Influencing factors and prognostic value of left ventricular systolic dysfunction in patients with complete occlusion of the left anterior descending artery reperfused by primary percutaneous coronary intervention.

BACKGROUND: The aim of this study was to perform a retrospective analysis of patients with acute anterior wall ST-segment elevation myocardial infarction (AAW-STEMI) whose left anterior descending (LAD) artery was completely occluded and reperfused by primary percutaneous coronary intervention (PPCI) and to determine the influencing factors and prognostic value of left ventricular systolic dysfunction (LVSD) in the acute phase of acute myocardial infarction (AMI). METHODS: A total of 304 patients with AAW-STEMI were selected. The selected patients were divided into two groups: the preserved left ventricular ejection fraction (pLVEF) group (LVEF ≥ 50%, n = 185) and the reduced left ventricular ejection fraction (rLVEF) group (LVEF < 50%, n = 119). The influencing factors of LVSD and their predictive value for LVSD were analyzed. Patients were followed up by examining outpatient records and via telephone. The predictive value of LVSD for the cardiovascular mortality of patients with AAW-STEMI was analyzed. RESULTS: Age, heart rate (HR) at admission, number of ST-segment elevation leads (STELs), peak creatine kinase (CK) and symptom to wire-crossing (STW) time were independent risk factors for LVSD (P < 0.05). The receiver operating characteristic (ROC) analysis showed that the peak CK had the strongest predictive value for LVSD, with an area under the curve (AUC) of 0.742 (CI, 0.687 to 0.797) as the outcome. At a median follow-up of 47 months (interquartile range, 27 to 64 months), the Kaplan‒Meier survival curves up to 6-year follow-up revealed a total of 8 patients succumbed to cardiovascular disease, with 7 (6.54%) in the rLVEF group and 1 (0.56%) in the pLVEF group, respectively (hazard ratio: 12.11, [P = 0.02]). Univariate and multivariate Cox proportional hazards regression analysis demonstrated that rLVEF was an independent risk predictor of cardiovascular death in patients with AAW-STEMI discharged after PPCI (P < 0.01). CONCLUSIONS: Age, HR at admission, number of STELs, peak CK, and STW time may be used to identify patients with a high risk of heart failure (HF) in a timely manner and initiate early standard therapy for incident LVSD in the acute phase of AAW-STEMI reperfused by PPCI. A trend toward increased cardiovascular mortality at follow-up was significantly linked to LVSD.

Superior mesenteric artery embolism after radiofrequency ablation in regularly anticoagulated patients with paroxysmal atrial fibrillation: a case report.

BACKGROUND: Superior mesenteric artery embolism (SMAE) is a rare cause of acute abdomen, and the fatality rate is extremely high if it is not diagnosed and treated in time. Due to the lack of knowledge and experience of nonspecialist physicians, it is easy to misdiagnose. Radiofrequency ablation (RFA) has become the first-line treatment strategy for atrial fibrillation (AF). Thromboembolic events are some of the major complications after RFA, whereas SMAE is rarely reported. CASE PRESENTATION: A 70 year-old woman with paroxysmal AF who regularly took anticoagulant drugs for 3 months experienced abdominal pain after RFA. At the outset, she was misdiagnosed as mechanical intestinal obstruction. When the patient presented with blood in the stool, abdominal enhancement computed tomography was conducted and showed a small bowel perforation. Immediate laparotomy was performed, and the final diagnosis was SMAE. CONCLUSION: It is suggested that for unexplained abdominal pain after RFA of AF, the possibility of SMAE should be considered, and a targeted examination should be carried out in time to confirm the diagnosis and give appropriate treatment.

Impact of patent foramen ovale on short-term outcomes in children with biliary atresia undergoing living donor liver transplantation: a retrospective cohort study.

OBJECTIVE: To investigate the impact of patent foramen ovale (PFO) on the short-term outcomes of living donor liver transplantation (LDLT) in children with biliary atresia. METHODS: With the approval of the hospital ethics committee, 304 children with biliary atresia who underwent LDLT in our center from January 2020 to December 2021 were enrolled. According to the results of echocardiography before the operation, the subjects were divided into the PFO group (n = 73) and the NoPFO group (n = 231). The baseline characteristics; intraoperative recipient-related data and donor-related data; incidence of postreperfusion syndrome (PRS); postoperative mechanical ventilation time; ICU stay duration; postoperative hospital stay duration; liver function index; incidences of postoperative complications including acute renal injury (AKI), graft dysfunction, hepatic artery thrombosis (HAT) and portal vein thrombosis (PVT); and one-year survival rate were compared between the two groups. RESULTS: The median age in the PFO group was 6 months and that in the NoPFO group was 9 months (P < 0.001), and the median height (65 cm) and weight (6.5 kg) in the PFO group were significantly lower than those in the NoPFO group (68 cm, 8.0 kg) (P < 0.001). The preoperative total bilirubin level (247 vs. 202 umol/L, P = 0.007) and pediatric end-stage liver disease (PELD) score (21 vs. 16, P = 0.001) in the PFO group were higher than those in the NoPFO group. There were no significant differences in the intraoperative PRS incidence (46.6% vs. 42.4%, P = 0.533 ), postoperative mechanical ventilation time (184 vs. 220 min, P = 0.533), ICU stay duration (3.0 vs. 2.5 d, P = 0.267), postoperative hospital stay duration (22 vs. 21 d, P = 0.138), AKI incidence (19.2% vs. 24.7%, P = 0.333), graft dysfunction incidence (11.0% vs. 12.6%, P = 0.716), HAT incidence (5.5% vs. 4.8%, P = 0.762), PVT incidence (2.7% vs. 2.2%, P = 0.675) or one-year survival rate (94.5% vs. 95.7%, P = 0.929) between the two groups. CONCLUSION: The presence of PFO has no negative impact on short-term outcomes in children with biliary atresia after LDLT.

Correlation between Obstructive Sleep Apnea Syndrome (OSAS) and Cognitive Dysfunction in Elderly Patients with Hypertension.

INTRODUCTION: Obstructive sleep apnea syndrome (OSAS) is a common clinical disease that seriously affects the quality of life and health of patients. This study aimed to explore the correlation between OSAS and cognitive dysfunction in elderly patients with hypertension. METHODS: A total of 106 elderly hypertensive patients were included and divided into OSAS group (n = 45) and non-OSAS group (n = 61), according to whether they combined with OSAS. OSAS was monitored with a portable polysomnography monitor by monitoring sleep and breathing. The cognitive dysfunction of the patients was evaluated using the Montreal Cognitive Assessment (MoCA). Basic data and MoCA scores of the patients were compared between the OSAS group and non-OSAS group. The correlation between OSAS and cognitive dysfunction in patients was evaluated using Pearson's correlation analysis. RESULTS: The proportion of men (38 vs. 22, p = 0.000), atrial fibrillation (31 vs. 19, p = 0.000), body mass index (27.32 ± 3.85 vs. 21.27 ± 5.90, p = 0.002), systolic pressure (167.76 ± 14.31 vs. 153.22 ± 12.79, p = 0.008), homocysteine (29.71 ± 6.27 vs. 12.50 ± 4.19, p = 0.005), cognitive dysfunction (15 vs. 10, p = 0.042) in patients of the OSAS group were significantly higher compared to patients of the non-OSAS group. Visual space/executive ability (3.12 ± 1.23 vs. 4.75 ± 1.03, p = 0.021), memory (2.48 ± 0.31 vs. 3.71 ± 0.42, p = 0.039), attention (4.15 ± 1.21 vs. 5.12 ± 1.87, p = 0.041), total MoCA scores (20.11 ± 5.09 vs. 25.76 ± 4.31, p = 0.017) in patients in the OSAS group were significantly lower compared to patients in the non-OSAS group. OSAS was positively correlated with cognitive dysfunction in elderly patients with hypertension (r = 0.224, p < 0.05). CONCLUSIONS: OSAS was positively correlated with cognitive dysfunction in elderly patients with hypertension, so OSAS could increase the risk of cognitive dysfunction through its own adverse effects or its accompanying disease status.

ROCK1 knockdown inhibits non-small-cell lung cancer progression by activating the LATS2-JNK signaling pathway.

Rho-associated kinase 1 (ROCK1) regulates tumor metastasis by maintaining cellular cytoskeleton homeostasis. However, the precise role of ROCK1 in non-small-cell lung cancer (NSCLC) apoptosis remains largely unknown. In this study, we examined the function of ROCK1 in NSCLS survival using RNA interference-mediated knockdown. Our results showed that ROCK1 knockdown reduced A549 lung cancer cell viability in vitro. It also inhibited A549 cell migration and proliferation. Transfection of ROCK1 siRNA was associated with increased expression of large tumor suppressor kinase 2 (LATS2) and c-Jun N-terminal kinase (JNK). Moreover, ROCK1 knockdown-induced A549 cell apoptosis and inhibition of proliferation were suppressed by LATS2 knockdown or JNK inactivation, suggesting that ROCK1 deficiency triggers NSCLC apoptosis in a LATS2-JNK pathway-dependent manner. Functional analysis further demonstrated that ROCK1 knockdown dysregulated mitochondrial dynamics and inhibited mitochondrial biogenesis. This effect too was reversed by LATS2 knockdown or JNK inactivation. We have thus identified a potential pathway by which ROCK1 downregulation triggers apoptosis in NSCLC by inducing LATS2-JNK-dependent mitochondrial damage.

Opa1 Reduces Hypoxia-Induced Cardiomyocyte Death by Improving Mitochondrial Quality Control.

Mitochondrial dysfunction contributes to cardiovascular disorders, especially post-infarction cardiac injury, through incompletely characterized mechanisms. Among the latter, increasing evidence points to alterations in mitochondrial quality control, a range of adaptive responses regulating mitochondrial morphology and function. Optic atrophy 1 (Opa1) is a mitochondrial inner membrane GTPase known to promote mitochondrial fusion. In this study, hypoxia-mediated cardiomyocyte damage was induced to mimic post-infarction cardiac injury in vitro. Loss- and gain-of-function assays were then performed to evaluate the impact of Opa1 expression on mitochondrial quality control and cardiomyocyte survival and function. Hypoxic stress reduced cardiomyocyte viability, impaired contractile/relaxation functions, and augmented the synthesis of pro-inflammatory mediators. These effects were exacerbated by Opa1 knockdown, and significantly attenuated by Opa1 overexpression. Mitochondrial quality control was disturbed by hypoxia, as reflected by multiple mitochondrial deficits; i.e., increased fission, defective fusion, impaired mitophagy, decreased biogenesis, increased oxidative stress, and blunted respiration. By contrast, overexpression of Opa1 normalized mitochondrial quality control and sustained cardiomyocyte function. We also found that ERK, AMPK, and YAP signaling can regulate Opa1 expression. These results identify Opa1 as a novel regulator of mitochondrial quality control and highlight a key role for Opa1 in protecting cardiomyocytes against post-infarction cardiac injury.