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INTRODUCTION: With a surge in the prevalence of coronavirus disease-2019 (COVID-19) in Beijing starting in October 2022, hospitalisation rates increased markedly. This study aimed to evaluate factors associated with in-hospital mortality in patients with COVID-19. METHODS: Using data from hospitalised patients, sex-based differences in clinical characteristics, in-hospital management, and in-hospital mortality among patients diagnosed with COVID-19 were evaluated. Predictive factors associated with mortality in 1,091 patients admitted to the Beijing Anzhen Hospital (Beijing, China) for COVID-19 between October 2022 and January 2023 were also evaluated. RESULTS: Data from 1,091 patients hospitalised with COVID-19 were included in the analysis. In-hospital mortality rates for male and female patients were 14.9% and 10.4%, respectively. Multifactorial logistic analysis indicated that lymphocyte percentage (LYM%) (odds ratio [OR] 0.863, 95% confidence interval [CI] 0.805-0.925; p < 0.001), uric acid (OR 1.004, 95% CI: 1.002-1.006; p = 0.001), and high-sensitivity C-reactive protein (OR 1.094, 95% CI: 1.012-1.183; p = 0.024) levels were independently associated with COVID-19-related in-hospital mortality. Among female patients, multifactorial analysis revealed that LYM% (OR 0.856, 95% CI: 0.796-0.920; p < 0.001), older age (OR 1.061, 95% CI: 1.020-1.103; p = 0.003), obesity (OR 2.590, 95% CI: 1.131-5.931; p = 0.024), and a high high-sensitivity troponin I level (OR 2.602, 95% CI: 1.157-5.853; p = 0.021) were risk factors for in-hospital mortality. Receiver operating characteristic (ROC) curve analysis, including area under the ROC curve, showed that the efficacy of LYM% in predicting in-hospital death was 0.800 (sensitivity, 63.2%; specificity, 83.2%) in male patients and 0.815 (sensitivity, 87.5%; specificity, 64.4%) in female patients. CONCLUSION: LYM% is a consistent predictor of in-hospital mortality for both sexes. Older age and markers of systemic inflammation, myocardial injury, and metabolic dysregulation are also associated with a high mortality risk. These findings may help identify patients who require closer monitoring and tailored interventions to improve outcomes.
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BACKGROUND: Given the increasing number of patients who require dual antiplatelet (DAP) therapy and electrophysiological device (EPD) placement, perioperative antiplatelet management is a current challenge. In this study, we investigated the incidence of pocket hematoma formation after EPD placement in patients undergoing DAP therapy or an alternative low-molecular-weight heparin (LMWH) regimen. METHODS: This clinical observational study was performed from July 2010 to July 2012. In total, 171 patients were enrolled in the analysis after meeting the inclusion criteria. These patients were divided into two groups: 86 patients were treated with DAP therapy at the time of device implantation, and the DAP therapy was discontinued for 5 to 7 days and replaced with enoxaparin before device implantation in the other 85 patients. Adenosine phosphate (ADP)-mediated platelet aggregation and arachidonic acid-induced platelet aggregation were tested preoperatively. We compared the incidence of pocket hematoma between the two groups and the association of pocket hematoma development with ADP-mediated platelet aggregation and arachidonic acid-induced platelet aggregation. RESULTS: The incidence of pocket hematoma in the patients who continued DAP was lower than that in the patients who replaced the dual antiplatelet regimen with LMWH (3.49% vs. 16.47%, respectively; X (2) = 6.66, P < 0.01). Among the patients who continued DAP therapies, the rate of ADP-mediated platelet aggregation inhibition in patients with pocket hematomas was higher than that in patients without pocket hematomas. None of the patients undergoing DAP or enoxaparin therapy developed pocket infection, thromboembolic events, or other serious complications. Multiple logistic regression analysis revealed that LMWH therapy was an independent risk factor for the development of pocket hematoma (RR = 0.054, 95%CI = 0.012-0.251). Furthermore, patients undergoing LMWH therapy were 5.1-fold more likely to develop pocket hematomas than were DAP-treated individuals. CONCLUSION: Continuance of DAP therapy does not increase the risk of pocket hematoma formation after EPD placement.
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OBJECTIVE: To investigate the risk of acute myocardial infarction (AMI) following stress hyperglycemia after hip fracture. RESEARCH DESIGN AND METHODS: From February 2007 to February 2012, we carried out a prospective observational analysis of 1,257 consecutive patients with no history of diabetes who suffered hip fractures. Fasting blood glucose (FBG) and glycosylated hemoglobin tests as well as electrocardiography, ultrasonic cardiography, and chest X-ray examinations were performed after admission. All selected hip fracture patients were divided into stress hyperglycemia and non-hyperglycemia groups according to their FBG, and the incidence of AMI was monitored. RESULTS: Among the patients enrolled, the frequency of stress hyperglycemia was 47.89% (602/1,257) and that of AMI was 9.31% (117/1,257), and the occurrence of AMI in the stress hyperglycemia group was higher than in the non-hyperglycemia group (12.46 vs. 6.41%, P<0.05). In the stress hyperglycemia patients, FBG reached maximum levels at 2-3 days after hip fractures and then decreased gradually. The AMI incidence (62.67% [47/75]) of the stress hyperglycemia group was highest in the initial 3 days after hip fracture, significantly coinciding with the FBG peak time (P<0.05). In all patients with AMI, non-ST-segment elevation myocardial infarction occurred more often than ST-segment elevation myocardial infarction (62.39% [73/117] vs. 37.61% [44/117]). CONCLUSIONS: Stress-induced hyperglycemia after hip fracture increased the risk of AMI.