Prevalence, Outcomes, and Risk Factors of New-Onset Atrial Fibrillation in Critically Ill Patients.

The purpose of this article is to systematically evaluate the prevalence, outcomes, and risk factors of new-onset atrial fibrillation (AF) in critically ill patients.Medline, Embase, Science Citation Index, Wanfang, CNKI, and Wiley Online Library were thoroughly searched to identify relevant studies. Studies were assessed for methodological quality using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system. Odds ratio (OR) and weighted mean difference (WMD) with 95% confidence interval (CI) were used to assess the strength of the association. Heterogeneity, subgroup, sensitivity analyses, and publication bias were conducted.A total of 25 studies were included. The prevalence of new-onset AF ranged from 4.1% to 46%.The random-effects pooled prevalence was 10.7%. The pooled result jumped up to 35.8% in patients with septic shock. Pooled analysis showed significant associations between new-onset AF with intensive care unit (ICU) mortality and in-hospital mortality over those patients without AF (OR = 3.11; 95%CI 2.45-3.96 and OR = 1.63; 95%CI 1.27-2.08). The pooled analysis also indicated that both ICU and hospital length of stay are longer in patients with new-onset AF than those without AF (WMD = 1.87; 95%CI 0.89-2.84 and WMD = 2.73; 95%CI 0.77-4.69). Independent risk factors included increasing age, shock, sepsis, use of a pulmonary artery catheter and mechanical ventilation, fluid loading, and organ failures.New-onset AF incidence rate is high in critically ill patients. New-onset AF is associated with worse outcomes. Further studies should be done to explore how to prevent and treat new-onset AF in critically ill patients.

Blood pressure targets for acute ischemic stroke patients following endovascular thrombectomy: A meta-analysis.

OBJECTIVE: The objective of this meta-analysis was to explore the impact of different blood pressure levels following endovascular therapy on clinical outcomes, including safety and efficacy in acute ischemic stroke (AIS) patients. METHODS: A systematic search was performed on PubMed, Embase, Cochrane Library, and Web of Science databases, covering studies published before February 1, 2023. Our primary outcomes were 90-day mRs 0-2 score, 90-day mortality, incidence of symptomatic intracranial hemorrhage(sICH), and hemicraniectomy. RESULTS: The incidence of 90-day mRs= 2 score was no significant difference between different blood pressure values (OR=1.37, 95 % CI [0.82, 2.29], p = 0.23) with heterogeneity (I2 =85 %, p < 0.001). Subgroup analysis indicated that when the blood pressure targets were SBP< 140 mmHg (OR=1.73, 95 % CI [1.04, 2.90], p = 0.04) with heterogeneity (I2 =37 %, p = 0.20), and SBP< 130 mmHg (OR=1.58, 95 % CI [0.53, 4.70], p = 0.41) with heterogeneity (I2 =80 %, p = 0.02), there were statistic differences in the incidence of 90-day modified mRs 0-2 score. Regarding 90-day mortality, there was no significant difference between different blood pressure values (OR=0.75, 95 % CI [0.47, 1.21], p = 0.24; I2 =69 %, p = 0.007). As for the incidence of sICH, the difference was not statistically significant (OR = 0.82, 95 % CI [0.61, 1.09], p = 0.17; I2 =24 %, p = 0.26). However, subgroup analysis was performed due to different blood pressure values, and it was found that when the blood pressure targets were SBP＜140 mmHg (OR=0.49, 95 % CI [0.28, 0.87], p = 0.02) and SBP＜120 mmHg (OR = 0.84, 95 % CI [0.58, 1.23], p = 0.37), there were statistic differences in the incidence of sICH with SBP＜140 mmHg. Furthermore, SBP＜140 mmHg was associated with a lower incidence of hemicraniectomy (OR = 0.30, 95 % CI [0.15, 0.58], p＜0.001). PROSPERO Register Number: CRD42022376706 CONCLUSION: The present meta-analysis findings indicate that intensive treatment is advantageous for achieving successful reperfusion in acute ischemic stroke (AIS) patients undergoing endovascular therapy (EVT). For different blood pressure targets (SBP < 140mmhg, SBP < 130mmhg, SBP < 120mmhg), with a reduction in systolic blood pressure (SBP) to less than 140 mmHg appearing to confer the greatest benefit. Furthermore, this study provides a significant blood pressure target that could inform the design of future multicentre, open-label, blinded-endpoint, randomized controlled trials.

Coinfection with Hypervirulent Klebsiella pneumoniae and Aspergillus flavus in a Critically Ill Patient with Aspergillus Overlap Syndrome: A Case Report.

Pulmonary aspergillosis is generally categorized into three groups: allergic bronchopulmonary aspergillosis, chronic pulmonary aspergillosis and invasive pulmonary aspergillosis. Aspergillus overlap syndromes (AOS) defined as the occurrence of more than one form of aspergillus disease in a single individual is not common. We present a 62-year-old-male patient with tachypnea, hypoxemia and shock after 4 weeks of cough, expectoration and intermittent hemoptysis, and 2 days of hyperpyrexia. Cardiac arrest occurring during tracheal intubation was resuscitated successfully. Laboratory examination showed acute kidney failure and severe myelosuppression with leukopenia and thrombocytopenia. Chest computed tomography (CT) scan showed the cavity with aspergilloma in the right upper lung lobe, a mass of consolidation in the right lower lung lobe and hyperdense shadow bronchiectasis in the left lower lobe. Bronchoscopy showed lots of sputum occluding the opening of the right airway bronchus. Laboratory examination showed significantly increased C-reactive protein (CRP) and procalcitonin concentration, serum (1,3)-ß-D-glucan (BDG) and aspergillus immunoglobulin G (IgG) levels were also elevated. The metagenomic next-generation sequencing and sputum cultures revealed Klebsiella pneumoniae and Aspergillus flavus infection. Pulmonary aspergillosis, invasive aspergillosis infection and severe pneumonia were diagnosed. Initial caspofungin and meropenem followed by piperacillin-tazobactam sodium and voriconazole were administrated in combination. Continuous renal replacement therapy and mechanical ventilation were also performed. The patient's condition gradually recovered. Oral antifungal therapy was continued for 1 year after discharge and CT images gradually improved. Coinfections with K. pneumoniae and A. flavus in a patient with AOS will complicate clinical conditions. A search of PubMed showed few reports of similar cases. Clinicians should pay enough attention to the polymicrobial interactions and improve clinical management strategies, especially in critically ill patient with AOS.

Identification of potential biomarkers and immune cell infiltration in acute myocardial infarction (AMI) using bioinformatics strategy.

Acute myocardial infarction (AMI) was considered a fatal disease resulting in high morbidity and mortality; platelet activation or aggregation plays a critical role in participating in the pathogenesis of AMI. The current study aimed to reveal the underlying mechanisms of platelets in the confrontation of AMI and potential biomarkers that separate AMI from other cardiovascular diseases and healthy people with bioinformatic strategies. Immunity analysis revealed that the neutrophil was significantly decreased in patients with SCAD compared with patients with ST-segment elevation myocardial infarction (STEMI) or healthy controls; monocytes and neutrophils showed potential in distinguishing patients with STEMI from patients with SCAD. Six differentially expressed genes (DEGs) showed great performances in differentiating STEMI patients from SCAD patients with AUC greater than 0.9. Correlation analysis showed that these six DEGs were significantly positively correlated with neutrophils; three genes were negatively correlated with monocytes. Weighted gene co-expression network analysis (WGCNA) found that module 'royalblue' had the highest correlation with STEMI; genes in STEMI-related module were enriched in cell-cell interactions, blood vessels' biological processes, and peroxisome proliferator-activated receptor (PPAR) signaling pathway; four genes (FN1, CD34, LPL, and WWTR1) represented the capability of identifying patients with STEMI from healthy controls and patients with SCAD; two genes (ARG1 and NAMPTL) were considered as novel biomarkers for identifying STEMI from SCAD; FN1 represented the potential as a novel biomarker for STEMI. Our findings indicated that the distribution of neutrophils could be considered as a potential molecular trait for separating patients with STEMI from SCAD.

Widely heterogeneous humoral and cellular immunity after mild SARS-CoV-2 infection in a homogeneous population of healthy young men.

BACKGROUND: We studied humoral and cellular responses against SARS-CoV-2 longitudinally in a homogeneous population of healthy young/middle-aged men of South Asian ethnicity with mild COVID-19. METHODS: In total, we recruited 994 men (median age: 34 years) post-COVID-19 diagnosis. Repeated cross-sectional surveys were conducted between May 2020 and January 2021 at six time points - day 28 (n = 327), day 80 (n = 202), day 105 (n = 294), day 140 (n = 172), day 180 (n = 758), and day 280 (n = 311). Three commercial assays were used to detect anti-nucleoprotein (NP) and neutralizing antibodies. T cell response specific for Spike, Membrane and NP SARS-CoV-2 proteins was tested in 85 patients at day 105, 180, and 280. RESULTS: All serological tests displayed different kinetics of progressive antibody reduction while the frequency of T cells specific for different structural SARS-CoV-2 proteins was stable over time. Both showed a marked heterogeneity of magnitude among the studied cohort. Comparatively, cellular responses lasted longer than humoral responses and were still detectable nine months after infection in the individuals who lost antibody detection. Correlation between T cell frequencies and all antibodies was lost over time. CONCLUSION: Humoral and cellular immunity against SARS-CoV-2 is induced with differing kinetics of persistence in those with mild disease. The magnitude of T cells and antibodies is highly heterogeneous in a homogeneous study population. These observations have implications for COVID-19 surveillance, vaccination strategies, and post-pandemic planning.

α7nAChR Deletion Aggravates Myocardial Infarction and Enhances Systemic Inflammatory Reaction via mTOR-Signaling-Related Autophagy.

Alpha7 nicotinic acetylcholine receptor (α7nAChR) has been previously reported to play an alleviative role in myocardial infarction (MI). In this study, we investigated its specific mechanism. α7nAChR-/- mice and its control (α7nAChR+/+) were used for the study of α7nAChR. Left anterior descending coronary artery occlusion was conducted for the creation of mice MI model and lipopolysaccharide (LPS) was used as inflammatory stressor in murine peritoneal macrophages. Triphenyltetrazolium chloride (TTC) staining and echocardiography was used for the detection of infarct size and cardiac function, respectively. Western blot was conducted for the testing of autophagy-related proteins and enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR) was used for the testing of proinflammatory cytokines. Rapamycin was used for the induction of autophagy through inhibiting mammalian target of rapamycin (mTOR)-related signaling. We found that knocking out α7nAChR enhanced the cardiac infarct size and damaged cardiac function in MI. α7nAChR deficiency increased the levels of several proinflammatory cytokines in serum and spleen from MI mice as well as murine macrophages under inflammatory stress. α7nAChR deletion decreased the level of autophagy in spleen from MI mice and macrophages under inflammatory stress. Rapamycin alleviated the cardiac function and systemic inflammatory reaction in MI mice as well as inflammatory reaction in macrophages under inflammatory stress, which was attenuated by knocking out α7nAChR. Our current study investigated the mechanism of α7nAChR-mediated cardio-protective and anti-inflammatory effect related to mTOR-related autophagy, which might provide a novel insight in the treatment of MI.