Objective: The coronavirus disease 2019 (COVID-19) pandemic disrupted healthcare systems worldwide, leading to increased mortality rates across various conditions. This study assessed the impact of COVID-19 on excess in-hospital mortality among emergency department patients and examined variations by community income levels, thereby highlighting socioeconomic disparities. Methods: This retrospective cross-sectional study used data from the National Emergency Department Information System in Korea. Cancer patients who visited emergency departments between January 27 and December 31 in 2019 (pre-COVID) and 2020 (during COVID) were included. The primary outcome was in-hospital mortality. The main exposure was the COVID-19 outbreak, with county per capita income tax serving as the interaction variable. The risk-adjusted in-hospital mortality rates were calculated. A multilevel linear regression model with an interaction term was used to estimate the difference-in-difference between the periods based on county income tax. Results: A total of 206,400 cancer patients were included 110,879 pre-COVID and 95,521 during COVID with an unadjusted in-hospital mortality rate of 1.0%. The risk-adjusted mortality rate was significantly higher during COVID than pre-COVID (1.2% vs. 0.9%, P<0.01). Using the highest socioeconomic status group (Q1) as the reference, the excess inhospital mortality odds during COVID were higher in Q3 (adjusted odds ratio [aOR], 1.32; 95% confidence interval [CI], 1.17-1.54) and Q4 (aOR, 1.43; 95% CI, 1.15-1.77). Conclusion The COVID-19 pandemic exacerbated in-hospital mortality disparities among cancer patients, imposing a greater burden on lower socioeconomic groups. These findings highlight the importance of implementing equitable healthcare strategies to protect vulnerable populations during health emergencies.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Our study hypothesizes that the interaction between depression, alcohol intake, and smoking status can significantly influence the risk of acute coronary syndrome (ACS). We aim to investigate the magnitude of the association between depression and ACS risk and explore how alcohol intake and smoking status affect this association. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure of interest was the presence of depression, as measured using the Beck Depression Inventory score at baseline. The primary outcome was the occurrence of ACS observed in the biennial follow-up surveys. We used Cox proportional regression analysis to estimate the effect of depression on ACS incidence. We conducted interaction and joint effect analyses to explore the interactions between depression and health-related habits including alcohol intake and smoking with regard to ACS incidence. Results: During 16 years of follow-up among 3,254 individuals, we documented 88 cases of new-onset ACS (2.2 cases per 1,000 personyears). We found no association between depression and ACS risk; furthermore, the effect of depression on ACS risk by alcohol intake and smoking status did not differ significantly. In the analysis to observe the joint effect of smoking and depression, the multivariate hazard ratios of ACS were 1.26 (95% confidence interval [CI], 0.67–2.36) for non-smoking and depression, 1.52 (95% CI, 0.83–2.82) for smoking and non-depression, and 2.79 (95% CI, 1.21–6.41) for smoking and depression compared with non-smoking and non-depression. Conclusion Our study reveals the combined effect of depression and smoking on ACS risk, highlighting the potential benefits of concurrent interventions for both depression and smoking for cardiovascular health.

Purpose: As people living with cancer increase in the aging society, cancer-related emergency department (ED) visits are also increasing. This study aimed to investigate the epidemiologic characteristics of non-emergent cancer-related ED visits using a nationwide ED database. Materials and Methods: A cross-sectional study was conducted using the National Emergency Department Information System (NEDIS) database. All cancer-related ED visits between 2016 and 2020 were included. The study outcome was non-emergent ED visits, defined as patients triaged into non-emergent condition at both the time of arrival at ED and discharge from ED and were discharged without hospitalization. Results: Among 1185871 cancer-related ED visits over 5 years, 19.0% (n=225491) were classified as non-emergent visits. While abdominal pain and fever are the top chief complaints in both emergent and non-emergent visits, non-emergent visits had high proportions of abdomen distension (4.8%), ascite (2.4%), and pain in lower limb (2.0%) compared with emergent visits. The cancer types with a high proportion of non-emergent visits were thyroid (32.4%) and prostate cancer (30.4%). Adults compared with children or older adults, female, medical aid insurance, urban/rural ED, direct-in compared with transfer-in, and weekend visit were associated with high odds for non-emergent visits. Conclusion Approximately 20% of cancer-related ED visits may be potentially non-emergent. A significant number of non-emergent patients visited the ED due to cancer-related symptoms. To improve the quality of care for people living with cancer, the expansion of supportive care resources besides of ED, including active symptom control, is necessary.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Objective: Previous studies have provided inconclusive results on the association between depression and stroke risk, and the potential modifying effect of comorbid insomnia on this association remains unclear. Our study aimed to clarify the independent roles of depression and insomnia as risk factors for stroke and to investigate the possibility of an interaction effect between these two conditions on stroke incidence. Methods: We used data from the Korean Genome and Epidemiology Study. The primary exposure was depression, measured by the Beck Depression Inventory. The secondary exposure was insomnia. The main outcome was the occurrence of stroke observed in biennial follow-up surveys. Cox proportional regression analysis was performed to estimate the effects of depression and insomnia on stroke incidence. We also conducted interaction analysis to investigate the interaction between depression and insomnia on stroke incidence. Results: During 16 years of follow-up involving 3,301 individuals, we documented 172 cases of new-onset stroke (4.3 cases per 1,000 person-years). Cox proportional logistic regression analysis showed that severe depression significantly increased the risk of stroke (hazard ratio [HR]: 2.06, 95% confidence interval [CI]: 1.13–3.75), whereas mild and moderate depression did not increase this risk. Interaction analysis demonstrated that stroke risk was increased with only moderate (HR: 2.04, 95% CI: 1.04–4.00) and severe (HR: 3.01, 95% CI: 1.43–6.31) depression among individuals without insomnia. Conclusion Although general depression does not significantly increase stroke risk, moderate-to-severe depression may increase this risk, particularly in individuals without insomnia.

Purpose: There has been no report of sex-specific, pediatric age-adjusted shock index (PASI) for pediatric trauma patients in previous studies. We aimed to determine the association between the PASI and in-hospital mortality of pediatric trauma patients and whether this association differs depending on sex. Materials and Methods: This is a prospective, multinational, and multicenter cohort study using the Pan-Asian Trauma Outcome Study (PATOS) registry in the Asia-Pacific region, conducted in pediatric patients who visited the participating hospitals. The main exposure of our study was abnormal (elevated) PASI measured in an emergency department. The main outcome was in-hospital mortality. We performed a multivariable logistic regression analysis to estimate the association between abnormal PASI and study outcomes after adjusting for potential confounders. An interaction analysis between PASI and sex was also conducted. Results: Of 6280 pediatric trauma patients, 10.9% (686) of the patients had abnormal PASI. In multivariable logistic regression analysis, abnormal PASI was significantly associated with increased in-hospital mortality [adjusted odds ratios (aOR), 1.74; 95% confidence interval (CI), 1.13–2.47]. Abnormal PASI had interaction effects with sex for in-hospital mortality (aOR, 1.86; 95% CI, 1.19–2.91 and aOR, 1.38; 95% CI, 0.58–2.99 for male and female, respectively) (p<0.01). Conclusion Abnormal PASI is associated with increased in-hospital mortality in pediatric trauma patients. The prediction power of PASI for in-hospital mortality was maintained only in male patients.

Background: We conducted a comprehensive meta-analysis of prospective cohort studies to analyze the effect of circulating vitamin D level on the risk of sudden cardiac death (SCD) and cardiovascular disease (CVD) mortality. Methods: Prospective cohort studies evaluating the association between circulating vitamin D and risk of SCD and CVD mortality were systematically searched in the PubMed and Embase. Extracted data were analyzed using a random effects model and results were expressed in terms of hazard ratio (HR) and 95% confidence interval (CI). Restricted cubic spline analysis was used to estimate the dose-response relationships. Results: Of the 1,321 records identified using the search strategy, a total of 19 cohort studies were included in the final meta-analysis. The pooled estimate of HR (95% CI) for low vs. high circulating vitamin D level was 1.75 (1.49–2.06) with I 2 value of 30.4%. In subgroup analysis, strong effects of circulating vitamin D were observed in healthy general population (pooled HR, 1.84; 95% CI, 1.43–2.38) and the clinical endpoint of SCD (pooled HRs, 2.68; 95% CI, 1.48– 4.83). The dose-response analysis at the reference level of < 50 nmol/L showed a significant negative association between circulating vitamin D and risk of SCD and CVD mortality. Conclusion Our meta-analysis of prospective cohort studies showed that lower circulating vitamin D level significantly increased the risk of SCD and CVD mortality.