Introduction: With population aging rampant globally, Europe faces unique challenges and achievements in chronic disease prevention. Despite this, comprehensive studies examining the diabetes burden remain absent. We investigated the burden of type 1 and type 2 diabetes, alongside high fasting plasma glucose (HFPG), in Europe from 1990-2019, to provide evidence for global diabetes strategies.Methods: Disease burden estimates due to type 1 and type 2 diabetes and HFPG were extracted from the GBD 2019 across Eastern, Central, and Western Europe. We analyzed trends from 1990 to 2019 by Joinpoint regression, examined correlations between diabetes burden and Socio-demographic indices (SDI), healthcare access quality (HAQ), and prevalence using linear regression models. The Population Attributable Fraction (PAF) was used to described diabetes risks.Results: In Europe, diabetes accounted for 596 age-standardized disability-adjusted life years (DALYs) per 100,000 people in 2019, lower than globally. The disease burden from type 1 and type 2 diabetes was markedly higher in males and escalated with increasing age. Most DALYs were due to type 2 diabetes, showing regional inconsistency, highest in Central Europe. From 1990-2019, age-standardized DALYs attributable to type 2 diabetes rose faster in Eastern and Central Europe, slower in Western Europe. HFPG led to 2794 crude DALYs per 100,000 people in 2019. Type 1 and type 2 diabetes burdens correlated positively with diabetes prevalence and negatively with SDI and HAQ. High BMI (PAF 60.1%) and dietary risks (PAF 34.6%) were significant risk factors.Conclusion: Europe’s diabetes burden was lower than the global average, but substantial from type 2 diabetes, reflecting regional heterogeneity. Altered DALYs composition suggested increased YLDs. Addressing the heavy burden of high fasting plasma glucose and the increasing burden of both types diabetes necessitate region-specific interventions to reduce type 2 diabetes risk, improve healthcare systems, and offer cost-effective care.

The drug-coated balloon (DCB) is an emerging percutaneous coronary intervention (PCI) device that delivers drugs to diseased vessels to decrease the rate of vascular stenosis. Recent clinical studies have demonstrated that DCBs tend to have both good safety and efficacy profiles, leading to extended application indications in the clinic, including in-stent restenosis (ISR) for metal stents such as drug-eluting stents (DESs), small vascular disease, bifurcation disease, large vascular disease, acute coronary syndrome (ACS), and high bleeding risk. However, some previous clinical data have suggested that DCBs performed less effectively than DESs. No studies or reviews have systematically discussed the improvement strategies for better DCB performance until now. Drug loss during the process of delivery to the target lesion and inefficient delivery of the coating drug to the diseased vascular wall are two key mechanisms that weaken the efficiency of DCBs. This review is the first to summarize the key influencing factors of DCB efficiency in terms of balloon structure and principles, and then it analyzes how these factors cause outcomes in practice based on current clinical trial studies of DCBs in the treatment of different types of lesions. We also provide some recommendations for improving DCBs to contribute to better DCB performance by improving the design of DCBs and combining other factors in clinical practice.

Objective: This study aimed to understand the temporal trends in the disease burden of stroke and its attributable risk factors in China, along with the future trends in the next 25 years, that is important for effective prevention strategies and improvement, and to provide new insights into the age- and sex-specific incidence, prevalence, mortality, disability-adjusted life-years (DALYs) and their trends from 1990 to 2019, and the prediction in the next 25 years.Methods: The Global Burden of Disease Study (2019) was used to extract the data on age- and sex-specific incidence, mortality, and disability-adjusted life-years (DALYs) of stroke in China, 1990–2019. We estimated the estimated annual percentage change (EAPC) to access the temporal trends of the disease burden of stroke. The R package called Nordpred was used to perform an age-period-cohort analysis to predict the prevalence of stroke.Results: The number of incidence cases, deaths, and DALYs of stroke increased from 1990 to 2019. Overall downward trends were observed in the age-standardized incidence rate (ASIR) from 1990 to 2019. Significant temporal trends in mortality and DALYs of stroke were observed. High systolic blood pressure, smoking, and high-sodium diet were the main driving forces for stroke. The DALYs lost attributable to smoking were different for male and female patients. In the next 25 years, the number of new cases and deaths from stroke should continue to increase. The ASIR and age-standardized mortality rate (ASMR) should show a downward trend among male and female patients.Conclusion: Despite the overall rates of stroke declined over the period from 1990 to 2019, the absolute number of people affected by stroke has substantially increased. There has been a substantial increase in the burden of stroke due to risk factors and will continue to increase in the next 25 years.

The findings of the last decade suggest a complex link between inflammatory cells, coagulation, and the activation of platelets and their synergistic interaction to promote venous thrombosis. Inflammation is present throughout the process of venous thrombosis, and various metabolic pathways of erythrocytes, endothelial cells, and immune cells involved in venous thrombosis, including glucose metabolism, lipid metabolism, homocysteine metabolism, and oxidative stress, are associated with inflammation. While the metabolic microenvironment has been identified as a marker of malignancy, recent studies have revealed that for cancer thrombosis, alterations in the metabolic microenvironment appear to also be a potential risk. In this review, we discuss how the synergy between metabolism and thrombosis drives thrombotic disease. We also explore the great potential of anti-inflammatory strategies targeting venous thrombosis and the complex link between anti-inflammation and metabolism. Furthermore, we suggest how we can use our existing knowledge to reduce the risk of venous thrombosis.