Pre-analytical stability of coagulation parameters in plasma stored at room temperature

Introduction: Haemostasis testing is influenced by many pre-analytical variables, such as storage time and temperature, which can affect the stability of coagulation factors and influence the results of coagulation assays. We investigated the stability of haemostasis tests after storage of aliquoted plasma at RT, including the variability of measurement principle and reagent used for determination. Methods: Blood samples from 20 healthy volunteers were obtained, processed to PPP and aliquoted. Aliquots were stored at RT for 0 hour, 2 hours, 4 hours, 6 hours, 8 hours, 12 hours, 24 hours and 48 hours. PT, aPTT, fibrinogen, D-Dimers and coagulation factors (FII, FV, FVII, FX, FVIII, FIX, FXI, FXII) were determined by STA-R Max (R) and ACL-TOP (R). VWF:Ag and vWF:RCo were determined by AcuStar (R). Clinically relevant changes, compared to the initial measurement, were denoted as a percentage change of > 10% according to the 99% CI. Results: For both analysers, a clinically relevant change of > 10% was observed for FV after 2 hours, FVIII after 4 hours and for aPTT, FII, FVII, FX and FXII after 48 hours of storage at RT. Statistically significant, but no clinically relevant differences were observed after 48-hours storage for PT, fibrinogen and FIX. D-Dimers, FXI, vWF: Ag and vWF: RCo were found stable up to 48 hours at RT. Conclusion: Overall, compared to the limits given by the current CLSI guidelines, for most coagulation parameters investigated in this study a longer storage period could be accepted. Time intervals for FVIII and FV dosage were shorter than recommended by the CLSI guidelines. For PT determination, our findings were consistent

The G534E polymorphism of the gene encoding the factor VII–activating protease is associated with cardiovascular risk due to increased neointima formation

The G534E polymorphism (Marburg I [MI]) of factor VII–activating protease (FSAP) is associated with carotid stenosis and cardiovascular disease. We have previously demonstrated that FSAP is present in atherosclerotic plaques and it is a potent inhibitor of vascular smooth muscle proliferation and migration in vitro. The effect of wild-type (WT)- and MI-FSAP on neointima formation in the mouse femoral artery after wire-induced injury was investigated. Local application of WT-FSAP led to a 70% reduction in the neointima formation, and this effect was dependent on the protease activity of FSAP. MI-FSAP did not inhibit neointima formation in vivo. This is due to a reduced proteolytic activity of MI-FSAP, compared to WT-FSAP, toward platelet-derived growth factor BB, a key mediator of neointima development. The inability of MI-FSAP to inhibit vascular smooth muscle accumulation explains the observed linkage between the MI-polymorphism and increased cardiovascular risk. Hence, FSAP has a protective function in the vasculature, and analysis of MI polymorphism is likely to be clinically relevant in restenosis

Ocular pulse amplitude in diabetes mellitus

BACKGROUND—The influence of diabetes mellitus on ocular pulse amplitude (OPA), an indirect measure of choroidal perfusion, is unclear.
METHODS—OPA, using the Langham ocular blood flow (OBF) system, applanation intraocular pressure (IOP), systemic blood pressure (BP), heart rate, and haemoglobin (Hb) A(1c) were measured in patients with insulin dependent diabetes mellitus (IDDM) with no (DR-0, n = 22) non-proliferative (DR-1, n = 24), and proliferative (DR-2, n = 18) diabetic retinopathy.
RESULTS—Neither local (OPA, IOP) nor systemic perfusion parameters (BPs, HR) nor HbA(1c) were significantly altered in DR-0, DR-1, or DR-2 IDDM patients.
CONCLUSION—Choroidal circulation remains unaffected as diabetic retinopathy advances.