[Bibliometrics Analysis of Studies on Hypertrophic Cardiomyopathy From 2018 to 2022].

Objective To analyze the research progress and hot topics in hypertrophic cardiomyopathy from 2018 to 2022.Methods The publications in the field of hypertrophic cardiomyopathy from January 1,2018 to December 31,2022 were retrieved from Web of Science core collection database and included for a bibliometric analysis.Results A total of 6355 publications were included,with an average citation frequency of 7 times.The year 2021 witnessed the most publications (1406).The analysis with VOSviewer showed that the research on sudden death related to hypertrophic cardiomyopathy,especially the predictive value of late gadolinium-enhanced cardiac MRI in sudden death,was a hot topic.In addition,gene detection and the new drug mavacamten became hot research topics.The United States was the country with the largest number of publications and the highest citation frequency in this field.Chinese scholars produced the second largest number of publications,which,however,included few high-quality research results.Conclusions Risk stratification and prevention of sudden death is still an important and hot research content in the field of hypertrophic cardiomyopathy.Chinese scholars should carry out multi-center cooperation in the future to improve the research results.

[Risk analysis for hospital mortality after operations for type A aortic dissection].

OBJECTIVE: To analyze the risk factors for hospital mortality after operations for type A aortic dissection. METHODS: Totally 766 consecutive patients (586 male and 180 female patient, aged (45±12) years, ranging from 16 to 78 years), who underwent surgery for type A aortic dissection from January 2001 to December 2010, were studied retrospectively. Preoperative and operation related clinic factors were analyzed by univariate analysis, followed by Logistic regression model, to identify the risk factors of hospital mortality. RESULTS: Overall, 37 patients (4.8%) died during hospitalization. On univariate analysis, significant risk factors for hospital mortality were male, acute status, renal dysfunction, cardiac dysfunction, cardiopulmonary bypass time, duration of operation, volume of blood transfusion, re-operation for bleeding (χ2=4.008-27.093, P<0.05). On Logistic regression model, independent risk factors were acute status (OR=2.784, 95%CI: 1.166-6.649, P=0.021), renal dysfunction (OR=6.285, 95%CI: 1.738 - 22.723, P=0.005), cardiac dysfunction (OR=3.052, 95%CI: 1.083-8.606, P=0.035), re-operation for bleeding (OR=3.690, 95%CI: 1.262-10.791, P=0.017), volume of blood transfusion (OR=1.033, 95%CI: 1.008-1.058, P=0.010). Additionally, male (OR=0.387, 95%CI: 0.177-0.848, P=0.018) was protective factor, and alternatively, female was indeed one of the independent risk factors for hospital mortality. CONCLUSION: Female, acute status, renal dysfunction, cardiac dysfunction, re-operation for bleeding, volume of blood transfusion were independent risk factors for hospital mortality after operations for type A aortic dissection.

Reimplantation versus remodeling: a meta-analysis.

BACKGROUND: Reimplantation and remodeling procedure are two different techniques for valve-sparing aortic root surgery. A number of comparative series have been published but, to date, there has been no meta-analysis comparing outcomes following the two techniques. METHODS: This meta-analysis was performed in accordance with the Cochrane Handbook for Systematic Reviews. A public domain database (MEDLINE) was searched to identify relevant series. Pooled risk ratios (RR) were calculated using fixed effects models for early (30-day) mortality, late deaths, and reoperation related to moderate or severe aortic insufficiency (AI) during follow-up. RESULTS: The search identified seven eligible series, totaling 672 patients (367 reimplantation patents). There was no significant difference in early (30-day) mortality (pooled RR 1.06; 95% CI 0.36 to 3.10; p = 0.92) and late deaths (pooled RR 0.57; 95% CI 0.18 to 1.87; p = 0.36) between reimplantation and remodeling groups. However, reimplantation technique has less chance for reoperation related to moderate or severe AI during follow-up (pooled RR 0.46; 95% CI 0.23 to 0.92; p = 0.03). CONCLUSION: Comparing with remodeling, reimplantation technique has less chance for reoperation related to moderate or severe AI during long-term follow-up.

[Expression of connective tissue growth factor and pathological remodeling in ascending thoracic aortic aneurysm].

OBJECTIVE: To study the expression of connective tissue growth factor (CTGF) and its significance in sporadic ascending thoracic aortic aneurysm (AAA), and initially to investigate the mechanisms of pathological remodeling in AAA. METHODS: AAA specimens were taken from 18 patients during elective surgical intervention, and 18 control specimens of ascending aorta were obtained from patients undergoing coronary artery bypass surgery. Specimens were stained with HE and Masson to evaluate the arrangement and aggregation of cells and collagen types I and III; immunohistochemistry staining was performed using antibodies directed against markers of CTGF; real-time PCR analysis was performed to quantify the expression level of CTGF and collagen types I and III. RESULTS: Pathological results show degradation of elastin and hyperplasia of collagen fibers as well as disordered arrangement of smooth muscle cells in AAA. When compared with controls, protein levels of CTGF were significantly increased [(44 ± 4)% vs. (33 ± 5)%, P < 0.01]. Similar patterns were shown in mRNA levels of CTGF (P < 0.01). Using real-time PCR method, elevated levels (relative expression ratio of mRNA: 10.54/3.8 and 1.79/1.19, respectively; P < 0.01, both) of collagen types I and III were observed. CTGF expression had a correlation with both collagen fibers and aortic aneurysm diameter (r = 0.784, P < 0.01; r = 0.793, P < 0.01). CONCLUSIONS: These results indicate increased expression of aortic collagen types I and III as well as CTGF in AAA specimens, which is likely to be responsible for the aortic wall pathological remodeling. The expression of CTGF was positively correlated with the aortic diameter. As a cytokines factor can stimulate collagen synthesis, CTGF may be involved in the pathogenesis and progression of AAA.

High fructose causes cardiac hypertrophy via mitochondrial signaling pathway.

High fructose diet can cause cardiac hypertrophy and oxidative stress is a key mediator for myocardial hypertrophy. Disruption of cystic fibrosis transmembrane conductance regulator (CFTR) leads to oxidative stress. This study aims to reveal mitochondrial oxidative stress-related signaling pathway in high fructose-induced cardiac hypertrophy. Mice were fed high fructose to develop cardiac hypertrophy. Fructose and H2O2 were used to induce cardiomyocyte hypertrophy in vitro. Mitochondria-targeted antioxidant SkQ1 was applied to investigate the possible role of mitochondrial reactive oxygen species (ROS). CFTR silence was performed to detect the role of CFTR in high fructose-induced myocardial hypertrophy. ROS, glutathione (GSH), mitochondrial function and hypertrophic markers were measured. We confirmed that long-term high fructose diet caused cardiac hypertrophy and diastolic dysfunction and elevated mitochondrial ROS. However, SkQ1 administration prevented heart hypertrophy and mitochondrial oxidative stress. Cadiomyocytes incubated with fructose or H2O2 exhibited significantly increased cell areas but SkQ1 treatment ameliorated cardiomyocyte hypertrophy induced by high fructose or H2O2 in vitro. Those results revealed that the underlying mechanism for high fructose-induced heart hypertrophy was attributed to mitochondrial oxidative stress. Moreover, CFTR expression was decreased by high fructose intervention and CFTR silence resulted in an increase in mitochondrial ROS, which suggested high fructose diet affected mitochondrial oxidative stress by regulating CFTR expression. Electron transport chain impairment might be related to mitochondrial oxidative damage. In conclusion, our findings indicated that mitochondrial oxidative stress plays a central role in pathogenesis of high fructose-induced cardiac hypertrophy. High fructose decreases CFTR expression to regulate mitochondrial oxidative stress.