Association between anticholinergic medication uses and the risk of pneumonia in elderly adults: a meta-analysis and systematic review.

OBJECTIVE: To conduct a meta-analysis and systematic review on the association between anticholinergic medication uses and the risk of pneumonia in elderly adults. MATERIALS AND METHODS: Medical databases were searched included PubMed, Web of Science, EBSCO and Google Scholar (up to December 7, 2022). Studies evaluating association between anticholinergic medication uses and the risk of pneumonia in elderly adults were included. Studies without available data were excluded. We made meta-analysis by using adjusted odds ratio (aOR) with 95% confidence intervals (CIs) from random-effects model. The risk of bias was assessed using ROBINS-I tool and statistical heterogeneity using the I2 statistic. Registration: INPLASY202330070. RESULTS: A total of six studies with 107,012 participants were included. Meta-analysis results showed that anticholinergic medication uses was related with an increased risk of pneumonia (aOR = 1.59; 95%CI, 1.32-1.92) and stroke-associated pneumonia (aOR = 2.02; 95%CI, 1.76-2.33). Moreover, risk estimates of pneumonia for high-potency anticholinergics (aOR = 1.96; 95%CI, 1.22-3.14) were higher than those for low-potency anticholinergics (aOR = 1.58; 95%CI, 1.27-1.97). And increased risk of pneumonia was associated with the anticholinergic medication uses within 30 days (aOR = 2.13; 95%CI, 1.33-3.43), within 90 days (aOR = 2.03; 95%CI, 1.26-3.26) and chronic use (aOR = 1.65; 95%CI, 1.09-2.51). CONCLUSIONS: The risk of pneumonia is increased in elderly adults with anticholinergic medication, especially with higher-potency anticholinergic drugs and in the initiation phase of anticholinergic medication. Clinicians should monitor their use in older patients carefully, especially when the pneumonia-related signs and symptoms are identified.

Anticholinergic medication could increase the risk of pneumonia in elderly adults.The risk of pneumonia was higher in the initiation phase of anticholinergic medication and when the older patients was medicated with higher-potency anticholinergic drugs.Clinicians should monitor anticholinergic drugs use in older patients carefully, especially when the pneumonia-related signs and symptoms are identified.

RESPIRATORY MECHANICS AND NEURAL RESPIRATORY DRIVE OF UNTREATED GASPING DURING CARDIAC ARREST IN A PORCINE MODEL.

ABSTRACT: Introduction: Although the effects on hemodynamics of gasping during cardiac arrest (CA) have received a lot of attention, less is known about the respiratory mechanics and physiology of respiration in gasping. This study aimed to investigate the respiratory mechanics and neural respiratory drive of gasping during CA in a porcine model. Method: Pigs weighing 34.9 ± 5.7 kg were anesthetized intravenously. Ventricular fibrillation (VF) was electrically induced and untreated for 10 min. Mechanical ventilation (MV) was ceased immediately after the onset of VF. Hemodynamic and respiratory parameters, pressure signals, diaphragmatic electromyogram data, and blood gas analysis data were recorded. Results: Gasping was observed in all the animals at a significantly lower rate (2-5 gaps/min), with higher tidal volume ( VT ; 0.62 ± 0.19 L, P < 0.01), and with lower expired minute volume (2.51 ± 1.49 L/min, P < 0.001) in comparison with the baseline. The total respiratory cycle time and the expiratory time tended to be lengthened. Statistically significant elevations in transdiaphragmatic pressure, the pressure-time product of diaphragmatic pressure, and the mean of root mean square diaphragmatic electromyogram values (RMSmean) were observed ( P < 0.05, P < 0.05, and P < 0.001, respectively); however, VT /RMSmean and transdiaphragmatic pressure/RMSmean were reduced at all time points. The partial pressure of oxygen showed a continuous decline after VF to reach statistical significance in the 10th minute (9.46 ± 0.96 kPa, P < 0.001), whereas the partial pressure of carbon dioxide tended to first rise and then fall. Conclusions: Gasping during CA was characterized by high VT , extremely low frequency, and prolonged expiratory time, which may improve hypercapnia. During gasping, increased work of breathing and insufficient neuromechanical efficacy of neural respiratory drive suggested the necessity of MV and appropriate management strategies for MV during resuscitation after CA.

Prognostic role of dysregulated circRNAs in patients with non-small cell lung cancer: a meta-analysis.

BACKGROUND: Lung cancer is the leading cause of cancer incidence and mortality. Non-small cell lung cancer (NSCLC) accounts for the vast majority of lung cancer, which lacks comprehensive prognostic biomarkers to predict the prognosis of patients. This research was performed to assess the potential prognostic role of circular RNAs (circRNAs) in patients with NSCLC. METHODS: We searched the following databases: PubMed, Web of Science, Embase, and Ovid MEDLINE(R) up to May 20, 2019 to identify studies which explored the association between circRNAs and NSCLC. Newcastle-Ottawa Scale (NOS) was applied to assess the quality of the included studies. Pooled hazard ratios (HRs) and the corresponding 95% confidence interval (CI) were calculated to assess the prognostic value of circRNAs in patients with NSCLC. Subgroup analyses were performed to explain heterogeneity among the included studies. Publication bias was estimated using Begg's funnel plot. Sensitivity analysis was performed to test the stability of pooled results. RESULTS: A total of 19 eligible studies including 1,650 NSCLC patients were included in this research. Pooled results indicated that the up-regulated expression of circRNAs was significantly associated with worse prognosis of patients with NSCLC (HR =2.08, 95% CI: 1.81-2.40). CONCLUSIONS: Our finding indicated that circRNAs could serve as prognostic biomarkers in patients with NSCLC. However, further large-scale prospective studies about the clinical significance of circRNAs are of great need in order to obtain conclusive results.

Alterations in Respiratory Mechanics and Neural Respiratory Drive After Restoration of Spontaneous Circulation in a Porcine Model Subjected to Different Downtimes of Cardiac Arrest.

Background The potential alterations of respiratory pathophysiology after cardiopulmonary resuscitation (CPR) are relatively undefined. While untreated arrest is known to affect post-cardiopulmonary resuscitation circulation, whether it affects respiratory pathophysiology remains unclear. We aimed to investigate the post-cardiopulmonary resuscitation changes in respiratory mechanics and neural respiratory drive with varying delays (5 or 10 minutes) in the treatment of ventricular fibrillation (VF). Methods and Results Twenty-six male Yorkshire pigs were used. Anesthetized pigs weighing 38±5 kg were randomized into 3 groups (n=10 each in the VF5 and VF10 groups, with VF kept untreated for 5 and 10 minutes, respectively, and n=6 in the sham group without VF). Defibrillation was attempted after 6 minutes of cardiopulmonary resuscitation. Pulse-induced contour cardiac output, respiratory mechanics, diaphragmatic electromyogram, blood gas, lung imaging, and histopathology were evaluated for 12 hours. Significantly elevated mean root mean square of diaphragmatic electromyogram, transdiaphragmatic pressure, and minute ventilation were observed, but reduced minute ventilation/mean root mean square, dynamic pulmonary compliance, and Pao2 were noted in both VF groups. Despite recovery of spontaneous breathing, the abnormalities in respiratory mechanics and neural respiratory drive, Pao2, and extravascular lung water continued to last for >12 hours. The changes in imaging (P=0.027) and histopathology (P=0.012) were more severe in the VF10 group compared with the VF5 group. Conclusions There is an uncoupling between the respiratory center and ventilation after restoration of spontaneous circulation. Prolonged untreated arrest from cardiac arrest contributes to more serious alterations in lung pathophysiology.

Endovascular hypothermia improves post-resuscitation myocardial dysfunction by increasing mitochondrial biogenesis in a pig model of cardiac arrest.

The aim of the study was to investigate the effects of endovascular hypothermia on mitochondrial biogenesis in a pig model of prolonged cardiac arrest (CA). Ventricular fibrillation was electrically induced, and animals were left untreated for 10 min; then after 6min of cardiopulmonary resuscitation (CPR), defibrillation was attempted. 25 animals that were successfully resuscitated were randomized into three groups: Sham group (SG, 5, no CA), normal temperature group (NTG, 5 for 12 h observation and 5 for 24 h observation), and endovascular hypothermia group (EHG, 5 for 12 h observation and 5 for 24 h observation). The core temperatures (Tc) in the EHG were maintained at 34 ±â€¯0.5 °C for 6 h by an endovascular hypothermia device (Coolgard 3000), then actively increased at the speed of 0.5 °C per hour during the next 6 h to achieve a normal body temperature, while Tc were maintained at 37.5 ±â€¯0.5 °C in the NTG. Cardiac and mitochondrial functions, the quantification of myocardial mitochondrial DNA (mtDNA), peroxisome proliferator-activated receptor coactivator-1α (PGC-1α), nuclear respiratory factor (NRF)-1, and NRF-2 were examined. Results showed that myocardial and mitochondrial injury and dysfunction increased significantly at 12 h and 24 h after CA. Endovascular hypothermia offered a method to rapidly achieve the target temperature and provide stable target temperature management (TTM). Cardiac outcomes were improved and myocardial injuries were alleviated with endovascular hypothermia. Compared with NTG, endovascular hypothermia significantly increased mitochondrial activity and biogenesis by amplifying mitochondrial biogenesis factors' expressions, including PGC-1α, NRF-1, and NRF-2. In conclusions, endovascular hypothermia after CA alleviated myocardial and mitochondrial dysfunction, and was associated with increasing mitochondrial biogenesis.

Airflow obstruction was associated with elevation of brachial-ankle pulse wave velocity but not ankle-brachial index in aged patients with chronic obstructive pulmonary disease.

OBJECTIVE: Both brachial-ankle pulse wave velocity (baPWV) and ankle-brachial index (ABI) are important predictors for cardiovascular disease (CVD). Patients with chronic obstructive pulmonary disease (COPD) are at high risk of CVD. But the association between airflow obstruction and baPWV or ABI was still unclear. The study was aimed to investigate the influencing factors on arterial stiffness in aged COPD patients. METHODS: 67 aged patients with COPD and 67 age- and sex-matched controls without COPD were enrolled in this study. COPD patients were grouped into four groups according to the Global Initiative for Chronic Obstructive Lung Disease Guidelines (GOLD). Both baPWV and ABI were evaluated. Spirometry indices, blood pressure, smoking history and related laboratory parameters were also collected. RESULTS: Comparing with controls, all COPD patients had significantly higher baPWV (1933 ± 355 cm/s versus 1515 ± 256 cm/s, P < 0.001) but not ABI (P = 0.196). And baPWV values were significantly highest at GOLD stage 4. Forced expiratory volume in 1 s (FEV1) was the most significant factor influencing baPWV, after adjusting for age, systolic blood pressure and other traditional cardiovascular risk factors (ß = -0.463, P = 0.014). CONCLUSION: Arterial stiffness was serious in aged patients with COPD. Spirometry index FEV1 was a possible important predictor for the severity of arterial stiffness of COPD patients.