[Early and midterm outcomes of artificial chordae transplant in mitral valve repair].

OBJECTIVE: To summarize the early and midterm outcomes of artificial chordae transplant in mitral valve repair. METHODS: A total of 50 patients underwent mitral valve repair with artificial chordae transplant from January 2009 to January 2010 in General Hospital of Shenyang Military Command. Follow-up was conducted on 48 cases (96%) for 3-4 years. RESULTS: No early postoperative mortality occurred. All cases had cardiac function New York Heart Association (NYHA) grade I/II at discharge. Among 48 cases, one died of cerebral infarction after 13 months and the reminder survived and no one underwent reoperation. Among survivors, 45 cases were in cardiac function NYHA grade I and another 2 in grade II. Echocardiography showed that postoperative 3 years left atrial diameter, left ventricular end-diastolic dimension, left ventricular end-systolic dimension and the ratio of regurgitation beam area and left atrial area were significantly smaller than those preoperative ones (39.5% ± 9.7% vs 5.6% ± 0.1%, P < 0.01) and left ventricular ejection fraction increased markedly (0.55 ± 0.06 vs 0.67 ± 0.07, P < 0.01). There was no instance of artificial chordae rupture. CONCLUSION: Gore-Tex artificial chordae transplant is a safe and effective technique in mitral valve repair with excellent early and midterm operative outcomes.

Polymorphism of 8q24 rsl3281615 and breast cancer risk : a meta-analysis.

Several genome-wide association studies on breast cancer have reported similar findings of a new cancer susceptibility locus, 8q24 rsl3281615. Subsequent case-control studies have rapidly investigated the association between the single nucleotide polymorphism of rsl3281615 at chromosome 8q24 and breast cancer risk, but the effect of 8q24 rsl3281615 polymorphism on breast cancer is still unclear due to the inconsistence among those studies. Given the contradictory findings, a meta-analysis was performed to determine the association between 8q24 rsl3281615 polymorphism and breast cancer risk. 12 eligible case-control studies with a total of 42,508 cases and 53,928 controls were finally included into this meta-analysis by searching the PubMed, Embase, and China Biology Medicine (CBM) databases. We estimated the summary odds ratio (OR) with its corresponding 95 % confidence interval (95 % CI) to assess this association. Meta-analyses of total 12 studies showed 8q24 rsl3281615 polymorphism was significantly associated with an increased risk of breast cancer in all contrast models (OR(G vs. A) = 1.10, 95 % CI 1.05-1.14, P (OR) < 0.001; OR(GG vs. AA) = 1.20, 95 % CI 1.11-1.29, P (OR) < 0.001; OR(AG vs. AA) = 1.08, 95 % CI 1.05-1.12, P (OR) < 0.001; OR(GG vs. AA +AG) = 1.13, 95 % CI 1.07-1.19, P (OR) < 0.001; OR(GG+AG vs. AA) = 1.13, 95 % CI 1.07-1.19, P (OR) < 0.001). Meta-analyses of studies with high quality showed that 8q24 rsl3281615 polymorphism was still significantly associated with an increased risk of breast cancer under the five genetic contrast models. Sensitivity analyses by sequential omission of any individual studies and subgroup analyses by ethnicity further identified the significant association between 8q24 rsl3281615 polymorphism and breast cancer risk. Conclusively, this meta-analysis shows a significant association between 8q24 rsl3281615 polymorphism and breast cancer risk.

Myocardial ischaemic and diazoxide preconditioning both increase PGC-1alpha and reduce mitochondrial damage.

OBJECTIVES: Pretreatment with diazoxide, a mitochondrial ATP-sensitive potassium channel (mito KATP) opener, was found to protect the rat heart against ischaemia-reperfusion (I/R) injury by mimicking ischaemic preconditioning (IPC). However, the protection mechanisms have not been fully clarified yet.We hypothesize that molecular regulation of mitochondrial energetics is integral to this cardioprotective programme. We explored the involvement of peroxisome proliferator-activated receptor gamma coactivator-1-1alpha (PGC-1alpha) in the effect of IPC and diazoxide preconditioning (DPC) with regard to its role in protection against I/R injury. METHODS: 30 Wistar rats were used to establish the Langendorff isolated perfused heart model. Rats were randomly divided into 5 groups, 6 in each group: (1) the I/R group: after 30 min of equilibration perfusion, the heart was subjected to 30 min of ischaemia and 1 h of reperfusion; (2) the IPC group: after 10 min of equilibration perfusion, the heart was subjected to two times 5 min ischaemia and 5 min of reperfusion, followed by 30 min of ischaemia and 1 h of reperfusion; (3) the DPC group: after 10 min of equilibration perfusion, the heart was given two times a K-H perfusion solution containing diazoxide (100 micromol/l) for 5 min then a non-diazoxide K-H perfusion solution for 5 min, followed by 30 min of ischaemia and 1 h of reperfusion; (4) a blank control group: an equal amount of saline was used instead of diazoxide. The perfusion procedure was the same as in the DPC group; (5) the dimethyl sulfoxide (DMSO) group: DMSO was applied instead of diazoxide, and the perfusion procedure was the same as in the DPC group. Cardiac apex muscle was cut for frozen section. Immunohistochemistry staining of PGC-1alpha was performed and average absorbance was calculated. An electron microscope was used for Flameng scoring of the myocardial mitochondria. RESULTS: The average absorbance values of PGC-1alpha were: I/R group (3.88 +/- 1.72), IPC group (10.94 +/- 5.23), DPC group (8.40 +/- 3.64), blank control group (3.55 +/- 1.56) and DMSO group (4.16 +/- 0.52), respectively. The expression of PGC- 1alpha was significantly increased in the IPC and DPC groups and the differences were statistically significant compared to the I/R, blank control and DMSO groups, i.e., P < 0.01 for IPC group and P < 0.05 for DPC group. However, there was no significant difference between the IPC and DPC groups (P > 0.05). Flameng score: IPC group (0.44 +/- 0.13), DPC group (0.47 +/- 0.10), I/R group (1.78 +/- 0.14), blank control group (1.70 +/- 0.03) and DMSO group (1.68 +/- 0.06). The Flameng score of the IPC and DPC groups was statistically significantly different as compared to the I/R group, blank control group and DMSO group (P < 0.01), but no significant difference was detected between the IPC and DPC groups (P > 0.05). CONCLUSION: IPC and DPC have a protective effect on myocardial mitochondria, and their mechanism of action may be related to activation and over-expression of PGC-1alpha.

Role of nitric oxide during early phase myocardial ischemic preconditioning in rats.

BACKGROUND: To date, there have been no reports on altered nitric oxide (NO) content in ischemia/reperfusion with regard to in vivo preconditioning procedures. These studies are important for understanding the mechanisms of NO during early myocardial ischemic preconditioning. The aim of the present study was to investigate the mechanisms of NO during early myocardial ischemic preconditioning by measuring levels of NO and cyclic guanosine monophosphate (cGMP), as well as activity of nitric oxide synthase (NOS) in ischemia/reperfusion with respect to preconditioning in rats. METHODS: Sixty-six female Sprague-Dawley rats were randomly divided into four groups: ischemic preconditioning group (IP), ischemia/reperfusion group (I/R), control group (CON), and preconditioning procedure group (PC). In the PC group, rats were further divided into PC1-, PC1 +, PC2-, PC2 +, PC3-, and PC3 + subgroups. Rats underwent left coronary artery occlusion and reperfusion, and subsequently, NOS activity and levels were assessed with spectrophotometric analysis. cGMP contents were measured with radioimmunoassay. RESULTS: The level of NO and cGMP, as well as the activity of NOS, were significantly higher in the IP group compared to the I/R and CON groups (P < 0.05). During preconditioning prior to prolonged ischemia, NO and cGMP levels varied markedly with ischemia and reperfusion. The levels of NO repeatedly increased when the heart was exposed to three episodes of 5-minute ischemia, and were almost completely reversed during each reperfusion period. NO and cGMP levels were significantly different between the 5-minute period of ischemia and the same period of reperfusion during preconditioning. CONCLUSIONS: NO plays an important role during early phase myocardial ischemic preconditioning in rats. NO and cGMP could be triggers and mediators of early phase myocardial ischemic preconditioning. Altered NOS activity following ischemic stress could be the primary inducer of higher NO levels detected. NO and cGMP fluctuations might be the trigger for protection during early phase myocardial ischemic preconditioning.