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.

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: A regional pandemic may result in a crisis in providing emergency care to the community and disrupt emergency medical services. This study examined how the recent coronavirus disease 2019 pandemic impacted emergency department (ED) preparedness nationwide by describing the current ED operations. Methods: A cross-sectional survey was developed and distributed nationwide to emergency physicians. All 57 severe emergency care centers and 35 selected local emergency medical institutions nationwide were invited to participate. The survey consisted of basic ED information, infection guidelines, and operations for ED, preemptive pretriage area details, ED quarantine area details, cohort isolation and preemptive quarantine area, and difficulties or problems in treating infectious patients. Results: Forty-nine severe emergency care centers (86%) and 24 (68.6%) local emergency medical institutions answered the survey. Most EDs (95.9% and 91.7% of severe emergency care centers and local emergency medical institutions, respectively) operated under infection guidelines. In addition, 51% and 72.3% of preemptive pretriage areas in severe emergency care centers and local emergency medical institutions, respectively, placed doctors. Both negative and normal pressurized ED quarantine areas were more placed in severe emergency care centers (3 and 3 vs. 0.5 and 1 of severe emergency care centers and local emergency medical institutions, respectively). In severe emergency care centers, the preemptive quarantine areas were operated more than the cohort isolation areas (63.3% vs. 40.8%). Common difficulties expressed by EDs were delayed polymerase chain reaction test results (4.5 and 4.1 of severe emergency care centers and local emergency medical institutions, respectively) and a fear of infection with ED shutdown (4.4 and 4.1 of severe emergency care centers and local emergency medical institutions, respectively). Conclusion This study surveyed how ED care was changed by the pandemic and how current resources are redeployed nationwide. These results may be used as a basis for future ED pandemic preparedness.

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.

Purpose: Sleep apnea (SA) is a risk factor for coronary artery disease (CAD), and SA and CAD increase the incidence of sudden cardiac arrest (SCA). This study aimed to investigate the effect of SA on the incidence of SCA and explore the effect of varying degrees of SA with or without CAD on the incidence of SCA. Materials and Methods: This prospective multi-center, case-control study was performed using the phase II Cardiac Arrest Pursuit Trial with Unique Registry and Epidemiologic Surveillance (CAPTURES-II) database for SCA cases and community-based controls in Korea. The matching ratio of cases to controls was 1:1, and they were randomly matched within demographics, including age, sex, and residence. The primary variable was a history of SA, and the second variable was a history of CAD. We conducted a conditional logistic regression analysis to estimate the effect of SA and CAD on the SCA risk, and an interaction analysis between SA and CAD. Results: SA was associated with an increased risk of SCA [adjusted odds ratio (AOR) (95% confidence interval, CI): 1.54 (1.16–2.03)], and CAD was associated with an increased risk of SCA [AOR (95% CI): 3.94 (2.50–6.18)]. SA was a risk factor for SCA in patients without CAD [AOR (95% CI): 1.62 (1.21–2.17)], but not in patients with CAD [AOR (95% CI): 0.56 (0.20–1.53)]. Conclusion In the general population, SA is risk factor for SCA only in patients without CAD. Early medical intervention for SA, especially in populations without pre-existing CAD, may reduce the SCA risk.ClinicalTrials.gov (NCT03700203)