EchoNavigator virtual marker and Agilis NxT steerable introducer facilitate transseptal transcatheter closure of mitral paravalvular leak.

BACKGROUND: Paravalvular leak (PVL), also known as paravalvular prosthetic regurgitation, is not a rare complication after surgical valve replacement, and it may cause varying degrees of heart failure. The transcatheter closure of PVL is technically demanding and challenging. CASE SUMMARY: A 68-year-old man presented with degenerative mitral regurgitation with heart failure, New York Heart Association functional class 3. He received bioprosthetic mitral valve replacement in December 2019. PVL was noted at the location of the aorto-mitral curtain in transesophageal echocardiography without signs of endocarditis or dehiscence of the bioprosthetic valve. Transseptal transcatheter closure of the mitral PVL was performed efficiently using the EchoNavigator virtual marker and Agilis NxT steerable introducer. CONCLUSION: This case highlights that the EchoNavigator virtual marker and Agilis NxT steerable introducer can facilitate transseptal transcatheter closure of mitral PVL by reducing the procedure time and contrast media.

Oxidative Stress-Induced Growth Inhibitor (OSGIN1), a Target of X-Box-Binding Protein 1, Protects Palmitic Acid-Induced Vascular Lipotoxicity through Maintaining Autophagy.

Saturated free fatty acids (FFAs) strongly correlate with metabolic syndromes and are well-known risk factors for cardiovascular diseases (CVDs). The mechanism of palmitic acid (PA)-induced vascular lipotoxicity under endoplasmic reticulum (ER) stress is unknown. In the present paper, we investigate the roles of spliced form of X-box-binding protein 1 (XBP1s) target gene oxidative stress-induced growth inhibitor 1 (OSGIN1) in PA-induced vascular dysfunction. PA inhibited the tube formation assay of primary human umbilical vein endothelial cells (HUVECs). Simultaneously, PA treatment induced the XBP1s expression in HUVECs. Attenuate the induction of XBP1s by silencing the XBP1s retarded cell migration and diminished endothelial nitric oxide synthase (eNOS) expression. OSGIN1 is a target gene of XBP1s under PA treatment. The silencing of OSGIN1 inhibits cell migration by decreasing phospho-eNOS expression. PA activated autophagy in endothelial cells, inhibiting autophagy by 3-methyladenine (3-MA) decreased endothelial cell migration. Silencing XBP1s and OSGIN1 would reduce the induction of LC3 II; therefore, OSGIN1 could maintain autophagy to preserve endothelial cell migration. In conclusion, PA treatment induced ER stress and activated the inositol-requiring enzyme 1 alpha-spliced XBP1 (IRE1α-XBP1s) pathway. OSGIN1, a target gene of XBP1s, could protect endothelial cells from vascular lipotoxicity by regulating autophagy.

Ochratoxin A-Induced Nephrotoxicity: Up-to-Date Evidence.

Ochratoxin A (OTA) is a mycotoxin widely found in various foods and feeds that have a deleterious effect on humans and animals. It has been shown that OTA causes multiorgan toxicity, and the kidney is the main target of OTA among them. This present article aims to review recent and latest intracellular molecular interactions and signaling pathways of OTA-induced nephrotoxicity. Pyroptosis, lipotoxicity, organic anionic membrane transporter, autophagy, the ubiquitin-proteasome system, and histone acetyltransferase have been involved in the renal toxicity caused by OTA. Meanwhile, the literature reviewed the alternative or method against OTA toxicity by reducing ROS production, oxidative stress, activating the Nrf2 pathway, through using nanoparticles, a natural flavonoid, and metal supplement. The present review discloses the molecular mechanism of OTA-induced nephrotoxicity, providing opinions and strategies against OTA toxicity.

Selective Activation of Endoplasmic Reticulum Stress by Reactive-Oxygen-Species-Mediated Ochratoxin A-Induced Apoptosis in Tubular Epithelial Cells.

Ochratoxin A (OTA), one of the major food-borne mycotoxins, impacts the health of humans and livestock by contaminating food and feed. However, the underlying mechanism of OTA nephrotoxicity remains unknown. This study demonstrated that OTA induced apoptosis through selective endoplasmic reticulum (ER) stress activation in human renal proximal tubular cells (HK-2). OTA increased ER-stress-related JNK and precursor caspase-4 cleavage apoptotic pathways. Further study revealed that OTA increased reactive oxygen species (ROS) levels, and N-acetyl cysteine (NAC) could reduce OTA-induced JNK-related apoptosis and ROS levels in HK-2 cells. Our results demonstrate that OTA induced ER stress-related apoptosis through an ROS-mediated pathway. This study provides new evidence to clarify the mechanism of OTA-induced nephrotoxicity.

Age correlates with hypotension during propofol-based anesthesia for endoscopic retrograde cholangiopancreatography.

OBJECTIVE: Endoscopic retrograde cholangiopancreatography (ERCP) is a procedure used for diagnostic and therapeutic purposes. Most of the patients may feel pain, anxiety, and discomfort during this procedure, so conscious sedation is usually used during ERCP. General anesthesia would be considered if conscious sedation fails to achieve the requirement of the endoscopists. Several studies showed that propofol-based sedation could provide a better recovery profile. However, propofol has a narrow therapeutic window and complications may occur beyond this window. The present study aimed to find out the complications and the associated risk factors during ERCP procedure under propofol-based deep sedation. METHODS: We retrospectively reviewed data from anesthetic and procedure records of the patients who underwent ERCP under propofol-based deep sedation from January 2006 to July 2010 at Far Eastern Memorial Hospital, Taipei, Taiwan. All propofol-based deep sedations were conducted by anesthesiologists. The incidence of complications was determined and the independent risk factors identified by the multivariable logistic regression model. RESULT: Propofol-based deep sedation was provided for 552 patients who received ERCP procedure. The majority of the patients were male, the mean age was 60 ± 16 years and American Society of Anesthesiologists physical status II-III. Almost 30% of patients experienced hypotension during the procedure, although no mortality or morbidity was associated with this complication. Sex, age, anesthetic time, American Society of Anesthesiologists status, hypertension, and arrhythmia were significantly different (p < 0.05) between patients with hypotension and without hypotension during the procedure. Multivariable logistic regression identified sex and age to be the independent predictors of hypotension. CONCLUSION: Hypotension was the most frequent anesthetic complication during procedure under propofol-based deep sedation, but this method was safe and effective under appropriate monitoring. Age is the strongest predictor of hypotension and therefore propofol-based deep sedation should be conducted with caution in the elderly.