Comparison of perventricular and percutaneous ultrasound-guided device closure of perimembranous ventricular septal defects.

Background: Ultrasound-guided percutaneous device closure of perimembranous ventricular septal defects (PmVSD) is a minimally invasive recent treatment approach. Perventricular PmVSD device closure is an emerging radiation-free intervention, yet it comes with certain limitations. No studies compared both of these treatment approaches. Methods: We performed a retrospective institutional data comparison of percutaneous (PCP Group, n = 138) and perventricular (PVP Group, n = 67) ultrasound-guided device closure procedures in 205 patients with PmVSD between March 2017 and December 2022. Results: Patients of the PCP and PVP groups had a median age of 4.9 years (IQR, 3.1-14.0) and 5.3 years (IQR, 3.4-13.1) respectively. The median PmVSD diameter in the PCP Group was 4.0 mm (IQR, 3.3-5.3) and 5.2 mm (IQR, 4.0-7.0) in the PVP Group (p = 0.001). There was no significant difference in success rates between the PCP and PVP Groups (intention-to-treat population, 88.4% vs. 92.5%, p = 0.36; as-treated population, 88.4% vs. 89.3%, p = 0.84). 5/8 failed percutaneous cases that were shifted to the perventricular approach were successful. Compared to the PVP Group, patients of the PCP group experienced a significant decrease in ventilation time, drainage volume, and postoperative hospital stay (p < 0.001). The median follow-up period was 24 months (IQR, 6-42) for the PCP group and 61 months (IQR, 53-65) for the PVP group. The overall severe adverse event rate was 0% in the PCP group and 3.0% in the PVP group. Conclusions: Perventricular and percutaneous ultrasound-guided device closure of PmVSD are both effective and safe treatment options. The percutaneous approach offers less trauma and faster recovery and may be the preferred approach in selected patients.

Sufentanil: a risk factor for lactic acidosis in patients after heart valve surgery.

BACKGROUNDS: Hyperlactatemia is a common metabolic disorder after cardiac surgery with cardiopulmonary bypass. Epinephrine use has been identified as a potential cause of increased lactate levels after cardiac surgery. Stress can lead to an increase in catecholamines, mainly epinephrine, in the body. Exogenous epinephrine causes hyperlactatemia, whereas endogenous epinephrine released by stress may have the same effect. Opioids are the most effective anesthetics to suppress the stress response in the body. The authors sought to provide evidence through a retrospective data analysis that helps investigate the relationship between intraoperative opioid dosage and postoperative lactic acidosis after cardiac surgery. METHODS: The clinical data of 215 patients who underwent valvular heart surgery with cardiopulmonary bypass from July 2016 to July 2019 were analyzed retrospectively. Blood lactate levels were measured at 0.1 h, 2 h, 4 h, and 8 h after surgery. Patients with continuous increases in lactate levels and lactate levels exceeding 5 mmol/L at two or more time points were included in the lactic acidosis group, whereas the other patients were included in the control group. First, univariate correlation analysis was used to identify parameters that were significantly different between the two groups, and then multivariate regression analysis was conducted to elucidate the independent risk factors for lactic acidosis. Fifty-one pairs of patients were screened by propensity score matching analysis (PSM). Then, lactic acid levels at four time points in both groups were analyzed by repeated measures ANOVA. RESULTS: he EF (heart ejection fraction) (OR = 0.94, P = 0.003), aortic occlusion time (OR = 10.17, P < 0.001) and relative infusion rate (OR = 2.23, P = 0.01) of sufentanil was an independent risk factor for lactic acidosis after valvular heart surgery. The patients were further divided into two groups with the mean sufentanil infusion rate as the reference point. The data were filtered with PSM (Propensity Score Matching). Lactic acid values in both groups peaked at 4 h after surgery and then declined. The rate of lactic acid decline was significantly faster in the group with a higher sufentanil dosage than in the lower group. The difference was statistically significant (P < 0.05). There was also a significant difference in lactic acid levels at the four time points (0.1 h, 2 h, 4 h and 8 h after surgery) in both groups (P < 0.001). CONCLUSION: The inadequate intraoperative infusion rate of sufentanil is an independent risk factor for lactic acidosis after heart valve surgery. The possibility of lactic acidosis caused by this factor after cardiac surgery should be considered, which is helpful for postoperative patient management.

Transcatheter closure of atrial septal defect with deficient posterior-inferior or inferior vena cava rim under echocardiography only: a feasibility and safety analysis.

BACKGROUND: The safe closure of atrial septal defect with deficient posterior-inferior or inferior vena cava rim is a controversial issue. Few studies have been conducted on the closure of atrial septal defect with deficient posterior-inferior or inferior vena cava rim without fluoroscopy. This study evaluated the feasibility and safety of echocardiography-guided transcatheter closure of atrial septal defect with deficient posterior-inferior or inferior vena cava rim. METHODS: The data of 136 patients who underwent transcatheter atrial septal defect closure without fluoroscopy from March 2017 to March 2020 were retrospectively analysed. The patients were classified into the deficient (n = 45) and sufficient (n = 91) posterior-inferior or inferior vena cava rim groups. Procedure and the follow-up results were compared between the two groups. RESULTS: Atrial septal defect indexed diameter and the device indexed diameter in the deficient rim group were both larger than that in the sufficient rim group (22.12 versus 17.38 mm/m2, p < 0.001; 24.77 versus 21.21 mm/m2, p = 0.003, respectively). There was no significant difference in the success rate of occlusion between two groups (97.78% in the deficient rim group versus 98.90% in the sufficient rim group, p = 1.000). During follow-up, the incidence of severe adverse cardiac events was not statistically significant (p = 0.551). CONCLUSIONS: Atrial septal defect with deficient posterior-inferior or inferior vena cava rim can safely undergo transcatheter closure under echocardiography alone if precisely evaluated with transesophageal or transthoracic echocardiography and the size of the occluder is appropriate. The mid-term results after closure are similar to that for an atrial septal defect with sufficient rim.

Circular RNA PVT1 silencing prevents ischemia-reperfusion injury in rat by targeting microRNA-125b and microRNA-200a.

Circular RNAs (circRNAs) are essential regulators associated with many cardiac conditions, including myocardial infarction (MI). This study aimed to explore circRNA expression during MI development in an animal model and in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Microarray and real-time quantitative PCR showed that the circRNA PVT1 (circPVT1) was expressed at high levels in MI tissues and H/R-triggered cardiomyocytes. Loss-of-function assays were utilized for examining the influence of circPVT1 on cardiac function and cardiomyocyte properties. Cardiac function was measured by echocardiography at 7 d after MI. Reduced circPVT1 expression significantly decreased MI-triggered myocardial infarct size by 60% and prevented MI-triggered reductions in fractional shortening (%FS) and ejection fraction (EF%). Results of LDH, CCK-8, EdU staining, colony formation assays, and flow cytometry showed that circPVT1 silencing restored cell viability and proliferation while decreased apoptosis. Mechanistic experiments indicated that microRNAs (miR)-125b and miR-200a associated with circPVT1. We demonstrated that circPVT1 functioned as a competitive endogenous RNA (ceRNA) to sponge both miR-125b and miR-200a. Gain-of-function assays showed that miR-125b and miR-200a upregulation partially eliminated the effects of circPVT1 on cardiomyocyte properties. In addition, we found that the previously reported p53/TRAF6, SIRT7, Keap1/Nrf2, and PDCD4 pathways were regulated by the circPVT1/miR-125b/miR-200a axis. In conclusion, our study suggests that circPVT1 protects the myocardium from MI and H/R injury by preventing miR-125b- and miR-200a-mediated apoptotic signaling.

[Endovascular treatment of a rare type of aortic arch aneurysm derived from the fourth aortic arch].

OBJECTIVE: To report a rare type of aortic arch aneurysm. METHODS: Three cases of aortic arch aneurysm derived from the fourth aortic arch were retrospectively analyzed. The pathogenesis and treatment of this type of aortic arch aneurysm were investigated. RESULTS: Most of the aneurysm body was located in the Z2 zone, which was the stem from the fourth aortic arch in the embryonic development period. All of the 3 cases could not be explained by common etiology. We speculated that the cause might be developmental anomaly of the fourth aortic arch. All the 3 aortic arch aneurysms were totally excluded with a covered stent. The technical success rate was 100%. Endoleak of type I was seen in one case, which was resolved in a later open surgery. During the follow-up, no type of complications was found. CONCLUSION: To the best of our knowledge, this is the first report of this type of aortic arch aneurysm. The cause may be developmental anomaly of the fourth aortic arch. Endovascular treatment of this type of aortic arch aneurysm is feasible.

Association of epidermal growth factor receptor (EGFR) gene polymorphism with lung cancer risk: a systematic review.

Epidermal growth factor receptor (EGFR) is a member of the tyrosine kinase receptor family, which is thought to be involved in the development of cancer, as the EGFR gene is often amplified, and/or mutated in cancer cells. Lung cancer remains one of the most major causes of morbidity and mortality worldwide, accounting for more deaths than any other cancer cause. Gene polymorphism factor has been reported to be an important factor which increases the susceptibility of lung cancer. There lacks a well-documented diagnostic approach for the lung cancer risk, and the etiology of lung cancer is not clear. The current systematic review was performed to explore the association of EGFR gene polymorphism with lung cancer risk. In this review, association of EGFR 181946C > T, 8227G > A gene polymorphism with lung cancer was found, and EGFR Short genotype of cytosine adenine repeat number polymorphism was significantly associated with an increased risk of lung cancer.

A systematic review and meta-analysis of the association between angiotensin II type 1 receptor A1166C gene polymorphism and myocardial infarction susceptibility.

BACKGROUND AND AIM: Many reported studies have been conducted to investigate the association of angiotensin II type 1 receptor (AT1R) A1166C gene polymorphism with myocardial infarction (MI) susceptibility. However, the results from those reports are still conflicting. This meta-analysis was performed to study the relationship between AT1R A1166C gene polymorphism and MI risk. METHOD: The databases of PubMed, Embase, and Cochrane Library were searched as of 1 March 2012, and eligible investigations were recruited into this meta-analysis. RESULTS: Eighteen investigations were identified for the analysis of association between AT1R A1166C gene polymorphism and MI risk, 11 in Caucasians, three in Asians, two in Africans, one in the population of Brazil and one in the population of Durban, South Africa . There was a marked association between AT1R C allele and MI susceptibility for overall populations (odds ratio (OR)=1.12, 95% confidence interval (CI): 1.01-1.25, p=0.03), and AT1R AA genotype was associated with a lower risk of MI in overall populations (OR=0.87, 95% CI: 0.78-0.98, p=0.02). However, AT1R A1166C gene polymorphism was not associated with MI risk in the sub-groups of Caucasians, Asians, Africans, Brazil and Durban populations. CONCLUSIONS: C allele is a risk factor for the MI susceptibility in overall populations, and AA genotype might be a protective factor against the MI risk in overall populations. However, more case-control association investigations on larger, stratified populations are required in the future.

A meta-analysis of the relationship between glutathione S-transferase T1 null/presence gene polymorphism and the risk of lung cancer including 31802 subjects.

The relationship between glutathione S-transferase T1 (GSTT1) null/presence gene polymorphism and the risk of lung cancer from the published reports are still conflicting. This study was conducted to evaluate the relationship between GSTT1 null/presence gene polymorphism and the risk of lung cancer using meta-analysis method. The association studies were identified from PubMed, and Cochrane Library on July 1, 2012, and eligible investigations were included and synthesized using meta-analysis method. 51 reports were recruited into this meta-analysis for the association of null genotype of GSTT1 with lung cancer susceptibility, consisting of 15,140 patients with lung cancer and 16,662 controls. There was a marked association between GSTT1 null genotype and lung cancer risk in overall populations (OR = 1.15, 95 % CI 1.04-1.27, P = 0.007). Furthermore, GSTT1 null genotype was associated with the lung cancer risk in Asians (OR = 1.47, 95 % CI 1.23-1.76, P < 0.0001). However, GSTT1 null genotype was not associated with the risk of lung cancer in Caucasians, Brazilian population and Africans. In conclusion, GSTT1 null genotype is associated with the lung cancer in overall populations and in Asians.

A meta-analysis of the association between glutathione S-transferase P1 gene polymorphism and the risk of adenocarcinomas of lung cancer.

BACKGROUND: Results of the published reports on the relationship between glutathione S-transferase P1 (GSTP1) gene polymorphism and the adenocarcinomas of lung cancer are still debated. OBJECTIVE: This meta-analysis was performed to evaluate the association between GSTP1 A/G gene polymorphism and the risk of adenocarcinomas of lung cancer. METHODS: The association investigations were identified from PubMed and Cochrane Library, and eligible studies were included and synthesized using meta-analysis method. RESULTS: 16 reports were included into this meta-analysis for the association of GSTP1 A/G gene polymorphism and the risk of adenocarcinomas of lung cancer. The G allele and GG genotype were not associated with the susceptibility of risk of adenocarcinomas. Furthermore, in the sensitivity analysis, the results were similar with those from the non-sensitivity analysis. CONCLUSIONS: GSTP1 G allele or GG genotype is not a biomarker to be associated with the susceptibility of adenocarcinomas of lung cancer.

Association of glutathione S-transferase P1 gene polymorphism with the histological types of lung cancer: a meta-analysis.

The conclusions of the published reports on the relationship between glutathione S-transferase P1 (GSTP1) A/G gene polymorphism and the histological types of lung cancer are still debated. GSTP1 is one of the important mutant sites reported at present. This meta-analysis was performed to evaluate the association between GSTP1 and histological types of lung cancer. The association investigations were identified from PubMed and Cochrane Library, and eligible studies were included and synthesized using meta-analysis method. Seventeen reports were included into this meta-analysis for the association of GSTP1 A/G gene polymorphism and histological types of lung cancer. The G allele and GG genotype were not associated with the susceptibility of risk of squamous cell carcinomas, adenocarcinomas, small cell carcinoma, non-small cell carcinoma or large cell carcinoma. However, in the sub-group analysis, there was an association between G allele/GG genotype with the risk of squamous cell carcinomas in East-Asians and GG genotype was associated with the risk of small cell carcinoma in Caucasians. In conclusion, GSTP1 A/G gene polymorphism is not associated with the susceptibility of squamous cell carcinomas, adenocarcinomas, small cell carcinoma, non-small cell carcinoma or large cell carcinoma.

Lack of association of glutathione S-transferase M3 gene polymorphism with the susceptibility of lung cancer.

OBJECTIVE: The conclusions of published reports on the relationship between the glutathione S-transferase M3 (GSTM3) A/B gene polymorphism and the risk of lung cancer are still debated. This meta-analysis was performed to evaluate the association between GSTM3 and the risk of lung cancer. METHODS: Association investigations were identified from PubMed, Embase, and Cochrane Library, and eligible studies were included and synthesized using a meta-analysis method. RESULTS: Eight reports were included into this meta-analysis for the association of GSTM3 A/B gene polymorphism and lung cancer susceptibility, covering 1,854 patients with lung cancer and 1,926 controls. No association between the GSTM3 A/B gene polymorphism and lung cancer was found in this meta-analysis (B allele: OR = 1.25, 95% CI: 0.89-1.76, P = 0.20; BB genotype: OR = 1.53, 95% CI: 0.71-3.32, P = 0.28; AA genotype: OR = 0.85, 95% CI: 0.59-1.23, P = 0.39). CONCLUSIONS: The GSTM3 A/B gene polymorphism is not associated with lung cancer susceptibility. However, more studies on the relationship between GSTM3 A/B gene polymorphism and the risk of lung cancer should be performed in the future.

Association of glutathione S-transferase P1 gene polymorphism with the susceptibility of lung cancer.

The conclusions of the published reports on the relationship between glutathione S-transferase P1 (GSTP1) gene polymorphism and the risk of lung cancer are still debated. GSTP1 is one of the important mutant sites reported at present. This meta-analysis was performed to evaluate the association between GSTP1 and the risk of lung cancer. The association investigations were identified from PubMed and Cochrane Library, and eligible studies were included and synthesized using meta-analysis method. Forty-four reports were included into this meta-analysis for the association of GSTP1 A/G gene polymorphism and lung cancer susceptibility, consisting of 12,363 patients with lung cancer and 13,948 controls. The association between GSTPI G allele and lung cancer risk was found in this meta-analysis (OR 1.08, 95 % CI 1.02-1.15, P = 0.01). However, the GG genotype and AA genotype were not associated with the susceptibility of lung cancer. Furthermore, there was no association between GSTP1 A/G gene polymorphism and the risk of lung cancer in Caucasians, and East-Asians. In conclusion, GSTP1 G allele is associated with the lung cancer susceptibility. However, more studies on the relationship between GSTP1 A/G gene polymorphism and the risk of lung cancer should be performed in the future.