CONCLUSION: Preoperative and postoperative measurement of serum CEA, SCC and Cyfra21-1 (especially Cyfra21-1) is helpful in the diagnosis, prediction of prognosis and monitor of postoperative recurrence in patients with esophageal cancer.