Cardiovascular disease remains the main cause of mortality in individuals with diabetes mellitus (DM) and also results in significant morbidity. Premature and more aggressive atherosclerotic disease, coupled with an enhanced thrombotic environment, contributes to the high vascular risk in individuals with DM. This prothrombotic milieu is due to increased platelet activity together with impaired fibrinolysis secondary to quantitative and qualitative changes in coagulation factors. However, management strategies to reduce thrombosis risk remain largely similar in individuals with and without DM. The current review covers the latest in the field of antithrombotic management in DM. The role of primary vascular prevention is discussed together with options for secondary prevention following an ischaemic event in different clinical scenarios including coronary, cerebrovascular, and peripheral artery diseases. Antiplatelet therapy combinations as well as combination of antiplatelet and anticoagulant agents are examined in both the acute phase and long term, including management of individuals with sinus rhythm and those with atrial fibrillation. The difficulties in tailoring therapy according to the variable atherothrombotic risk in different individuals are emphasized, in addition to the varying risk within an individual secondary to DM duration, presence of complications and predisposition to bleeding events. This review provides the reader with an up-to-date guide for antithrombotic management of individuals with DM and highlights gaps in knowledge that represent areas for future research, aiming to improve clinical outcome in this high-risk population.

In recent years, newer drug classes for the treatment of type 2 diabetes mellitus have been released with significant effects on glucose lowering and weight reduction. One of the most promising classes in achieving these goals has been the glucagon-like peptide (GLP)-1 agonists. However, a difficulty with the use of these agents is the need for subcutaneous injections, which can be inconvenient to individuals living with type 2 diabetes. More recently, a GLP-1 agonist has been developed, semaglutide, that can be administered orally which has at least similar effects to the subcutaneous preparation from which this compound is derived. In this review article, we discuss the glycemic and cardiovascular effects of the GLP-1 agonists with special emphasis on oral semaglutide and the potential role of this therapy in individuals with type 2 diabetes.

Aim: To examine the impact of interrupting prolonged sitting with frequent short bouts of light‐intensity activity on glycaemic control in people with type 1 diabetes (T1D). Materials and Methods: In total, 32 inactive adults with T1D [aged 27.9 ± 4.7 years, 15 men, diabetes duration 16.0 ± 6.9 years and glycated haemoglobin 8.4 ± 1.4% (68 ± 2.3 mmol/mol)] underwent two 7‐h experimental conditions in a randomised crossover fashion with >7‐day washout consisting of: uninterrupted sitting (SIT), or, interrupted sitting with 3‐min bouts of self‐paced walking at 30‐min intervals (SIT‐LESS). Standardised mixed‐macronutrient meals were administered 3.5 h apart during each condition. Blinded continuous glucose monitoring captured interstitial glucose responses during the 7‐h experimental period and for a further 48‐h under free‐living conditions. Results: SIT‐LESS reduced total mean glucose (SIT 8.2 ± 2.6 vs. SIT‐LESS 6.9 ± 1.7 mmol/L, p = .001) and increased time in range (3.9‐10.0 mmol/L) by 13.7% (SIT 71.5 ± 9.5 vs. SIT‐LESS 85.1 ± 7.1%, p = .002). Hyperglycaemia (>10.0 mmol/L) was reduced by 15.0% under SIT‐LESS (SIT 24.2 ± 10.8 vs. SIT‐LESS 9.2 ± 6.4%, p = .002), whereas hypoglycaemia exposure (<3.9 mmol/L) (SIT 4.6 ± 3.0 vs. SIT‐LESS 6.0 ± 6.0%, p = .583) was comparable across conditions. SIT‐LESS reduced glycaemic variability (coefficient of variation %) by 7.8% across the observation window ( p = .021). These findings were consistent when assessing discrete time periods, with SIT‐LESS improving experimental and free‐living postprandial, whole‐day and night‐time glycaemic outcomes ( p < .05). Conclusions: Interrupting prolonged sitting with frequent short bouts of light‐intensity activity improves acute postprandial and 48‐h glycaemia in adults with T1D. This pragmatic strategy is an efficacious approach to reducing sedentariness and increasing physical activity levels without increasing risk of hypoglycaemia in T1D.

Background: Estimated glucose disposal rate (eGDR) is a practical measure of Insulin Resistance (IR) which can be easily incorporated into clinical practice. We profiled eGDR in younger adults with type 1 diabetes mellitus (T1DM) by their demographic and clinical characteristics. Methods: In this single centre study, medical records of TIDM were assessed and eGDR tertiles correlated with demographic and clinical variables. Results: Of 175 T1DM individuals, 108 (61.7%) were males. Mean age (±SD) was 22.0 ± 1.6 years and median time from diagnosis 11.0 years (range 1–23). Individuals were predominantly Caucasian (81.7%), with 27.4% being overweight (BMI: 25–30 kg/m²) and 13.7% obese (BMI > 30 kg/m²). Mean total cholesterol (TC) levels were significantly lower in high and middle eGDR tertiles (4.4 ± 1 and 4.3 ± 0.8 mmol/l, respectively) compared with low eGDR tertile (4.8 ± 1, p < 0.05 for both). Triglyceride (TG) levels showed a similar trend at 1.1 ± 0.5 and 1.1 ± 0.5 mmol/l for high and middle eGDR tertile compared to low eGDR tertile (1.5 ± 1 mmol/l, p < 0.05 for both). Renal function was similar across eGDR tertiles and no difference in retinopathy was detected. Conclusion: TC and TG are altered in individuals with T1DM and low eGDR, suggesting that this subgroup requires optimal lipid management to ameliorate their vascular risk.

Diabetes is a metabolic condition with a rising global prevalence and is characterised by abnormally high blood glucose levels. Cardiovascular disease (CVD) accounts for the majority of deaths in diabetes and, despite improvements in therapy, mortality and hospitalisations in this cohort remain disproportionally higher compared to individuals with normal glucose metabolism. One mechanism for increased CVD risk is enhanced thrombosis potential, due to altered function of the cellular and acellular arms of coagulation. Different mechanisms have been identified that mediate disordered blood clot formation and breakdown in diabetes, including dysglycaemia, insulin resistance, and metabolic co-morbidities. Collectively, these induce platelet/endothelial dysfunction and impair the fibrinolytic process, thus creating a prothrombotic milieu. Despite these abnormalities, current antithrombotic therapies are largely similar in diabetes compared to those without this condition, which explains the high proportion of patients experiencing treatment failure while also displaying an increased risk of bleeding events. In this narrative review, we aimed to summarise the physiological functioning of haemostasis followed by the pathological effects of diabetes mellitus on platelets and the fibrin network. Moreover, we carefully reviewed the literature to describe the current and future therapeutic targets to lower the thrombosis risk and improve vascular outcomes in diabetes.