Objectives. The purpose of this study was to review the experiences with transcatheter closure of mitral PVL after surgical valve replacement. Background. Transcatheter closure of paravalvular leak (PVL) is an intricate alternative to surgical closure. But it represents one of the most intricate procedures in the field of structural heart interventions, especially for patients with mitral PVL. Methods. From January 2015 through January 2019, 35 patients with mitral PVL after valve replacement underwent transcatheter closure. We reviewed the catheter techniques, perioperative characteristics, and prognosis. The median follow-up was 26 (3–48) months. Results. Acute procedural success was achieved in 33/35 (94.3%) patients. Twenty-five patients had single mitral prosthetic valve replacements; 10 had combined aortic and mitral prosthetic valve replacements previously; 28 had mechanical valves; and 7 had bioprosthetic valves. All percutaneous procedures were performed with local anesthesia except for seven transapical cases with general anesthesia. Multiple approaches were used: transfemoral, transapical, and transseptal via an arteriovenous loop. Multiple devices were deployed. There were no hospital deaths. The procedural time was 67–300 (124 ± 62) minutes. Fluoroscopic time was 17–50 (23.6 ± 12.1) minutes. The hospital stay was 5–17 (8.3 ± 3.2) days. Complications included recurrent hemolysis, residual regurgitation, acute renal insufficiency, and anemia. Twenty-seven (77.1%) patients improved by ≥1 New York Heart Association functional class at the 1-year follow-up. Conclusions. Transcatheter mitral PVL closure requires complex catheter techniques. However, this minimally invasive treatment could provide reliable outcomes and shorter hospital stays in selected patients. This trial is registered with NCT02917980.
This study was designed to investigate whether berbamine (BA)‐induced cardioprotective effects were related to 5′ adenosine monophosphate‐activated protein kinase (AMPK)/nuclear factor erythroid 2‐related factor (Nrf2) signaling and changes in the mitochondria in myocardial ischemia/reperfusion (I/R) injury. C57/BL6 mice were exposed to BA (10 mg/kg/d), with or without administration of the AMPK specific inhibitor compound C (5 mg/kg/d) or the Nrf2 specific inhibitor ML‐385 (30 mg/kg/d), and then subjected to a myocardial I/R operation. As expected, BA significantly improved post‐ischemic cardiac function, reduced infarct size and apoptotic cell death, decreased oxidative stress, and improved the mitochondrial state. Furthermore, BA markedly increased AMPK activation, Nrf2 nuclear translocation, and the levels of NAD(P)H quinone dehydrogenase and heme oxygenase‐1. Nevertheless, these BA‐induced changes were abrogated by compound C. In addition, ML‐385 also canceled the cardioprotective effects of BA but had little effect on AMPK activation. Our results demonstrate that BA alleviates myocardial I/R injury and the mitochondrial state by inhibiting apoptosis and oxidative stress via the AMPK/Nrf2 signaling pathway.
Background
Small cell lung cancer (SCLC) is clinically the most aggressive subtype of lung cancer, and accounts for about 15% of all newly diagnosed lung cancer cases. Approximately 1/3 of SCLC patients are diagnosed with limited-stage SCLC (LS-SCLC). The standard of treatment for most patients with LS-SCLC is concurrent chemoradiotherapy. LS-SCLC is sensitive to first-line therapy, but has a high recurrence rate and patients show a poor response to second-line treatment. Referring to extensive-stage SCLC (ES-SCLC), durvalumab plus platinum-etoposide chemotherapy has been approved by the Food Drug Administration and National Medical Products Administration. It is hoped that durvalumab will produce good results for LS-SCLC patients.
Case Description
In this article, we report the case of a 75-year-old male patient with LS-SCLC of the left lung (tumor, node metastasis stage cT3N0M0 IIB) who received 2 cycles durvalumab plus neoadjuvant chemotherapy. The neoadjuvant therapy was favorable and no adverse events were observed. The assessment of the tumor via Resist1.1 by videography indicated a complete response. Then a thoracoscopic resection of the left lower lobe of the lung was performed under general anesthesia. The operation was successful, and the patient’s postoperative recovery was good. Fortunately, the postoperative pathology results showed pathological complete response. After the surgery, the patient received 3 cycles of adjuvant therapy. Now, the patient is still alive and there is no sign of tumor recurrence.
Conclusions
This case highlights the benefits of neoadjuvant programmed death-ligand 1 (PD-L1) inhibitor plus chemotherapy and radical surgery for patients with LS-SCLC and identifies a significant treatment option for LS-SCLC patients.
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