Infective endocarditis after surgical aortic or mitral valve replacement: A nationwide population-based study.

OBJECTIVE: Evidence regarding the incidence of prosthetic valve endocarditis and its association with the use of mechanical or biologic prosthetic valves is limited. METHODS: Patients who underwent aortic or mitral valve replacement in the years 2000 to 2017 were identified from Taiwan's National Health Insurance Research Database and grouped according to the type of prosthesis used (mechanical or biologic). Propensity score matching was performed to reduce confounding. RESULTS: A total of 22,844 patients were included, with 11,950 (52.2%) and 10,934 (47.8%) in the mechanical prosthesis and biologic prosthesis groups, respectively. After matching, each group contained 5441 patients. During follow-up, patients with a biologic prosthesis had a significantly higher risk of infective endocarditis (IE) than those with a mechanical valve (3.4% vs 1.9%; subdistribution hazard ratio, 1.78; 95% CI, 1.40-2.26). Moreover, biologic prostheses were associated with greater risks of all-cause mortality and redo valve surgery, but lesser risks of ischemic stroke, hemorrhagic stroke, major bleeding, and gastrointestinal bleeding. In subgroup analysis, biologic prostheses were consistently associated with a greater risk of IE in all subgroups, specifically single-valve replacement-aortic, single-valve replacement-mitral, double-valve replacement, active IE (IE diagnosed during index hospitalization), any IE (active or old), and not having a history of IE. CONCLUSIONS: In this nationwide population-based retrospective cohort study, biologic prosthesis use was associated with a greater risk of IE during follow-up compared with mechanical valve use. However, mechanical valve use was associated with a greater risk of ischemic stroke and hemorrhagic complications.

Effects of dexmedetomidine on surgery for type A acute aortic dissection outcome.

No study has evaluated the effect of dexmedetomidine in patients who received surgery for type A aortic dissection. This is the first study to evaluate the effect of dexmedetomidine in aortic dissection patients. This study was executed using data from the Chang Gung Research Database in Taiwan. The CGRD contains the multi-institutional standardized electronic medical records from seven Chang Gung Memorial hospitals, the largest medical system in Taiwan. We retrospectively evaluate patients who received surgery for acute type A aortic dissection between January 2014 and December 2018. Overall, 511 patients were included, of whom 104 has received dexmedetomidine infusion in the postoperative period. One-to-two propensity score-matching yielded 86 cases in the dexmedetomidine group and 158 cases in the non-dexmedetomidine group. The in-hospital mortality and composite outcome including all-cause mortality, acute kidney injury, delirium, postoperative atrial fibrillation, and respiratory failure, were considered primary outcomes. The in-hospital mortality and composite outcome were similar between groups. The risk of Acute Kidney Injury Network stage 3 acute kidney injury was significantly lower in the dexmedetomidine group than in the non-dexmedetomidine group (8.1% vs 19.0%; OR, 0.38; 95% CI, 0.17-0.86; p = 0.020. The risk of newly-onset dialysis was also significantly lower in the dexmedetomidine group than in the non-dexmedetomidine group (4.7% vs 13.3%; OR, 0.32; 95% CI, 0.11-0.90; p = 0.031). Post-operative dexmedetomidine infusion significantly reduced the rate of severe acute kidney injury and newly-onset dialysis in patients who received surgery for acute type A aortic dissection.

CCDC167 as a potential therapeutic target and regulator of cell cycle-related networks in breast cancer.

According to cancer statistics reported in 2020, breast cancer constitutes 30% of new cancer cases diagnosed in American women. Histological markers of breast cancer are expressions of the estrogen receptor (ER), the progesterone receptor (PR), and human epidermal growth factor receptor (HER)-2. Up to 80% of breast cancers are grouped as ER-positive, which implies a crucial role for estrogen in breast cancer development. Therefore, identifying potential therapeutic targets and investigating their downstream pathways and networks are extremely important for drug development in these patients. Through high-throughput technology and bioinformatics screening, we revealed that coiled-coil domain-containing protein 167 (CCDC167) was upregulated in different types of tumors; however, the role of CCDC167 in the development of breast cancer still remains unclear. Integrating many kinds of databases including ONCOMINE, MetaCore, IPA, and Kaplan-Meier Plotter, we found that high expression levels of CCDC167 predicted poor prognoses of breast cancer patients. Knockdown of CCDC167 attenuated aggressive breast cancer growth and proliferation. We also demonstrated that treatment with fluorouracil, carboplatin, paclitaxel, and doxorubicin resulted in decreased expression of CCDC167 and suppressed growth of MCF-7 cells. Collectively, these findings suggest that CCDC167 has high potential as a therapeutic target for breast cancer.

Nationwide cohort study of tricuspid valve repair versus replacement for infective endocarditis.

OBJECTIVES: The aim of this study was to compare the outcomes of tricuspid valve (TV) repair versus replacement for patients with infective endocarditis (IE). METHODS: In this nationwide population-based cohort study, we identified 704 patients from Taiwan National Health Insurance Research Database who underwent TV surgery due to IE between 2000 and 2013. Of them, 412 (58.5%) underwent TV repair and 292 (41.5%) underwent TV replacement, and their perioperative and late outcomes were analysed. Confounding was reduced using the inverse probability of treatment weighting on propensity score. RESULTS: After inverse probability of treatment weighting, the in-hospital mortality rate between the 2 groups was not significantly different. However, patients who received TV repair had lower rates of perioperative complications, including massive blood transfusion, de novo dialysis and deep wound infection; longer ICU and hospital stays; and higher hospital cost. Regarding late outcomes, TV repair was associated with lower risks of all-cause readmission [subdistribution hazard ratio (HR) 0.68, 95% confidence interval (CI) 0.60-0.78; P < 0.001], readmission for adverse liver outcomes (subdistribution HR 0.75, 95% CI 0.58-0.97; P = 0.025), new permanent pacemaker implantation (subdistribution HR 0.27, 95% CI 0.15-0.48; P < 0.001) and all-cause mortality (HR 0.60, 95% CI 0.51-0.71; P < 0.001) than TV replacement. CONCLUSIONS: For IE, TV repair is associated with better early and late outcomes than TV replacement. A repair-first strategy is recommended for patients with IE for whom TV surgery is indicated.

Fatty acid metabolic enzyme acyl-CoA thioesterase 8 promotes the development of hepatocellular carcinoma.

Dysregulated metabolism is an emerging hallmark of cancer development, and upregulated lipid synthesis is one of the important tumor metabolic features. However, lipolysis may also contribute to cancer pathogenesis by altering free fatty acid (FFA) metabolism. In the present study, we investigated the importance of the lipolytic enzyme acyl-CoA thioesterase 8 (ACOT8) in hepatocellular carcinoma (HCC) development. Bioinformatic analysis of published microarrays regarding clinical specimens revealed that both ACOT8 gene copy number and mRNA expression were increased in HCC tissues when compared to these variables in non-tumor tissues. ACOT8 silencing with specific shRNA stably expressed in Huh7 and Hep3B HCC cell lines showed that ACOT8 protein expression and overall thioesterase activity were reduced following ACOT8 knockdown. In vitro tumorigenic assays revealed that ACOT8 knockdown inhibited anchorage-dependent and ­independent growth of HCC cell lines. This growth inhibition was partially rescued by addition of the FFA, myristic acid, indicating the importance of FFA in cancer metabolism. In summary, lipolytic enzyme ACOT8 is frequently upregulated in HCC clinical specimens. More importantly, ACOT8 silencing leads to inhibition of cell growth in HCC in vitro.