PURPOSE. There is considerable evidence for systemic vascular dysfunction in primary openangle glaucoma (POAG). We performed nailfold capillary video microscopy to observe directly the nature of nonocular microvasculature abnormalities in POAG. METHODS.We enrolled 199 POAG patients and 124 control subjects from four sites. We used JH-1004 capillaroscopes to perform nailfold capillary video microscopy on the fourth and fifth digits of each subject's nondominant hand. Videos were evaluated for hemorrhages, dilated capillary loops > 50 lm, and avascular zones > 100 lm by graders masked to case status. Multivariable odds ratios (ORs) and 95% confidence intervals (CIs) for POAG were obtained by means of logistic regression analyses that were applied to data from all cases and controls. Corresponding estimates of moderate or severe POAG versus mild POAG (based on the Hodapp-Anderson-Parrish scale) were obtained among cases only. RESULTS.After controlling for demographic factors, family history of glaucoma, systemic diseases, and use of anticoagulation and antiplatelet therapy, for each 100 nailfold capillaries assessed, all types of microvascular abnormalities were significantly associated with POAG. Specifically, the presence of any dilated capillaries (OR ¼ 2.9; 95% CI, 1.6-5.6), avascular zones (OR ¼ 4.4; 95% CI, 1.7-11.3) and hemorrhages (OR ¼ 12.2; 95% CI, 5.9-25.1) were associated with POAG. Among cases, the frequency of microvascular abnormalities was not associated with glaucoma severity (P ‡ 0.43).CONCLUSIONS. These data provided support for nonocular capillary bed abnormalities in POAG. Comparable vascular abnormalities in the optic nerve may render it susceptible to glaucomatous damage.
The aim of this study was to examine the effect of the traditional oral anticoagulant, warfarin (W), and new anticoagulants, apixaban (A) and rivaroxaban (R), on the level of thrombotic biomarkers in patients with atrial fibrillation (AF). Circulating plasma levels of von Willebrand factor (vWF), prothrombin fragment 1.2 (F1.2), microparticle tissue factor (MP-TF), and plasminogen activator inhibitor (PAI-1) were analyzed as potential markers of clot formation in 30 patients with AF prior to ablation surgery. Patients with AF were divided into 2 groups based on their usage (n = 21) and nonusage (n = 9) of any oral anticoagulant. Furthermore, those on anticoagulants were divided based on their use of newer (R and A, 16) or traditional (W, 4) anticoagulants. A statistical increase (P < .05) in the levels of vWF, MP-TF, and PAI-1 were seen in anticoagulated patients with AF, whereas F1.2 and PAI-1 were increased in nonanticoagulated patients with AF compared to normal. There was no statistical difference (P > .05) in levels of any thrombotic biomarker between patients treated with the traditional anticoagulant, W, and those treated with new anticoagulants, R and A. Our data suggest that, despite the use of traditional or newer anticoagulants, prothrombotic biomarkers are still generated at increased levels in patients with AF. Further studies to confirm these findings are warranted.
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