Our data support a role of HD-induced release of hemoglobin in the pathogenesis of endothelial dysfunction in patients with end-stage renal disease. Approaches that oxidize free plasma hemoglobin may restore NO bioavailability and may have potential beneficial effects on vascular function. (Influence of Hemodialysis on Endothel-Depending Dilatation of Peripheral Arteries; NCT00764192).
Age-dependent alterations of the vessel wall may predispose older individuals to increased cardiovascular pathology. Aging is associated with an impaired bioactivity of nitric oxide (NO). Plasma nitrite reflects NO-synthase activity under fasting conditions and is an important storage pool of NO. To test the hypothesis that aging is associated with an impaired capacity of the vasculature to increase plasma nitrite during exercise, 29 young and 28 old healthy individuals (25 +/- 1 years and 58 +/- 2 years; P < 0.001) without major cardiovascular risk factors were enrolled. Exercise stress was similar in both groups. Baseline nitrite did not differ (107 +/- 8 vs. 82 +/- 10 nmol/l, young vs. old; n.s.) although a trend toward higher nitrite levels in young individuals was seen. In young subjects, exercise increased plasma nitrite by 38 +/- 7% (P < 0.001) compared to only 13 +/- 8% (P = n.s.) in older subjects. L-NMMA blocked increases of nitrite. Endothelial function, as defined by flow-mediated-dilation (FMD) of the brachial artery via ultrasound, was impaired in older subjects (5.4 +/- 0.4% vs. 6.7 +/- 0.3%; P < 0.01). Multivariate analysis showed that age (P = 0.007), BMI (P = 0.010), and LDL (P = 0.021) were independent predictors of nitrite increase. The fact that aging is associated with an impaired capacity of the vasculature to adequately increase nitrite to physiological stimuli may contribute to attenuated maintenance and further deterioration of vascular homeostasis with aging.
Non-Chicken Wing LAA morphologies are associated with a specific echocardiographic flow pattern in patients with AF. Since evidence exists that LAA flow pattern are indicative of an enhanced risk of thrombus formation, 3D-TEE might be a valuable tool warranting future studies to test whether these morphological and functional characteristics permit risk stratification in AF.
The aim of our study was to evaluate possible associations of circulating monocyte subsets with cardiovascular risk and the extent of coronary artery disease (CAD). Monocytes in peripheral blood have been divided into functional subsets on the basis of their expression of the lipopolysaccharide receptor CD14 and the Fc-γ receptor CD16 (1-4). CD14 ++ CD16cells represent the major monocyte population, highly express CCR2 and are often described as "classical" monocytes. The tissue macrophage-like CD14 + CD16 + subset displays elevated levels of the chemokine receptors CX 3 CR1, CXCR4 and CCR5 but lower expression of CCR2 than CD14 ++ CD16monocytes (2, 3). These CD16 + monocytes can produce pro-inflammatory cytokines, show lower expression of scavenger receptor type-A (SR-A) but higher antigen-presenting capacity, ox-LDL uptake, fractalkine-induced adhesiveness and migratory potential in the subendothelium, which may favour patrolling or egression from atherosclerotic plaques (2-6). Current data have demonstrated a higher degree of heterogeneity in the CD16 + subset: CD14 ++ CD16 + monocytes differ from CD14 low CD16 + cells by secretion of tumour necrosis factor (TNF)-α and by expression of VEGFR1 and Tie2 (4, 7-10). Recent study has further revealed an inverse correlation of CD14 ++ CD16monocyte counts to left ventricular recovery after myocardial infarction (11).
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