Background: Platelet concentrates are conventionally stored at room temperature (20–24°C), which preserves platelet viability but is associated with progressive metabolic deterioration and increased risk of bacterial contamination. Cold storage (4°C) has re-emerged as a potential alternative strategy; however, its impact on platelet metabolism, activation, and hemostatic function during extended storage remains incompletely characterized. Aim: To evaluate metabolic and functional changes in apheresis platelet concentrates during storage under cold and room temperature conditions. Methods: Apheresis platelet concentrates obtained from two healthy donors were stored in platelet additive solution with or without pathogen inactivation. Platelets were stored at 20–24°C (up to 7 days) or 4°C (up to 21 days). Metabolic parameters (pH, glucose, lactate), activation markers (CD62P, Annexin V), and hemostatic function (thromboelastography) were assessed at predefined time points. Because this was an exploratory pilot study with two independent donors, the analysis was primarily descriptive and no inferential statistical comparisons were performed. Results: Cold storage was associated with slower glucose consumption and lower lactate accumulation during the early storage period, accompanied by a progressive decline in pH during prolonged storage. Cold-stored platelets showed increased CD62P expression and phosphatidylserine exposure, as reflected by Annexin V binding, particularly during prolonged storage. Thromboelastographic analysis showed relative preservation of clot strength during the first 7 days of cold storage, with mean maximum amplitude values remaining approximately 72–79 mm during this period. Conclusion: Cold storage was associated with distinct metabolic and functional changes, including slower early glucose consumption, lower lactate accumulation, increased platelet activation and phosphatidylserine exposure, and relative preservation of clot strength during the first 7 days. Given the exploratory design and limited sample size, these findings should be considered preliminary and require confirmation in larger experimental and clinical studies.
Background Atherosclerosis is a lipid-driven inflammatory disease in which plasma lipoproteins and cellular cholesterol pools contribute to coronary artery disease (CAD). Lipoprotein subfractions and erythrocyte membrane cholesterol (EMC) have each been linked to CAD, but their combined behavior across angiographic stages remains insufficiently characterized. EMC may also be relevant to blood flow properties and microcirculatory function. Methods We studied 122 patients undergoing coronary angiography and 64 controls. CAD severity was classified by the number of diseased vessels. Plasma lipid profile, LDL and HDL subfractions, atherogenic indices, EMC, and C-reactive protein were analyzed using multivariable regression, ANCOVA, ROC analysis, and an exploratory multi-marker approach. Results Conventional lipid parameters showed limited group differences, whereas sdLDL, HDL subfractions, EMC, CRP, and selected lipid ratios differed across CAD severity groups. EMC increased across CAD categories and remained associated with CAD after adjustment for conventional lipid variables. Among lipid-related variables, EMC showed the most consistent association with angiographically defined CAD. Conclusions EMC may provide complementary hemorheology- and microcirculation-relevant information in angiographically defined CAD. Lipoprotein subfractions and composite lipid indices may offer adjunctive characterization of CAD-related lipid remodeling.
Objective Patients with Chronic Obstructive Pulmonary Disease (COPD) often develop exacerbations that could be infective or non-infective and are prone to develop thrombosis. To assess thrombogenicity in this group, a functional biomarker of clot microstructure namely fractal dimension (d f) is utilised. This sub-group analysis intent to compare the changes in d f between infective and non-infective exacerbation of COPD.Methods 85 patients with acute exacerbations of COPD were recruited from the Emergency Department. Blood samples were taken to determine biomarkers of inflammation, haemostasis and rheology at four time points (0 h, 4-6 h, 24 h and 3-7 days).Results The biomarker of clot microstructure did not attain significance in the infective group when compared to the non-infective group at four time points.Conclusions The study demonstrates that exacerbation caused by infection does not cause more thrombogenicity compared to non-infective causes utilising clot microstructure.
Background: Hemorrhagic shock is associated with profound disturbances of microcirculatory perfusion in which alterations of blood rheology may contribute to tissue hypoxia and organ dysfunction. Historically, the concept of hemorrhagic shock has evolved from an initial focus on systemic hemodynamic failure toward recognition of the critical role of microcirculatory dysfunction and impaired tissue oxygen delivery. More recent experimental and clinical research has further emphasized the contribution of blood rheological abnormalities to the progression of hemorrhagic shock and organ dysfunction. However, the relative contribution of individual hemorheological parameters during progressive hemorrhagic shock remains insufficiently characterized. Objective: To investigate stage-dependent changes in blood rheology in an experimental rat model of hemorrhagic shock and to evaluate the relationship between conventional hemorheological parameters and a newly proposed computational rheological index derived from routine hematological variables. Methods: Hemorrhagic shock was induced in 60 anesthetized rats by controlled withdrawal of 2.0, 2.5, or 3.5 mL of arterial blood, corresponding to progressive stages of shock. 20 intact animals served as controls. Erythrocyte aggregation, erythrocyte deformability, plasma viscosity, hematocrit, and the computational rheological index were assessed 15 min after blood withdrawal. Results: Progressive blood loss resulted in stage-dependent deterioration of hemorheological properties. Erythrocyte aggregation demonstrated the greatest relative increase and was strongly associated with shock severity. Changes in erythrocyte deformability were less pronounced, whereas plasma viscosity and hematocrit remained relatively stable throughout the experimental stages. The computational rheological index exhibited changes parallel to erythrocyte aggregation, suggesting that it reflects progressive rheological impairment. Conclusions: Experimental hemorrhagic shock is accompanied by progressive deterioration of blood rheology, with erythrocyte aggregation representing the most sensitive laboratory marker. The proposed computational rheological index demonstrated a close association with experimentally observed rheological alterations and warrants further validation in independent experimental and clinical studies.
Background:Cardiovascular risk stratification in patients with hypertension and diabetes remains suboptimal. We evaluated the prognostic and incremental value of Dr. Noon CVD, a deep learning (DL)-based retinal biomarker, for 10-year atherosclerotic cardiovascular (ASCVD) mortality. Methods:This retrospective, single-center, primary prevention cohort study included 7,832 Korean patients with hypertension or diabetes diagnosed on or before retinal fundus photography (2005 to 2022). Patients with prior cardiovascular disease were excluded. The primary outcome of 10-year ASCVD mortality and a sensitivity analysis of 5-year mortality were stratified using 4-tier and 3-tier Dr. Noon CVD systems, respectively. Multivariable Cox proportional hazards models were adjusted for traditional risk factors and chronic kidney disease (CKD), and incremental predictive value was assessed using the change in the C-index (ΔC-index) and net reclassification improvement (NRI). Results:In the overall population, the Dr. Noon CVD score was independently associated with 10-year ASCVD mortality (hazard ratio [HR] trend, 1.49; 95% confidence interval [CI], 1.21 to 1.85; P < 0.001) after full adjustment for traditional factors and CKD. Adding Dr. Noon CVD to the clinical model significantly improved discrimination (ΔC-index, 0.030; P = 0.001) and risk reclassification (NRI, 0.484; 95% CI, 0.233 to 0.666; P < 0.001). This independent prognostic value was consistent in both hypertension (10-year HR trend, 1.48; P = 0.006) and diabetes (10-year HR trend, 1.42; P = 0.003) subgroups. The reclassification improvement was greater in the diabetes than the hypertension subgroup (10-year NRI, 0.481 vs. 0.413). The score's prognostic value was independent of diabetic retinopathy status. Conclusions:DL-based retinal imaging provides prognostic value for 10-year ASCVD mortality independent of the available clinical risk factors (age, sex, hypertension, diabetes, and CKD) and consistent under adjustment for available laboratory measures, supporting its role as an accessible opportunistic screening tool for long-term primary prevention in cardiometabolic clinics.
