Comparing Outcomes of Single-Incision Laparoscopic Herniorrhaphy in Newborns and Infants.

BACKGROUND: As surgical techniques progress, laparoscopic herniorrhaphy is now performed more often in premature babies. The aim of this study was to analyze the outcomes of newborns and infants who underwent single-incision laparoscopic herniorrhaphy (SILH) at our center. METHODS: We retrospectively reviewed patients younger than 12 months old who received SILH at our department from 2016 to 2020. SILH involved a 5 mm 30-degree scope and 3 mm instruments with a 3-0 Silk purse-string intracorporeal suture for closure of the internal ring. At the time of surgery, Group 1 newborns, whose corrected age was 2 months and below, were compared to the Group 2 infants, whose age was above 2 months. We assessed the patients' characteristics, anesthesia, surgical data, and complications. RESULTS: A total of 197 patients were included (114 newborns in Group 1 and 83 infants in Group 2). The mean age and body weight in Group 1 were 1.2 months and 3.8 kg, respectively, whereas in Group 2, they were 3.2 months and 6.7 kg, respectively. There were no significant differences in operative time (Group 1 = 34.1 min vs. Group 2 = 32.3 min, p = 0.26), anesthetic time (Group 1 = 80.0 min vs. Group 2 = 76.3 min, p = 0.07), length of hospitalization (Group 1 = 2.3 days vs. Group 2 = 2.4 days, p = 0.88), postoperative complications including omphalitis (Group 1 = 5.3% vs. Group 2 = 1.2%, p = 0.13), wound infection (Group 1 = 0.9% vs. Group 2 = 1.2%, p = 0.81), and hydrocele (Group 1 = 0.35% vs. Group 2 = 8.4%, p = 0.14). No recurrence, testicular ascent or atrophy, or mortality was observed in either group during the 2-year follow-up period. CONCLUSIONS: Single-incision laparoscopic herniorrhaphy is a safe and effective operation for inguinal hernia repair in infants, even those with prematurity, lower body weight at the time of surgery, or cardiac and/or pulmonary comorbidities. Comparable results revealed no significant differences in perioperative complications despite younger ages and lower body weights.

Splenic Torsion in Heterotaxy Syndrome with Left Isomerism: A Case Report and Literature Review.

Splenic torsion is an unusual condition that results in congenital abnormality, especially in the visceral abnormal arrangement. We report the case of an 8.5-year-old boy with features in the right upper quadrant. Radiological investigations revealed heterotaxy syndrome with polysplenia and a hypodense tumor in the right upper quadrant adjacent to several spleens. We initially treated it as an intra-abdominal tumor. Laparoscopy was performed to check the tumor condition and revealed a congestive tumor located in the abdomen of the right upper quadrant below the central liver, which was suspected to be a torsion spleen without attaching ligaments. Laparoscopic splenectomy was successfully carried out without complications. The pathological report shows splenic tissue with hemorrhagic infarction. Physicians should be vigilant of the differential diagnosis of the acute abdomen in adolescents.

Effect of qigong training on fatigue in haemodialysis patients: A non-randomized controlled trial.

BACKGROUND: Fatigue is a debilitating symptom in haemodialysis patients. Qigong presents a potentially safe modality of treatment for chronic fatigue patients but has not yet been evaluated in haemodialysis patients. OBJECTIVE: The aim of this study is to investigate whether qigong exercise affects fatigue in haemodialysis patients. DESIGN: A 6-month non-randomized control trial with six measurement periods was conducted. The qigong group was taught to practice qigong three times per week for six months. The control group received usual routine care. Main outcome measure Fatigue, as measured by the "Haemodialysis Patients Fatigue Scale". RESULTS: A total of 172 patients participated in this study, with 71 patients in the qigong group and 101 patients in the control group. The results indicated that all patients experienced mild to moderate fatigue. There was no difference between the qigong and control groups in fatigue at baseline. However, fatigue was lower in the qigong group than in the control group at 8 weeks (43.5 vs. 53.9), 12 weeks (44.7 vs. 53.6), 16 weeks (43.2 vs. 50.8), 20 weeks (42 vs. 50.2), and 24 weeks (41.4 vs. 48.4). The results, based on the generalized estimating equation method, showed that fatigue was significantly lower in the qigong group than in the control group (odds ratio=0.004, p=0.005). CONCLUSION: Fatigue in the qigong group showed a continuous decrease, which was maintained until the end of data collection at 24 weeks. Thus, qigong presents a potentially effective and safe method to reduce fatigue in haemodialysis patients.

Inhibition of HSP90-dependent telomerase activity in amyloid ß-induced apoptosis of cerebral endothelial cells.

Although apoptosis induced by amyloid ß (Aß) has been identified, the effect of Aß on telomerase activity in relation to apoptosis induction remains unclear. In the present study, Aß(1-40) and Aß(25-35), but not Aß(1-16) and Aß(35-25), reduce the viability of primary cerebral endothelial cells (CECs) in accordance with apoptosis induction. Increases in caspase 3 and PARP protein cleavage with reductions of the Bcl-2/Bax protein ratio accompanied by a loss in the mitochondria membrane potential were identified in Aß(1-40) and Aß(25-35)-treated CECs. A significant decrease in intracellular telomerase activity by Aß(1-40) and Aß(25-35) was detected; meanwhile, reduced telomerase activity by telomerase reverse transcriptase (TERT) siRNA enhanced the cytotoxic effect of Aß. The addition of serum might block the Aß(25-35)-induced cytotoxic effect via elevated telomerase activity in according with stimulating phospho-AKT protein expression, which was blocked by adding AKT inhibitor LY294002. Decreases in heat shock protein 90 (HSP90) and its client proteins including TERT, AKT, p53, CDK4 were observed in Aß(1-40) and Aß(25-35), but not Aß(1-16) and Aß(35-25), -treated CECs. The knockdown of HSP90 gene expression by HSP90 siRNA significantly inhibits telomerase activity with decreasing TERT protein expression. The application of HSP90 activity inhibitor geldanamycin (GA) and radicicol (RD) potentiates the telomerase inhibition and apoptosis induction of Aß in CECs. An increase in protein ubiquitination by Aß(25-35), but not Aß(35-25), treatment was examined, and Aß-inhibited HSP90 and TERT protein expression and telomerase activity was reversed by adding proteasome inhibitor, MG132. Additionally, increased TERT protein ubiquitination by Aß(25-35) was detected in CECs via immunoprecipitation/Western blotting analysis. The data of the present study firstly demonstrates that telomerase inhibition contributes to the apoptosis induction of Aß in CECs.

Lung abscess predicts the surgical outcome in patients with pleural empyema.

OBJECTIVES: Most cases of pleural empyema are caused by pulmonary infections, which are usually combined with pneumonia or lung abscess. The mortality of patients with pleural empyema remains high (up to 20%). It also contributes to higher hospital costs and longer hospital stays. We studied pleural empyema with combined lung abscess to determine if abscess was associated with mortality. METHODS: From January 2004 to December 2006, we retrospectively reviewed 259 patients diagnosed with pleural empyema who received thoracscopic decortications of the pleura in a single medical center. We evaluated their clinical data and analyzed their chest computed tomography scans. Outcomes of pleural empyema were compared between groups with and without lung abscess. RESULTS: Twenty-two pleural empyema patients had lung abscesses. Clinical data showed significantly higher incidences in the lung abscess group of pre-operative leukocytosis, need for an intensive care unit stay and mortality. CONCLUSION: Patients with pleural empyema and lung abscess have higher intensive care unit admission rate, higher mortality during 30 days and overall mortality than patients with pleural empyema. The odds ratio of lung abscess is 4.685. Physician shall pay more attention on high risk patient of lung abscess for early detection and management.

Granular cell tumor of the lung.

A nodular lesion in the medial segment of right middle lobe was discovered on a chest radiograph for chronic cough in a 42-year-old Asian woman. A chest computed tomography (CT) scan subsequently showed a right middle lobe (RML) nodular lesion, which exhibited intense fluorodeoxyglucose uptake on positron emission tomography scan. A thoracoscopic RML lobectomy was then performed and immunohistochemical study and Ki-67 proliferative index on the pathology sample demonstrated a benign granular cell tumor. Thirty-six months after surgery, the patient remains symptom-free and there has been no recurrence of the tumor on follow-up CT scan.

Activation of telomerase and cyclooxygenase-2 in PDGF and FGF inhibition of C2-ceramide-induced apoptosis.

In the present study, the roles of telomerase and prostaglandin E(2) (PGE(2)) in platelet-derived growth factor (PDGF's) and fibroblast growth factor-2 (FGF-2's) effects against C(2)-ceramide-induced cell death were investigated. C(2)-ceramide reduced the viability of NIH3T3 cells in a condition without calf serum (CS) in accordance with decreasing telomerase activity according to the TRAP assay. The addition of CS significantly protected cells from C(2)-ceramide-induced apoptosis through increased telomerase activity, and the phosphorylations of PDGF and the FGF-2-like receptor in NIH3T3 cells were detected. Adding PDGF and FGF-2 decreased the cytotoxic effect elicited by C(2)-ceramide through stimulating telomerase activity, which was blocked by adding a telomerase inhibitor (TI). Activations of ERKs and JNKs were detected in PDGF- and FGF-2-treated NIH3T3 cells, and the telomerase activities induced by PDGF and FGF were respectively inhibited by the addition of the ERK inhibitor, PD98059, and the JNK inhibitor, SP600125. Accordingly, induction of cyclooxygenase-2 (COX-2) protein expression and PGE(2) production was detected in PDGF- and FGF-2-treated NIH3T3 cells, and the telomerase activities stimulated by PDGF and FGF were reduced by adding a specific COX-2 inhibitor, NS398, through a decrease in PGE(2) production. Incubation of cells with PGE(2) or the EP1 agonist, 17-PT, but not the EP2 agonist, sulprostone, the EP3 agonist, butaprost, or the EP4 agonist, PGE(1) alcohol, significantly enhanced the telomerase activity of NIH3T3 cells. PGE(2) protection of NIH3T3 cells against C(2)-ceramide-induced cell death was identified by the MTT and LDH-release assays, and it was inhibited by adding the EP1 antagonist, SC-19220. Ceramide metabolites including ceramide-1-phosphate (C1P) and sphingosine-1-phosphate (S1P), and a standard control of exogenous ceramide C(2)-dihydroceramide show no effect on the telomerase activity and viability of NIH3T3 cells. The involvement of COX-2/PGE(2)-mediated telomerase activation by PDGF and FGF-2 against C(2)-ceramide-induced cell death is first demonstrated herein.

Plasma nuclear DNA and mitochondrial DNA as prognostic markers in corrosive injury patients.

STUDY OBJECTIVES: Ingestion of a corrosive substance produces an injury to the gastrointestinal tract and it is often difficult to evaluate the severity and prognosis of this injury. Increased concentrations of plasma nuclear DNA and mitochondrial DNA (mtDNA) have been found to be associated with the area of corrosion. This study examined the level of plasma DNA as it relates to the severity of corrosive injury. METHODS: Forty-eight consecutive patients were enrolled prospectively. The concentrations of plasma nuclear DNA and mtDNA were measured by real-time quantitative polymerase chain reaction assay at presentation to the emergency room and 12 h later. RESULT: The median age of the patients enrolled was 55 years (20 men and 28 women) with an overall mortality rate of 21%. Nineteen patients underwent operative intervention secondary to perforation. Findings included significantly elevated plasma nuclear DNA and mtDNA in the mortality group at presentation and 12 h after injury compared to the survival group. CONCLUSION: The concentrations of plasma nuclear DNA and mtDNA were elevated within 4 h after corrosive injury. The elevated concentrations of plasma nuclear DNA and mtDNA could be useful prognostic markers to correlate with the clinical outcome in corrosive patients.

Reactive oxygen species-dependent HSP90 protein cleavage participates in arsenical As(+3)- and MMA(+3)-induced apoptosis through inhibition of telomerase activity via JNK activation.

The effects of six arsenic compounds including As(+3), MMA(+3), DMA(+3), As(+5), MMA(+5), and DMA(+5) on the viability of NIH3T3 cells were examined. As(+3) and MMA(+3), but not the others, exhibited significant cytotoxic effects in NIH3T3 cells through apoptosis induction. The apoptotic events such as DNA fragmentation and chromosome condensation induced by As(+3) and MMA(+3) were prevented by the addition of NAC and CAT, and induction of HO-1 gene expression in accordance with cleavage of the HSP90 protein, and suppression of telomerase activity were observed in NIH3T3 cells under As(+3) and MMA(+3) treatments. An increase in the intracellular peroxide level was examined in As(+3)- and MMA(+3)-treated NIH3T3 cells, and As(+3)- and MMA(+3)-induced apoptotic events were blocked by NAC, CAT, and DPI addition. HSP90 inhibitors, GA and RD, significantly attenuated the telomerase activity in NIH3T3 cells with an enhancement of As(+3)- and MMA(+3)-induced cytotoxicity. Suppression of JNKs significantly inhibited As(+3)- and MMA(+3)-induced apoptosis by blocking HSP90 protein cleavage and telomerase reduction in NIH3T3 cells. Furthermore, Hb, SnPP, and dexferosamine showed no effect against As(+3)- and MMA(+3)-induced apoptosis, and overexpression of HO-1 protein or inhibition of HO-1 protein expression did not affect the apoptosis induced by As(+3) or MMA(+3). These data provide the first evidence to indicate that apoptosis induced by As(+3) and MMA(+3) is mediated by an ROS-dependent degradation of HSP90 protein and reduction of telomerase via JNK activation, and HO-1 induction might not be involved.

Differential apoptotic effect of wogonin and nor-wogonin via stimulation of ROS production in human leukemia cells.

We investigate the roles of methoxyl (OCH(3)) and hydroxyl (OH) substitutions at C8 of flavonoids on their apoptosis-inducing activities. Wogonin (Wog) and nor-wogonin (N-Wog) are structurally related flavonoids, and respectively contain an OH and OCH(3) at C8. In leukemia HL-60 cells, N-Wog exhibited more-potent cytotoxicity than Wog according to the MTT and LDH release assays, and the IC(50) values of Wog and N-Wog in HL-60 cells were 67.5 +/- 2.1 and 21.7 +/- 1.5 microM, respectively. Apoptotic characteristics including DNA ladders, apoptotic bodies, and hypodiploid cells accompanied by the induction of caspase 3 protein processing appeared in Wog- and N-Wog-treated HL-60 cells. Interestingly, an increase in intracellular peroxide production was detected in N-Wog- but not Wog-treated HL-60 cells by the DCHF-DA assay, and the reduction of intracellular peroxide by catalase (CAT) induced by N-Wog significantly reduced the N-Wog- but not the Wog-induced cytotoxic effect according to the MTT assay in accordance with the blocking of DNA ladder formation and caspase 3 and PARP protein processing elicited by N-Wog. We further analyzed the effect of six structurally related compounds, including 5-OH, 7-OH, 5,7-diOH, 5,7-diOCH(3), 7,8-diOCH(3), and 7-OCH(3)-8-OH flavones, on apoptosis induction in HL-60 cells. Results suggested that OH at C5 and C7 is essential for both the apoptosis-inducing activity of flavonoids, and OH at C8 may contribute to apoptosis induction ability. Evidence to support a distinct structure-activity relationship in apoptosis induction of flavonoids is provided for the first time in this study.

12-o-Tetradecanoylphorbol 13-acetate prevents baicalein-induced apoptosis via activation of protein kinase C and JNKs in human leukemia cells.

In the present study, we found that baicalein (BE), but not its glycoside baicalin (BI), induced apoptosis in human leukemia HL-60 and Jurkat cells, but not in primary murine peritoneal macrophages (PMs) or human polymorphonuclear (PMN) cells, by the MTT assay, LDH release assay, and flow cytometric analysis. Activation of the caspase 3, but not caspase 1, enzyme via inducing protein processing was detected in BE-induced apoptosis. The ROS-scavenging activity of BE was identified by the anti-DPPH radical, DCHF-DA, and in vitro plasmid digestion assay, and none of chemical antioxidants including allpurinol (ALL), N-acetyl-cystein (NAC), and diphenylene iodonium (DPI) affected BE-induced apoptosis in HL-60 cells. This suggests that apoptosis induced by BE is independent of the production of ROS in HL-60 cells. Interestingly, the apoptotic events such as DNA ladders formation and activation of the caspase 3 cascade were significantly blocked by TPA addition in the presence of membrane translocation of PKCalpha, and TPA-induced protection was reduced by adding the PKC inhibitors, GF-109203X and staurosporin. TPA addition induces the phosphorylation of JNKs and ERKs, but not p38, protein in HL-60 cells, and incubation of HL-60 cells with JNKs inhibitor SP600125, but not ERKs inhibitor, PD98059 or the p38 inhibitor SB203580, suppressed the protective effect of TPA against BE-induced apoptotic events including DNA ladders, apoptotic bodies, caspase 3 and D4-GDI protein cleavage in according with blocking JNKs protein phosphorylation. In addition, PKC inhibitor GF-109203X treatment blocks TPA-induced ERKs and JNKs protein phosphorylation, which indicates that activation of PKC locates at upstream of MAPKs activation in TPA-treated HL-60 cells. Additionally, a loss in mitochondrial membrane potential with a reduction in Bcl-2 protein expression, the induction of Bad protein phosphorylation, and translocation of cytochrome c from mitochondria to the cytosol were observed in BE-treated HL-60 cells, and these events were prevented by the addition of TPA. GF-109203X and SP600125 suppression of TPA against cytochrome c release induced by BE was identified. This suggests that activation of PKC and JNKs participate in TPA's prevention of BE-induced apoptosis via suppressing mitochondrial dysfunction in HL-60 cells.

Baicalein inhibition of oxidative-stress-induced apoptosis via modulation of ERKs activation and induction of HO-1 gene expression in rat glioma cells C6.

In the present study, we examined the protective mechanism of baicalein (BE) and its glycoside, baicalin (BI), on hydrogen-peroxide (H(2)O(2))-induced cell death in rat glioma C6 cells. Results of the MTT assay, LDH release assay, and morphological observation showed that H(2)O(2) addition reduced the viability of C6 cells, and this was prevented by the addition of BE but not BI. Incubation of C6 cells with BE significantly decreased the intracellular peroxide level induced by H(2)O(2) according to flow cytometric analysis using DCHF-DA as a fluorescent substrate. Suppression of H(2)O(2)-induced apoptotic events including DNA ladders, hypodiploid cells, and activation of caspases 3, 8, and, 9 by BE but not BI was identified in C6 cells. The cytotoxicity and phosphorylation of ERK proteins induced by H(2)O(2) were blocked by the ERK inhibitor PD98059. Catalase addition prevented H(2)O(2)-induced ROS production, ERKs protein phosphorylation, and cell death, and BE dose-dependently inhibited H(2)O(2)-induced ERK protein phosphorylation in C6 cells. These data suggest that ROS-scavenging activity is involved in BE prevention of H(2)O(2)-induced cell death via blocking ERKs activation. Additionally, BE but not BI induced heat shock protein 32 (HSP32; HO-1) protein expression in both time- and dose-dependent manners, but not heme oxygenase 2 (HO-2), heat shock protein 70 (HSP70), or heat shock protein 90 (HSP90) protein expression. In the absence of H(2)O(2), BE induces ERKs protein phosphorylation, and HO-1 protein expression induced by BE was blocked by the addition of cycloheximide, actinomycin D, and the ERK inhibitor PD98059. The addition of the HO inhibitor ZnPP inhibited the protective effect of BE against H(2)O(2)-induced cytotoxicity in C6 cells according to the MTT assay and apoptotic morphology under microscopic observation, accompanied by blocking the ROS-scavenging activity of BE in C6 cells. However, BE treatment was unable to protect C6 cells from C2-ceramide-induced cell death. These data indicate that BE possesses abilities to inhibit ROS-mediated cytotoxic effects through modulation of ERKs activation and induction of HO-1 protein expression. The role of HO-1 in ROS-scavenging activity of BE is proposed.

Quercetin inhibition of ROS-dependent and -independent apoptosis in rat glioma C6 cells.

In the present study, we investigated the protective mechanism of quercetin (QUE) and its glycosides, rutin (RUT) and quercitrin (QUI), on reactive oxygen species (ROS)-dependent (H(2)O(2)) and -independent (chemical anoxia) cell death in rat glioma C6 cells. Induction of HO-1 protein expression was detected in QUE- but not RUT- or QUI-treated C6 cells, and this was prevented by cycloheximide and actinomycin D. Incubation of C6 cells with QUE, but not RUT or QUI, protected C6 cells from H(2)O(2)- and chemical anoxia-induced cytotoxicity according to the MTT and LDH release assays. Apoptotic characteristics including chromatin condensation, DNA ladders, and hypodiploid cells appeared in H(2)O(2)-and chemical anoxia-treated C6 cells, and those events were significantly suppressed by adding QUE (but not RUT or QUI). Increases in caspase 3, 8, and 9 enzyme activities with decreases in pro-PARP and pro-caspase 3 protein levels and an increase in cleaved D4-GDI protein were identified in H(2)O(2)-and chemical anoxia-treated C6 cells, and these were blocked by the addition of QUE, but not by RUT or QUI. Intracellular peroxide levels increased with H(2)O(2) and decreased with chemical anoxia, and the addition of QUE reduced the intracellular peroxide levels induced by H(2)O(2). Results of an anti-DPPH radical assay showed that QUE, RUT, and QUI dose-dependently inhibited the production of DPPH radicals in vitro; however, QUE (but not RUT or QUI) prevention of DNA damage induced by OH radicals was identified with a plasmid digestion assay. Increases in phosphorylated ERK and p53 protein expressions were detected in H(2)O(2)- but not chemical anoxia-treated C6 cells, and the addition of QUE significantly blocked H(2)O(2)-induced phosphorylated ERK and p53 protein expressions. Adding the HO-1 inhibitors, SnPP, CoPP, and ZnPP, reversed the protective effect of QUE against H(2)O(2)- and chemical anoxia-induced cell death according to the MTT assay and morphological observations. Additionally, QUE exhibited inhibitory effects on LPS/TPA-induced transformation in accordance with a decrease in MMP-9 enzyme activity and iNOS protein expression in C6 cells. Taken together, the results of this study suggest that QUE exhibits an inhibitory effect on both ROS-dependent and -independent cell death, and induction of HO-1 protein expression is involved.

Comparison between video-assisted thoracoscopic thymectomy and transternal thymectomy for myasthenia gravis (analysis of 82 cases).

Video-assisted thoracoscopic surgery (VATS) provides a new approach to thymectomy for myasthenia gravis (MG). We compared the results of video-assisted thoracoscopic thymectomy (VATT) and transternal thymectomy (TT) in Taiwanese people with MG. From January 1997 to August 2002, we enrolled a total of 82 patients with MG who underwent TT and anterior mediastinal adipose tissue removal in our study. Of those, 51 patients underwent VATT, and 31 patients underwent TT. The men-to-women ratios were 18:33 and 15:16 in the VATT and TT groups, respectively. The mean age was 37.9 +/- 17.56 years in the VATT group and 35.6 +/- 16.8 years in the TT group (P = 0.55). Preoperative Osserman's classification revealed the following: class I: 11 (21.6%), 13 (41.9%); class IIA: 18 (35.3%), 11 (35.5%); class IIB: 18 (35.3%), 5 (16.1%); class III: 2 (3.9%), 0; and class IV: 2 (3.9%), 2 (6.5%), respectively, in the two groups (P = 0.06). During VATT, all but two patients were placed supine in the 45 degrees left lateral decubitus position under double-lumen intubated anesthesia. Usually three 1-cm incision wounds over anterior axillary line at the third, fifth, and sixth intercostal spaces were necessary. A total of 82 patients (51 with VATT and 31 with TT) were studied. There were no statistical differences between the two groups of patients in terms of sex, age, and severity of MG. In VATT and TT groups, postoperative hospital stays were 6.1 +/- 3.3 and 26.9 +/- 14.1 days, respectively (P = 0.001). Intensive care unit stays were 1.5 +/- 1.1 and 3.2 +/- 2.3 days, respectively (P = 0.018). Operative times were 180.0 +/- 53.4 and 248.2 +/- 71.9 minutes, respectively (P = 0.004). Thymus weights were 43.7 +/- 22.5 and 52.2 +/- 29.6 g, respectively (P = 0.141). Fifty-one VATT procedures were performed through a right-side approach without conversion. Most patients were extubated in the operating room or recovery room. The harvested thymus glands had an average weight of 49.4 g (range, 21.4-90 g). There were no surgical mortality cases. There was no statistically significant difference (P = 0.574) in the postoperative improvement classification between the two groups, with a mean of 4 years of follow-up. In the VATT group, 14 (27.5%) patients had complete remission without any medication, 14 (27.5%) patients were in class II, 21 (41.1%) patients were in class III, 2 (3.9%) patients were in class IV, and 0 (0%) patients were in class V, according to postoperative classification of DeFilippi et al. We concluded that VATT is technically feasible and safe and is associated with a favorable postoperative outcome compared with the transsternal approach.