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Proximal pulmonary artery masses are exceedingly rare, and their diagnosis and therapy are important and challenging for clinicians. This study reviews our experience exploring the value of a combination of transthoracic echocardiography and contrast echocardiography for the differential diagnosis of proximal pulmonary artery masses. Between January 2018 and June 2021, 44 patients diagnosed with a mass attached to the major pulmonary artery and straddling the bilateral pulmonary arteries or pulmonary valve on transthoracic echocardiography were referred to this study. Contrast echocardiography was performed in 17 patients. Masses were diagnosed based on their site of attachment, shape, size, mobility, hemodynamic consequences on transthoracic echocardiography, and tissue perfusion on contrast echocardiographic perfusion imaging. Pathological data were collected from medical records and analyzed. The most frequent location of proximal pulmonary artery masses was the major pulmonary artery trunk. Twelve patients underwent complete mass resection, whereas nine patients underwent percutaneous pulmonary artery biopsy puncture and had a pathological diagnosis. Another 24 patients were confirmed with the validation methods. Contrast echocardiography has good sensitivity and specificity for differentiating thrombi from pulmonary artery sarcomas (PAS). The mass types were distributed as follows: thrombi (19, 43%), PAS (15, 34%), metastatic tumors (6, 14%), vegetations (3, 7%), and primary benign lesions (1, 2%). The majority of proximal pulmonary artery masses were thrombi or PAS. A combination of transthoracic echocardiography and contrast echocardiography offers advantages in the early identification of proximal pulmonary masses and provides clinically important information about the characteristics of masses, especially for differentiating thrombi from PAS.
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Arteria Pulmonar , Trombosis , Ecocardiografía , Humanos , Valor Predictivo de las Pruebas , Arteria Pulmonar/diagnóstico por imagen , TóraxRESUMEN
@#Objective To compare the effects of transthoracic device closure and traditional surgical repair on atrial septal defect systemically. Methods A systematic literature search was conducted using the PubMed, EMbase, The Cochrane Library, VIP, CNKI, CBM, Wanfang Database up to July 31, 2018 to identify trials according to the inclusion and exclusion criteria. Quality was assessed and data of included articles were extracted. The meta-analysis was conducted by RevMan 5.3 and Stata 12.0 software. Results Thirty studies were identified, including 3 randomized controlled trials (RCTs) and 27 cohort studies involving 3 321 patients. For success rate, the transthoracic closure group was lower than that in the surgical repair group (CCT, OR=0.34, 95%CI 0.16 to 0.69, P=0.003). There was no statistical difference in mortality between the two groups (CCT, OR=0.43, 95%CI 0.12 to 1.52, P=0.19). Postoperative complication occurred less frequently in the transthoracic closure group than that in the surgical repair group (RCT, OR=0.30, 95%CI 0.12 to 0.77, P=0.01; CCT, OR=0.27, 95%CI 0.17 to 0.42, P<0.000 01). The risk of postoperative arrhythmia in the transthoracic closure group was lower than that in the surgical repair group (CCT, OR=0.56, 95%CI 0.34 to 0.90, P=0.02). There was no statistical difference in the incidence of postoperative residual shunt in postoperative one month (CCT, OR=4.52, 95%CI 0.45 to 45.82, P=0.20) and in postoperative one year (CCT, OR=1.03, 95%CI 0.29 to 3.68, P=0.97) between the two groups. Although the duration of operation (RCT MD=–55.90, 95%CI –58.69 to –53.11, P<0.000 01; CCT MD=–71.68, 95%CI -– 79.70 to –63.66, P<0.000 01), hospital stay (CCT, MD=–3.31, 95%CI –4.16, –2.46, P<0.000 01) and ICU stay(CCT, MD=–10.15, 95%CI –14.38 to –5.91, P<0.000 01), mechanical ventilation (CCT, MD=–228.68, 95%CI –247.60 to – 209.77, P<0.000 01) in the transthoracic closure group were lower than those in the traditional surgical repair group, the transthoracic closure costed more than traditional surgical repair during being in the hospital (CCT, MD=1 221.42, 95%CI 1 124.70 to 1 318.14, P<0.000 01). Conclusion Compared with traditional surgical repair, the transthoracic closure reduces the hospital stay, shortens the length of ICU stay and the duration of ventilator assisted ventilation, while has less postoperative complications. It is safe and reliable for patients with ASD within the scope of indication.
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BACKGROUND: This study aimed to investigate the specific causes for switching patients from minimally invasive transthoracic occlusion to surgical repair under cardiopulmonary bypass (CPB). By retrospectively analyzing 340 cases, we sought to provide the clinical reference for improving the success rate of minimally invasive transthoracic device closure of ventricular septal defect (VSD). METHODS: Among the 340 patients who underwent transthoracic closure of VSDs in the past 3 years at our hospital, 26 patients needed to be switched to surgical repair under CPB due to failure of transthoracic closure. We investigated the causes by retrospectively analyzing the findings from preoperative transthoracic echocardiography (TTE), intraoperative transesophageal echocardiography (TEE) and surgical exploration. RESULTS: Among the 340 patients who underwent transthoracic closure of VSDs, 26 patients (7.65%) were switched to surgical repair under CPB, which included 11 cases of membranous aneurysm (13.10%), 13 cases of perimembranous type (6.22%) and 2 cases of intracristal type (5.00%) according to their anatomic classifications. Among the 186 patients who underwent transthoracic closure during the first 17 months, 20 patients (10.75%) were switched to surgical repair under CPB. The main causes were failure of the delivery system to pass through the VSD in 7 patients, obvious residual shunts after releasing the occluder in 5 patients, significant shedding or shifting after releasing the occluder in 4 patients, significant regurgitation in adjacent valves in 3 patients and severe intraoperative complication (bleeding) in 1 patient. Among the 154 patients who underwent transthoracic closure during the late 17 months, 6 patients (3.90%) were switched to surgical repair under cardiopulmonary bypass. The main causes were significant residual shunts after releasing the occluder in 3 patients, significant regurgitation in adjacent valves in 2 patients after releasing the occluder and failure of the delivery system to pass through the VSD in 1 patient. CONCLUSIONS: Among all the anatomic classifications, membranous aneurysm VSD had the highest risk for switching from minimally invasive transthoracic closure to surgical repair under CPB. During the early period, the surgeons were not yet skilled with the minimally invasive transthoracic closure procedure, and the main causes of switching to surgical repair under CPB were that the delivery system could not pass through the ventricular septal defect and significant residual shunts persisted after releasing the occluder. In contrast, in the late period, the surgeons were skilled with the minimally invasive transthoracic closure procedure, and the main causes were significant residual shunts and obvious regurgitation in adjacent valves after releasing the occluder.
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BACKGROUND: The aim of this study is to discuss a novel surgical approach of percutaneous trans-jugular vein closure of atrial septal defect (ASD) with steerable introducer under echocardiographic guidance. METHODS: From January 2015 to June 2015, ten ASD patients underwent percutaneous trans-jugular vein ASD closure, the occluder placement could be perpendicular to the plane of ASD using the steerable introducer. RESULTS: All cases succeeded. The average procedure time was 27.4±5.6 minutes; and the average intracardiac operation time was 6.7±5.2 minutes. No patient showed the residual shunt after the procedure. There was no clinical death, no arrhythmia, no hemolysis, no infection, no jugular vein damage or occlusion during patients' hospitalization. The post-operation follow up after one month of the operation showed that there was no residual shunt, no falling off or detachment of occluders or other complications. CONCLUSIONS: It is a new surgical method with easy operation, mild damage and wider indication. Compared with the traditional percutaneous and transthoracic closure of ASD, it has obvious advantages.
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A disintegrin, metalloproteinase 8 (ADAM8), is overexpressed in the vast majority of lung cancers and can be a diagnostic marker of lung cancer. We have investigated the effect of ADAM8 on the cisplatin resistance in non-small-cell lung cancer (NSCLC) cell lines. Stable cell lines overexpressing ADAM8 in A549 and H460 cells were generated, both of which have low endogenous ADAM8. Ectopic expression of ADAM8 rendered cells more resistant to cisplatin-induced toxicity, increasing the half maximal inhibitory concentration (IC(50) ) values by 1.85-fold in A549 cells and 3.91-fold in H460 cells relative to mock-transfected cells. Moreover, silencing of ADAM8 in H647 cells with high endogenous level of ADAM8 sensitised them to cisplatin-induced toxicity, with a lower IC(50) value of 11.2 µM relative to an IC(50) of 25.3 µM in mock-transfected cells. Moreover, knockdown of ADAM8 caused a significant increase in cisplatin-induced apoptosis assessed by annexin-V/propidium iodide double staining, accompanying with enhanced cleavage of caspase-3 and poly(ADP-ribose) polymerase. Western blot analysis showed that a greater amount of phosphorylated signal transducer and activator of transcription 3 (STAT3) in ADAM8-overexpressing A549 cells compared to parental or mock-transfected cells. STAT3 silencing increased the susceptibility of ADAM8-overexpressing A549 cells to cisplatin. Both Bcl-2 and Mcl-1 in ADAM8-overexpressing A549 cells were profoundly diminished by STAT3 knockdown. Thus, ADAM8 is implicated in cisplatin resistance of NSCLC cells through activation of the STAT3 signalling pathway, and thus represents a potential therapeutic target in this malignancy.
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Proteínas ADAM/metabolismo , Antineoplásicos/farmacología , Apoptosis , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Cisplatino/farmacología , Neoplasias Pulmonares/metabolismo , Proteínas de la Membrana/metabolismo , Antineoplásicos/uso terapéutico , Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico , Línea Celular Tumoral , Cisplatino/uso terapéutico , Resistencia a Antineoplásicos , Silenciador del Gen , Humanos , Neoplasias Pulmonares/tratamiento farmacológicoRESUMEN
Pulmonary embolism (PE) by occlusion of the pulmonary arterial bed may lead to acute life-threatening but potentially reversible right ventricular failure, one of the most severe complications of thoracic surgery. Still, the incidence of acute pulmonary embolism after surgery is reduced by comprehensive anticoagulant prevention, improved surgical techniques, appropriate perioperative management and early ambulation. However, there is difficulty in diagnosing PE after thoracic surgery due to the lack of specific clinical manifestations. So that optimal diagnostic strategy and management according to the clinical presentation and estimated risk of an adverse outcome is fundamental.