Background: Impaired endothelial-dependent flow-mediated dilatation (FMD) has been used to demonstrate endothelial dysfunction in a wide variety of cardiovascular disease, but previous studies have excluded patients with atrial fibrillation(AF). We therefore hypothesised that endothelial dysfunction exists in AF and that this could be demonstrated by impaired FMD, and related to plasma indices of endothelial damage/dysfunction [soluble E-selectin (sE-sel), von Willebrand factor (vWf), and soluble thrombomodulin (sTM)], as well as total body nitrate/nitrite product (NOx, a measure of endothelial nitric oxide production).
Methods: We studied 40 patients with chronic permanent AF, who were compared to 26 sinus rhythm controls.
Background: Disturbances in mineral and vitamin D metabolism, which affect parathyroid hormone (PTH) synthesis, are well recognized in patients receiving dialysis. However, it is unclear at what stage of chronic kidney disease (CKD) these abnormalities develop.
Methods: The associations between CKD stages 3 and 5, and alterations of calcium, phosphate, vitamin D and PTH concentrations were assessed in 249 patients (mean age 61 years, 66% male) and 79 age- and sex-matched healthy controls.
Background: Atrial fibrillation (AF) is associated with a prothrombotic state, which is related to endothelial damage/dysfunction. Plasma levels of soluble E-selectin (sE-sel), von Willebrand factor (vWf), and soluble thrombomodulin (sTM) have been used as indexes of endothelial activation, damage/dysfunction, and endothelial damage, respectively. Nitric oxide is also made by a healthy endothelium, and a total body nitrate/nitrite product (NOx) is used as a measure of endothelial nitric oxide production.
View Article and Find Full Text PDFObjective: To report two cases of preimplantation genetic diagnosis (PGD) for myotonic dystrophy type I (DM1) where cross-over between the DMPK locus and a linked polymorphic marker APOC2 was detected.
Methods: Embryos from in vitro fertilisation (IVF) were biopsied at day 3 of development and single blastomeres collected. Diagnosis was performed by duplex or triplex fluorescent-polymerase chain reaction (F-PCR) to amplify DMPK and APOC2 loci, or DMPK with APOC2 and D19S112 polymorphic markers.
Background: Chronic elevation of plasma catecholamines and sympathetic stimulation in chronic heart failure (CHF) leads to increased production of free radicals, and so possibly to endothelial damage/dysfunction and atheroma formation. Abnormal oxidative stress may therefore be related to some of the high mortality and morbidity in CHF. The objective of the present prospective open study was to compare the effects of beta-blockers and ACE inhibitors in relation to oxidative stress and endothelial damage in CHF.
View Article and Find Full Text PDFBackground: Chronic renal failure is associated with impaired endothelium-dependent vasodilation and accelerated atherogenesis. To examine whether endogenous reactive oxygen species (ROS) modify endothelial function in renal failure, we evaluated the effect of the antioxidant vitamin C on endothelium-dependent responses in both the conduit and resistance vasculature of subjects with severe renal impairment.
Methods: Endothelial function of the forearm resistance vasculature was assessed using plethysmography to measure the dilator response to intra-arterial acetylcholine (Ach) (25 to 100 nmol/min).
Cardiac parasympathetic control has prognostic significance in heart failure, but the control mechanisms of this system remain poorly defined. We have demonstrated previously a facilitatory role for nitric oxide (NO) in the parasympathetic control of heart rate in young healthy human subjects. In view of the complex abnormalities of regional NO activity observed in chronic heart failure, we now aim to establish if this mechanism is active in subjects with this condition.
View Article and Find Full Text PDFCardiac vagal control has prognostic significance in cardiac disease, but the control mechanisms of this system remain poorly understood. We have previously demonstrated a role for NO in promoting vagal control of heart rate in humans. Here we examine the influence of L-arginine, the substrate for NO synthase, on this mechanism in healthy human subjects.
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