Association between Uric Acid and In-Hospital Heart Failure in Patients with Acute Myocardial Infarction Undergoing Percutaneous Coronary Intervention.

OBJECTIVE: To investigate the association of serum uric acid levels with in-hospital heart failure (HF) in patients with acute myocardial infarction (AMI) who are undergoing percutaneous coronary intervention (PCI). METHODS: Two hundred sixteen patients with AMI who were treated with PCI were enrolled in our study. Univariate and multivariate logistic regression analyses were performed to estimate the associations between uric acid levels and the risk of in-hospital HF in AMI patients. Analyses of the areas under the receiver operating characteristic (ROC) curve were performed to determine the accuracy of uric acid levels in predicting in-hospital HF. RESULTS: A dose-response relationship was found for the incidence of in-hospital HF and levels of uric acid, showing increased HF from the lowest to the highest tertile of uric acid. Compared with subjects in the bottom tertile, the adjusted odds ratio for in-hospital HF was 1.92 (95% CI 0.70-5.24) and 3.33 (95% CI 1.18-9.46) in the second tertile group and the third tertile group, respectively. Every 1 mg/dl increase in the serum uric acid level was associated with a 1.60-fold increased risk of incident in-hospital HF (OR, 1.60; 95% CI 1.22-2.11; P = 0.001). ROC curve analysis showed that the optimal cut-off value of uric acid to predict in-hospital HF was 5.75 mg/dl with a sensitivity of 69.2% and specificity of 56.3%. CONCLUSIONS: Our study showed that the serum uric acid level on admission is an independent predictor of in-hospital heart failure in patients with AMI.

Silencing of ATP2B1-AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA-mediated NF-κB signalling pathway.

Myocardial infarction (MI) is an acute coronary syndrome that refers to tissue infarction of the myocardium. This study aimed to investigate the effect of long intergenic non-protein-coding RNA (lincRNA) ATPase plasma membrane Ca2+ transporting 1 antisense RNA 1 (ATP2B1-AS1) against MI by targeting nuclear factor-kappa-B inhibitor alpha (NFKBIA) and mediating the nuclear factor-kappa-B (NF-κB) signalling pathway. An MI mouse model was established and idenepsied by cardiac function evaluation. It was determined that ATP2B1-AS1 was highly expressed, while NFKBIA was poorly expressed and NF-κB signalling pathway was activated in MI mice. Cardiomyocytes were extracted from mice and introduced with a series of mouse ATP2B1-AS1 vector, NFKBIA vector, siRNA-mouse ATP2B1-AS1 and siRNA-NFKBIA. The expression of NF-κBp50, NF-κBp65 and IKKß was determined to idenepsy whether ATP2B1-AS1 and NFKBIA affect the NF-κB signalling pathway, the results of which suggested that ATP2B1-AS1 down-regulated the expression of NFKBIA and activated the NF-κB signalling pathway in MI mice. Based on the data from assessment of cell viability, cell cycle, apoptosis and levels of inflammatory cytokines, either silencing of mouse ATP2B1-AS1 or overexpression of NFKBIA was suggested to result in reduced cardiomyocyte apoptosis and expression of inflammatory cytokines, as well as enhanced cardiomyocyte viability. Our study provided evidence that mouse ATP2B1-AS1 silencing may have the potency to protect against MI in mice through inhibiting cardiomyocyte apoptosis and inflammation, highlighting a great promise as a novel therapeutic target for MI.

[Long-term outcome of percutaneous balloon mitral valvuloplasty in patients with rheumatic mitral valve stenosis].

OBJECTIVE: To observe the outcome of percutaneous balloon mitral valvuloplasty (PBMV) in patients with rheumatic mitral valve stenosis. METHODS: From April 1992 to November 2008, 1768 patients underwent PBMV in our hospital.Clinical and echocardiographic follow up data were analyzed in 426 patients from April 1992 to August 1998. Left atrial pressure and the mitral valve gradient (MVG) were measured before and immediately after PBMV in all patients. RESULTS: PBMV was successful in 1748 out of 1768 patients (98.86%). Left atrial pressure decreased from (38 +/- 7) mm Hg (1 mm Hg = 0.133 kPa) to (12 +/- 4) mm Hg (P < 0.001), MVG decreased from (28 +/- 6) mm Hg to (8 +/- 3) mm Hg (P < 0.001) and the area of the mitral valve increased from (0.98 +/- 0.26) cm(2) to (1.97 +/- 0.39) cm(2) (P < 0.001) post PBMV. The main complications included death (n = 2), acute pericardial effusion (n = 1), severe mitral regurgitation (n = 12), cerebral embolism (n = 2) and pulmonary edema (n = 1). Ten years follow up was finished in 426 patients and 288 patients (67.6%) were still in NYHA class Ior II without mitral valve replace operation or repeated PBMV, restenosis was evidenced in 140 patients (33.3%) and 31 patients dead (7.5%). CONCLUSION: PBMV was an effective therapy option for patients with rheumatic mitral valve stenosis.