Background Given the higher incidence of emergency conditions in older inhabitants, the global increase in aged population will pose a challenge for emergency services. In this study we examined the burden caused to emergency health care by the aged population. Methods Consecutive patients aged 80 years or over visiting a high-volume, collaborative emergency department (ED) between 2015 and 2016 were included. The key factors under analysis were the incidence of emergency conditions and costs associated with emergency care. Results A total of 6944 patients (median age 85 years, range 80–104 years; 67% female) aged ≥80 years representing 1.5% of the local population, made 17,769 ED visits during the two-year observation period accounting for 15% of all ED visits. Forty-two percent ( n = 2884) of patients had a single ED visit, whereas 8.2% ( n = 570) made ≥5 ED visits/year for a total of 1400 visits (7.9%). Thirty-two percent of those aged ≥80 years required ED services each year. The number of ED visits increased with age ( p < 0.001); and was 768/1000 person-years among octogenarians and 1007/1000 among nonagenarians, in comparison to 233/1000 among those aged < 80 years. One in five of the study population were discharged with non-specific diagnoses. Typical diagnoses included pneumonia (4.8%), malaise and fatigue (4.5%) and heart failure (4.3%). Non-specific diagnoses were frequent, and examination of patients with non-specific diagnoses incurred costs similar to or higher than those of other patients. The mean cost per ED visit in older patients was 422 €. Conclusions We demonstrated a high incidence of emergency department visits in older patients. While our aim was not to solve how the growing demand should be met, it seems unlikely that increasing ED resources is feasible. Instead, the focus should be on chronic care of the aged and prevention of potentially avoidable ED visits.

Endotension after EVAR may cause subsequent aneurysm rupture. Endotension is evidently not associated with endoleak I to III provided that the endovascular graft is maintained in appropriate position and that free endovascular flow is observed. We propose to consider a nonoperative approach in the clinically asymptomatic patient with aneurysm enlargement after EVAR if endoleak is excluded by well-performed imaging techniques.

Cardiovascular diseases due to atherosclerosis are the leading cause of death globally. We aimed to investigate the potentially altered gene and pathway expression in advanced peripheral atherosclerotic plaques in comparison to healthy control arteries. Gene expression analysis was performed (Illumina HumanHT-12 version 3 Expression BeadChip) for 68 advanced atherosclerotic plaques (15 aortic, 29 carotid and 24 femoral plaques) and 28 controls (left internal thoracic artery (LITA)) from Tampere Vascular Study. Dysregulation of individual genes was compared to healthy controls and between plaques from different arterial beds and Ingenuity pathway analysis was conducted on genes with a fold change (FC) > ±1.5 and false discovery rate (FDR) < 0.05. 787 genes were significantly differentially expressed in atherosclerotic plaques. The most up-regulated genes were osteopontin and multiple MMPs, and the most down-regulated were cell death-inducing DFFA-like effector C and A (CIDEC, CIDEA) and apolipoprotein D (FC > 20). 156 pathways were differentially expressed in atherosclerotic plaques, mostly inflammation-related, especially related with leukocyte trafficking and signaling. In artery specific plaque analysis 50.4% of canonical pathways and 41.2% GO terms differentially expressed were in common for all three arterial beds. Our results confirm the inflammatory nature of advanced atherosclerosis and show novel pathway differences between different arterial beds.

No abstract

Background Atherosclerosis is a complex disease with hundreds of genes influencing its progression. In addition, the phenotype of the disease varies significantly depending on the arterial bed. Methodology/Principal Findings We characterized the genes generally involved in human advanced atherosclerotic (AHA type V–VI) plaques in carotid and femoral arteries as well as aortas from 24 subjects of Tampere Vascular study and compared the results to non-atherosclerotic internal thoracic arteries (n=6) using genome-wide expression array and QRT-PCR. In addition we determined genes that were typical for each arterial plaque studied. To gain a comprehensive insight into the pathologic processes in the plaques we also analyzed pathways and gene sets dysregulated in this disease using gene set enrichment analysis (GSEA). According to the selection criteria used (>3.0 fold change and p-value <0.05), 235 genes were up-regulated and 68 genes down-regulated in the carotid plaques, 242 genes up-regulated and 116 down-regulated in the femoral plaques and 256 genes up-regulated and 49 genes down-regulated in the aortic plaques. Nine genes were found to be specifically induced predominantly in aortic plaques, e.g., lactoferrin, and three genes in femoral plaques, e.g., chondroadherin, whereas no gene was found to be specific for carotid plaques. In pathway analysis, a total of 28 pathways or gene sets were found to be significantly dysregulated in atherosclerotic plaques (false discovery rate [FDR] <0.25). Conclusions This study describes comprehensively the gene expression changes that generally prevail in human atherosclerotic plaques. In addition, site specific genes induced only in femoral or aortic plaques were found, reflecting that atherosclerotic process has unique features in different vascular beds.