20 research outputs found

    Illustration of reactive hyperaemia peripheral arterial tonometry (PAT).

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    <p>Depicted are a measurement (A) with colour-coded intervals corresponding to parameters required for the reactive hyperaemia index equation (B). Tracings derive from beat-to-beat finger volume changes captured by plethysmographic finger cuffs on the index fingers of both hands. The interval 60–120 seconds post cuff release is best linked to coronary microvasculature dysfunction as published by Bonnetti et al. [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0178412#pone.0178412.ref017" target="_blank">17</a>]. Additionally the comparison of a pathologic (C) and a normal (D) hyperaemia responses as recorded by fingertip plethysmography is shown. RHI, reactive hyperaemia index.</p

    Non-cardiac vascular markers in patients with angina like symptoms and CAD or normal coronary arteries.

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    <p>Illustrated are carotid IMT (A), plaque score (B), reactive hyperaemia index (C), reflection magnitude (D), pulse wave velocity (E) and carotid distensibility (F). The continuous lines represent the mean±SD (————) and the dotted lines represent the median + interquartile range (— — —). CAD, coronary artery disease; NCA, normal coronary arteries; IMT, carotid intima media thickness; RHI, reactive hyperaemia index; PWV, pulse wave velocity; DC, distensibility coefficient; ns, non-significant.</p

    ROC-analysis for CAD estimation.

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    <p>Depicted are ROC-curves for pre- (A) and post-test probability (B) and added vascular markers. RHI<sup>-1</sup>, inverse reactive hyperaemia index.</p

    Markers in the cardiovascular continuum.

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    <p>The inner circle (yellow) states the stage of the cardiovascular continuum. The middle circle (blue) states the different pathophysiological process or categorises of the cardiovascular continuum stage. The outer circle (black) summarises a range of markers quantifying the pathophysiological process. Investigated markers (<b><i>bold & italic</i></b>) capable of differentiating between patients with CAD and NCA in our study are highlighted red. Investigated markers (<b><i>bold & italic</i></b>) without statistical significant differences between patients with CAD and NCA are highlighted orange. SNP, single nucleotide polymorphism; CRP, C-reactive protein; IL-6, interleukin 6; TNFα, tumour necrosis factor α; ICAM-1, intercellular adhesion molecule-1; LDL, low density lipoprotein; RH-PAT, reactive hyperaemia pulse amplitude tonometry; EPCs, endothelial progenitor cells; IMT, intima media thickness; ABI, ankle brachial index; LVH, left ventricular hypertrophy; ECG, electrocardiography; ACS, acute coronary syndrome; CAD, coronary artery disease; NCA, normal coronary arteries; TIA, transitory ischaemic attack; CT, computer tomography; MRI, magnet resonance imaging; GFR, glomerular filtration rate; BNP, brain natriuretic peptide. Adapted from Dzau et al. [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0178412#pone.0178412.ref015" target="_blank">15</a>].</p

    Association plot of the genomic region around (i) SLCO1B1, (ii) CYP4B1 and (iii)ADH1B showing both type and imputed SNPs with location of genes and recombination rate.

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    <p><i>P</i> values of SNPs are plotted (as −log<sub>10</sub> <i>P</i>) against their physical position on the chromosomes (NCBI Build 36). Estimated recombination rates from the HapMap CEU population show the local LD structure. The color of each SNP indicates linkage disequilibrium with the index SNP (rs4149056 or rs6663731 or rs1693457 respectively) based on pairwise <i>r</i><sup>2</sup> values from HapMap CEU data.</p
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