K. McNeill

ICL, Londinium, England, United Kingdom

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Publications (13)60.11 Total impact

  • M. Cecelja · B. Jiang · K. McNeill · T. Spector · P. Chowienczyk ·

    Artery Research 12/2014; 8(4). DOI:10.1016/j.artres.2014.09.068
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    ABSTRACT: Pulse wave velocity (PWV), a measure of arterial stiffness strongly predictive of cardiovascular risk in adults, is usually measured by sequential ECG-referenced carotid and femoral tonometry. A simplified technique, more suitable for use in children, employs simultaneous volumetric recording from a sensor applied over the carotid artery and a cuff applied over the femoral artery or arm and thigh pressure cuffs applied over the brachial and femoral arteries. The purpose of this study was to compare PWV computed over the carotid-femoral path (PWVcf) with that over the brachial-femoral path (PWVbf) using a volumetric system (Vicorder) and to compare values of PWVcf obtained by the volumetric and a tonometric method (SphygmoCor) in children. Vicorder PWVcf and PWVbf were compared in 156 children (3-18 years, 110 with chronic kidney disease), and PWVcf by Vicorder was compared to PWVcf by SphygmoCor in a subset of 122 patients. PWVcf by Vicorder was moderately correlated with PWVcf by SphygmoCor (R = 0.50, P < 0.000). PWVbf and PWVcf Vicorder were more closely correlated (R = 0.75, P < 0.0001), but with a significant systematic difference. Applying a correction factor to PWVbf measurements gave results similar to those obtained over the carotid-femoral path. Within-patient coefficients of variation for repeated measures were 5.9, 7.8, and 8.5% for PWVbf (Vicorder), PWVcf (Vicorder) and PWVcf (SphygmoCor), respectively. All PWV values showed a similar relation to age. Volumetric methods appear reproducible and are easy to use in children, but values obtained by Vicorder and SphygmoCor are not interchangeable even when measured over the same pathway.
    Journal of Hypertension 04/2014; 32(7). DOI:10.1097/HJH.0000000000000203 · 4.72 Impact Factor
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    ABSTRACT: Within the general population, levels of C-reactive protein (CRP) are positively associated with atherosclerotic cardiovascular disease (CVD). Whether CRP is causally implicated in atherogenesis or is the results of atherosclerosis is disputed. A role of CRP to protect endothelium-derived nitric oxide (EDNO) has been suggested. We examined the association of CRP with EDNO-dependent vasomotor function and subclinical measures of atherosclerosis and arteriosclerosis in patients with raised CRP resulting from rheumatoid arthritis (RA). Patients with RA (n = 59) and healthy control subjects (n = 123), underwent measures of high sensitivity CRP, flow-mediated dilation (FMD, dependent on EDNO), intima-media thickness (IMT, a measure of subclinical atherosclerosis) and aortic pulse wave velocity (PWV, a measure of arteriosclerosis). IMT and PWV were elevated in patients with RA compared to controls but FMD was similar in the two groups. In patients with RA, IMT and PWV were not correlated with CRP but FMD was positively independently correlated with CRP (P<0.01). These findings argue against a causal role of CRP in atherogenesis and are consistent with a protective effect of CRP on EDNO bioavailability.
    PLoS ONE 04/2010; 5(4):e10242. DOI:10.1371/journal.pone.0010242 · 3.23 Impact Factor

  • Artery Research 12/2009; 3(4):153-153. DOI:10.1016/j.artres.2009.10.152
  • A. Donald · Z. Maniou · K. Connell · K. McNeill · T. Sanders · P. Chowienczyk ·

    Artery Research 12/2009; 3(4):164-164. DOI:10.1016/j.artres.2009.10.070
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    ABSTRACT: Our aim was to examine the relative contributions of the first systolic shoulder (P1) and augmentation pressure (DeltaP(aug)) to central pulse pressure (cPP), their relation to central arterial stiffness (pulse wave velocity [PWV]) and arterial diameters, and their respective heritability estimates. cPP is augmented above P1 by DeltaP(aug) due to pressure waves reflected from the periphery of the circulation. Women (n = 496) from the Twins UK adult twin registry (112 monozygotic, 135 dizygotic pairs) age 21 to 81 years were studied. cPP, P1, and DeltaP(aug) were estimated using the SphygmoCor system (Atcor, West Ryde, Australia) from transformed radial waveforms. Carotid-femoral PWV was measured using the same system. Aortic and femoral artery diameters were measured by ultrasonography. Heritability was estimated using structural equation modeling. P1 and DeltaP(aug) accounted for 22% and 76%, respectively, of the variance in cPP. After adjustment for mean arterial pressure and heart rate, P1 strongly independently positively correlated with PWV (standardized regression coefficient, beta = 0.4, p < 0.0001), whereas DeltaP(aug) did not independently correlate with PWV but independently negatively correlated with the ratio of the diameter of the femoral to that of the abdominal aorta (beta = -0.12, p < 0.001). Estimates of heritability (h(2)) of cPP, PWV, P1, and DeltaP(aug) were 0.43, 0.34, 0.31, and 0.62, respectively, after adjustment for mean arterial pressure and heart rate. These results suggest that, in women, DeltaP(aug) is highly heritable, is associated with the ratio of distal to proximal arterial diameters, and, independent of PWV, is a major determinant of cPP.
    Journal of the American College of Cardiology 09/2009; 54(8):695-703. DOI:10.1016/j.jacc.2009.04.068 · 16.50 Impact Factor
  • M. Cecelja · B. Jiang · K. McNeill · B. Kato · T. Spector · P. Chowienczyk ·

    Artery Research 08/2008; 2(3):86-86. DOI:10.1016/j.artres.2008.08.287
  • Benyu Jiang · Baoming Liu · Karen L McNeill · Philip J Chowienczyk ·
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    ABSTRACT: Pulse wave velocity (PWV), the speed of propagation of arterial pressure waves through the arterial tree, is related to arterial stiffness and is an important prognostic marker for cardiovascular events. In clinical practice PWV is commonly determined by arterial tonometry, with a noninvasive pressure sensor applied sequentially over carotid and femoral arteries. The electrocardiogram (ECG) is used as a timing reference to determine the time delay or "transit time" between the upstroke of carotid and femoral pulse waveforms. Commercially available vascular ultrasound scanners provide a pulsed wave (PW) Doppler velocity signal, which should allow determination of carotid-femoral transit time and hence PWV. We compared carotid-femoral PWV measured by tonometry and by PW Doppler ultrasound (Seimens, Apsen scanner with 7 MHz linear transducer) in asymptomatic subjects (n = 62, 26 male, aged 21 to 72 y). To test for intra-subject and inter-observer variation, ten subjects were scanned by one observer on two occasions 2 wk apart and by two observers on same day. PWV by tonometry ranged from 5.3 to 15.0 m/s. There was no significant difference between mean values of PWV obtained by the two techniques (mean difference: 0.3 m/s, standard deviation of difference: 1.5 m/s), which were closely correlated (r = 0.83). The coefficient of variation for repeated measures on the same subject by the same observer was 10.1% and the inter-observer coefficient of variation was 5.8%. These results suggest a commercial ultrasound scanner can be used to measure PWV, giving results that are reproducible and closely correlated with those obtained by arterial tonometry. (E-mail: [email protected] /* */).
    Ultrasound in Medicine & Biology 04/2008; 34(3):509-12. DOI:10.1016/j.ultrasmedbio.2007.09.008 · 2.21 Impact Factor
  • M Wong · B Y Jiang · K McNeill · S Farish · B Kirkham · P Chowienczyk ·
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    ABSTRACT: Rheumatoid arthritis (RA) is associated with increased cardiovascular disease (CVD) risk that has been attributed to endothelial dysfunction and inflammation. Non-steroidal anti-inflammatory drugs (NSAIDs) and cyclo-oxygenase (COX)-2 inhibitors have been shown in some studies to improve endothelial function in subjects without RA. The aim of this study was to investigate the effects of COX inhibition on endothelial function in patients with RA. Patients with RA (n = 37) were randomized to receive a 2-week course of either indomethacin (75 mg bd), rofecoxib (12.5 mg bd), or placebo in a double-blind study. Endothelial function was measured using flow-mediated dilation (FMD) of the brachial artery in response to reactive hyperaemia. Arterial stiffness was also assessed using pulse wave analysis (PWA) through the measurement of the aortic augmentation index (AIx). Measurements of vascular function and inflammatory markers were taken before and at the end of the treatment period. There were no significant differences in changes in FMD, AIx, blood pressure (BP), serum creatinine, erythrocyte sedimentation rate (ESR), or high-sensitivity C-reactive protein (hsCRP) between groups. However, compared with the other treatment groups, there was a tendency for systolic BP to decrease in the placebo group (p = 0.063) and for creatinine to increase in the indomethacin and rofecoxib groups after treatment (p = 0.054). This study suggests that COX inhibition by indomethacin or rofecoxib do not improve endothelial function in patients with RA.
    Scandinavian Journal of Rheumatology 01/2007; 36(4):265-9. DOI:10.1080/03009740701286771 · 2.53 Impact Factor
  • K. de Saram · K. L. McNeill · J. M. Ritter · P. J. Chowienczyk ·

    Journal of Hypertension 06/2004; 22(Suppl. 2):S50. DOI:10.1097/00004872-200406002-00168 · 4.72 Impact Factor
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    K de Saram · K L McNeill · S Khokher · J M Ritter · P J Chowienczyk ·
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    ABSTRACT: Vitamin C may influence NO-dependent relaxation independently of effects on oxidant stress. We investigated effects of vitamin C (0.1 – 10 mmol l−1) on relaxation of pre-constricted rabbit aortic rings to acetylcholine (ACh), authentic NO and the NO-donors glyceryl trinitrate (GTN), nitroprusside (NP) and S-nitroso-N-acetyl-penicillamine (SNAP). DETCA (2 – 6 mmol l−1), a cell permeable inhibitor of endogenous Cu-Zn superoxide dismutase (SOD) was used to increase intracellular superoxide anion (O2−). Vitamin C reduced the response to ACh (71±7% inhibition of maximum relaxation at 10 mmol l−1) and inhibited relaxation to authentic NO. Vitamin C inhibited relaxation to GTN but potentiated relaxations to NP and SNAP, causing a parallel shift to a lower concentration range of the log dose-response curve by approximately one log unit at the highest dose. Vitamin C increased the concentration of NO in bath solution (plus EDTA, 1.0 mmol l−1) following the addition of SNAP from 53±14 to 771±101 nmol l−1 over the range 0.1 – 3.0 mmol l−1. DETCA inhibited relaxation to ACh (71±9% inhibition of maximum relaxation). This inhibition was abolished by a cell permeable SOD mimetic, but not by vitamin C. DETCA inhibited relaxation to SNAP but not that to NP nor to GTN. Vitamin C inhibits endothelium-dependent relaxations of rabbit aortic rings to ACh and authentic NO and does not reverse impaired relaxation resulting from increased intracellular oxidant stress. Vitamin C potentiates relaxation to the NO-donors NP and SNAP by a mechanism that could involve release of NO from nitrosothiols. British Journal of Pharmacology (2002) 135, 1044–1050; doi:10.1038/sj.bjp.0704541
    British Journal of Pharmacology 03/2002; 135(4):1044-50. DOI:10.1038/sj.bjp.0704541 · 4.84 Impact Factor
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    ABSTRACT: The object of the present study is to determine whether native (n) low-density lipoprotein (LDL) isolated from men with type II diabetes and abnormal endothelial function inhibits endothelium-dependent relaxation more than n-LDL isolated from nondiabetic control subjects. Endothelium-dependent vasodilation is impaired in men with type II diabetes and this may result from qualitative rather than quantitative abnormalities of LDL. Forearm blood flow responses to brachial artery infusions of acetylcholine (endothelium-dependent vasodilator) and nitroprusside (endothelium-independent vasodilator) were measured in 10 men with uncomplicated type II diabetes and 10 nondiabetic men of similar age and with similar plasma concentrations of LDL cholesterol. Native LDL was isolated by discontinuous density gradient ultracentrifugation using EDTA to prevent oxidation. Preconstricted rabbit aortic ring bioassay was used to determine inhibitory properties of n-LDL on endothelium-dependent relaxation by measuring relaxation to acetylcholine (and nitroprusside) in the presence and absence of n-LDL. Forearm blood flow responses to acetylcholine but not nitroprusside were significantly impaired (p < 0.01) in diabetic men compared with control subjects. Native LDL (10 and 100 microg protein/ml) from diabetic men inhibited relaxation to acetylcholine by 13.9 +/- 4.8% and 61.9 +/- 7.8% (mean inhibition for all doses +/- SE), respectively, whereas n-LDL from control subjects inhibited relaxation by 7.3 +/- 3.0% and 23.9 +/- 5.7% (p < 0.01 for a difference between diabetic and control n-LDL). Relaxation to nitroprusside was not significantly inhibited by n-LDL. A qualitative abnormality of LDL may account for endothelial dysfunction in men with type II diabetes.
    Journal of the American College of Cardiology 05/2000; 35(6):1622-7. DOI:10.1016/S0735-1097(00)00607-0 · 16.50 Impact Factor
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    L Fontana · K L McNeill · J M Ritter · P J Chowienczyk ·
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    ABSTRACT: Low density lipoprotein (LDL) inhibits endothelium-dependent relaxation. The mechanism is uncertain, but increased production of superoxide anion O2− with inactivation of endothelium-derived NO and formation of toxic free radical species have been implicated. We investigated effects of the cell permeable superoxide dismutase mimetic manganese (III) tetrakis (1-methyl-4-pyridyl) porphyrin (MnTMPyP), the free radical scavenger vitamin C and arginine (which may reduce O2− formation) on acute LDL-induced endothelial dysfunction in rabbit aortic rings, using LDL prepared by ultracentrifugation of plasma from healthy men and aortic rings from New Zealand white rabbits. LDL (150 μg protein ml−1 for 20 min) markedly inhibited relaxation of aortic rings (in Krebs' solution at 37°C and pre-constricted to 80% maximum tension with noradrenaline) to acetylcholine 82±10% (mean percentage difference between sum of relaxations after each concentration of acetylcholine in the presence and absence of LDL, ±s.e.mean, n=26, P<0.001) but not to the endothelium-independent agonist nitroprusside. MnTMPyP (10 μM) reduced inhibitory effects of LDL from 124±27 to 56±17% (n=6, P<0.05). Vitamin C (1 mM) reduced inhibitory effects of LDL from 59±8 to 22±5% (n=6, P<0.05). Inhibitory effects of LDL were similar in the absence or presence of arginine (84±12 vs 79±16%, n=14, P=0.55). Effects of L-arginine (10 mM) did not differ significantly from those of D-arginine (10 mM). Acute (20 min) exposure of aortic rings to LDL impairs endothelium-dependent relaxation which can be partially restored by MnTMPyP and vitamin C. This is consistent with LDL causing increased O2− generation. British Journal of Pharmacology (1999) 126, 730–734; doi:10.1038/sj.bjp.0702331
    British Journal of Pharmacology 02/1999; 126(3):730-4. DOI:10.1038/sj.bjp.0702331 · 4.84 Impact Factor