Publications
263 results found
Hayward CS, Kraidly M, Webb CM, et al., 2002, Assessment of endothelial function using peripheral waveform analysis: a clinical application, J Am Coll Cardiol, Vol: 40, Pages: 521-528, ISSN: 0735-1097
Webb CM, Collins P, 2002, Androgens and arterial disease, Textbook of men's health, Editors: Lunenfeld, London, Publisher: Parthenon Publishing, Pages: 360-364, ISBN: 9781842140116
Ong PJ, Linardou H, Graham HA, et al., 2001, Tamoxifen is not detrimental to endothelial function in postmenopausal women with breast cancer., Am Heart J, Vol: 142
BACKGROUND: Tamoxifen has mixed estrogen agonist and antagonist properties in estrogen-regulated tissues. Its effect on the cardiovascular system is not well defined. We carried out a study to investigate the effect of tamoxifen on peripheral vascular endothelial function. METHODS: Three groups of postmenopausal women (median age, 56 years; range, 39 to 69 years) with breast cancer were studied. Patients in group 1 (n = 10) were newly diagnosed with breast cancer and studied before and after 4 weeks treatment with tamoxifen. Group 2 women (n = 6) had been receiving long-term tamoxifen (3 to 5 years) and were studied while taking tamoxifen and 4 weeks after stopping it. The final group of 6 subjects were in remission from primary breast cancer and were not receiving or had previously received tamoxifen. Ultrasound assessments of endothelial function were done before and 4 weeks after the initiation or discontinuation of tamoxifen with the nontreatment group acting as control. All ultrasound imaging was made by a single investigator blinded to the therapeutic status of the subject. Brachial artery diameter was measured by ultrasound at baseline and 1 minute after reactive hyperemia. Flow-mediated reactivity (FMR) was defined as percent change in artery diameter from baseline 1 minute after reactive hyperemia. RESULTS: There was no change in FMR in patients before compared with 4 weeks after starting tamoxifen (4.06% +/- 1.44% vs 3.97% +/- 1.20%, respectively, mean +/- standard error of the mean [SEM], P =.97). There was no significant change in FMR on withdrawal from tamoxifen (1.84% +/- 1.98% vs -0.42% +/- 1.44% on tamoxifen vs off tamoxifen, mean +/- SEM, P =.36). FMR in subjects taking tamoxifen was no different from the control group (3.17% +/- 1.05% vs 3.16% +/- 0.91%, respectively, mean +/- SEM, P =.995). CONCLUSIONS: Tamoxifen does not appear to affect endothelial function in the short term in postmenopausal women with breast cancer.
Chong WCF, Ong PJL, Hayward C, et al., 2001, Effects of storage solutions on in vitro vasoreactivity of radial artery conduits, JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, Vol: 122, Pages: 470-475, ISSN: 0022-5223
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- Citations: 21
Mosca L, Barrett-Connor E, Wenger NK, et al., 2001, Design and methods of the raloxifene use for the heart (RUTH) study, AMERICAN JOURNAL OF CARDIOLOGY, Vol: 88, Pages: 392-395, ISSN: 0002-9149
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- Citations: 125
Mosca L, Collins P, Herrington DM, et al., 2001, Hormone replacement therapy and cardiovascular disease: a statement for healthcare professionals from the American Heart Association., Circulation, Vol: 104, Pages: 499-503
Hayward CS, Webb CM, Collins P, 2001, Effect of sex hormones on cardiac mass, LANCET, Vol: 357, Pages: 1354-1356, ISSN: 0140-6736
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- Citations: 83
Collins P, 2001, Vascular effects of hormones, MATURITAS, Vol: 38, Pages: 45-50, ISSN: 0378-5122
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- Citations: 13
Grothues F, Smith GS, Bellenger NG, et al., 2001, Comparison of interstudy reproducibility of Cardiovascular Magnetic Resonance and 2D-Echocardiography in a mixed study group and implications for clinical trial planning, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 37, Pages: 392A-392A, ISSN: 0735-1097
Adamson DL, Webb CM, Collins P, 2001, Esterified estrogens combined with methyltestosterone improve emotional well-being in postmenopausal women with chest pain and normal coronary angiograms, MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY, Vol: 8, Pages: 233-238, ISSN: 1072-3714
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- Citations: 28
Collins P, 2001, Sex steroids and the cardiovascular system <i>in vivo</i>:: actions in humans, Workshop on Hormone Replacement Therapy and Cardiovascular Disease, Publisher: PARTHENON PUBLISHING GROUP LTD, Pages: 107-115, ISSN: 1474-3930
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- Citations: 8
Stevenson JC, Flather M, Collins P, 2000, Coronary heart disease in women., NEW ENGLAND JOURNAL OF MEDICINE, Vol: 343, Pages: 1891-1891, ISSN: 0028-4793
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- Citations: 6
Rosano GMC, Webb CM, Chierchia S, et al., 2000, Natural progesterone, but not medroxyprogesterone acetate, enhances the beneficial effect of estrogen on exercise-induced myocardial ischemia in postmenopausal women, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 36, Pages: 2154-2159, ISSN: 0735-1097
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- Citations: 88
Figtree GA, Webb CM, Collins P, 2000, Tamoxifen acutely relaxes coronary arteries by an endothelium-, nitric oxide-, and estrogen receptor-dependent mechanism, JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, Vol: 295, Pages: 519-523, ISSN: 0022-3565
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- Citations: 46
Webb CM, Ghatei MA, McNeill JG, et al., 2000, 17β-Estradiol decreases endothelin-1 levels in the coronary circulation of postmenopausal women with coronary artery disease, Circulation, Vol: 102, Pages: 1617-1622, ISSN: 0009-7322
Background - Estrogen reverses acetylcholine-induced coronary vasoconstriction via the possible facilitation of endothelium-derived NO. Estrogen also affects endothelium-derived constrictor factors. We therefore investigated the effects of 17β-estradiol on coronary vasomotor responses to substance P (SP), and coronary sinus endothelin-1 and NO metabolite levels in postmenopausal women with coronary heart disease. Methods and Results - We studied 20 women; 14 received estrogen (mean age 65±2 years) and 6 served as ethanol control subjects (age 63±3 years). Intracoronary infusions of papaverine (8 mg) and SP were administered before and 20 minutes after 50 pg/min 17β-estradiol or 0.2 μL/min control. Coronary blood flow was calculated from the diameter, as measured with quantitative coronary angiography, and flow velocity, as measured with intracoronary Doppler. Coronary sinus plasma endothelin-1 and nitrite/nitrate (NO2/NO3) were measured at baseline, at peak velocity response to each infusion, and every 5 minutes during the estradiol infusion. Endothelin-1 levels were decreased after 20 minutes of estradiol (1.12±0.18 versus 0.86±0.17 pmol/L baseline2 versus estradiol, P=0.05). Endothelin-1 levels to SP decreased after 17β-estradiol (1.29±0.18 versus 1.04±0.15 and 1.3±0.16 versus 0.99±0.17 pmol/L for before versus after estradiol, 10 and 25 pmol/min SP; both P<0.05). NO2/NO3 levels did not change. There was no change in vasomotor responses to estradiol alone or to papaverine or SP before versus after estradiol. Conclusions - Short-term intracoronary 17β-estradiol administration decreases coronary endothelino-1 levels. There was no enhancement of vasomotor responses to SP after the administration of estrogen, suggesting that the effects of estrogen on coronary acetylcholine responses may be a specific and not a generalized effect on coronary vasoreactivity.
Webb CM, Ghatei MA, McNeill JG, et al., 2000, 17β-estradiol decreases endothelin-l levels in the coronary circulation of postmenopausal women with coronary artery disease, CIRCULATION, Vol: 102, Pages: 1617-1622, ISSN: 0009-7322
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- Citations: 58
Murray S, Collins PD, James MA, 2000, Can TENS reduce silent ischaemia? Insights into mechanism of action, Heart, Vol: 83, ISSN: 1355-6037
Background: Neurostimulation (the use of TENS and spinal cord stimulation (SCS)) has been reported to have primary anti-ischaemic properties in the treatment of refractory angina. However it is unknown whether this occurs due to an intrinsic property of neurostimulation itself, or whether it is a consequence of masking the discomfort of angina and thereby reducing sympathetic drive, which in turn reduces myocardial work and so reducing ischaemia and symptoms. Silent ischaemia offers a novel way to study this question, as the patients are unaware of chest discomfort, thereby removing this masking effect of TENS. Methods: A randomised cross-over study was used, with n=7 (all male). All patients had evidence of silent ischaemia on exercise tolerance testing (ETT) with documented coronary disease at angiography. All screening ETTs were fully interpretable with > 1 mm ST depression. Three full-Bruce protocol ETTs were carried out, each 2 weeks apart: a baseline study, a TENS phase and a placebo phase (in a randomised order). Data was analysed using the Wilcoxon rank-sum test. Results: Placebo TENS p value Exercise time (s) 338 (90.8) 366 (137) NS Max ST ↓ (mm) 1.9 (0.4) 1.7 (0.5) NS ST ↓ @ 70% exercise time (mm) 1.2 (0.6) 0.6 (0.3) NS Figures given as means (Standard deviation) Discussion: This is the first time that TENS has been used in silent ischaemia. TENS produced a non-significant trend towards reducing ECG signs of ischaemia. Whilst this may be a result of the small sample group used, previous cross-over studies have described significant results with as little as 6 patients. This result could suggest that TENS may have a weak anti-ischaemic effect, and that much of its clinical benefit comes from a reduction in perceived chest discomfort. Alternatively it may suggest that patients with silent ischaemia are "wired" differently in neuronal terms, and thus may unable to respond to TENS. This intriguing result requires further work to answer t
Murray S, Collins PD, James MA, 2000, A study of the "carry over" effect of neurostimulation in the treatment of angina pectoris, Heart, Vol: 83, ISSN: 1355-6037
Background: Neurostimulation (the use of TENS and spinal cord stimulation (SCS)) has been reported to have primary anti-ischaemic properties in the treatment of refractory angina. Furthermore this effect has been observed to act beyond the period of stimulation itself - the so-called carry-over effect. However there has been some doubt as to whether this is a real phenomenon or simply a confounding factor produced from non-randomised study protocols (such as ischaemic pre-conditioning). This study aimed to detect this effect using a placebo-controlled, randomised trial. Methods: A randomised cross-over study was used, with n=10 (8 M, 2F). All had chronic stable angina with > 1 mm ST depression on exercise tolerance test (ETT). Three full-Bruce protocol ETTs were carried out, each 2 weeks apart: a baseline study, a TENS phase and a placebo phase (in a randomised order). During the TENS phase, the device was used for 1 hour tds, and for 1 hour prior to the ETT; the device was NOT used during the test itself. Data was analysed using the Wilcoxon rank-sum test. Results: Mean (SD) Baseline Control TENS p value Max ST ↓: 2.3mm (0.6) 2.1mm (0.8) 1.9mm (0.5) p=NS Time to Max ST ↓: 338 secs (106) 324 secs (83) 374 secs (93) p=0.01 ST↓ at 3 mins: 1.0mm (0.5) 1.1mm (0.7) 0.7mm (0.5) p=0.01 RPP: 209 (67) 193 (52) 197 (77) p=NS Discussion: This is the first time the carry-over effect has been demonstrated in a randomised controlled study. The ischaemic threshold has been increased in the treatment group in that a similar ST depression was achieved in each case, but that the time to reach that level is prolonged by pre-treatment with TENS. ST depression at a fixed time-point is also diminished. This is also the first time (to our knowledge) that TENS has been used in chronic stable angina. Further work is underway to assess its potential role in these cases.
Murray S, Carson K, Collins PD, et al., 2000, A cost analysis of Spinal Cord Stimulation (SCS) in patients with refractory angina pectoris, Heart, Vol: 83, ISSN: 1355-6037
Background: SCS has previously been shown to reduce the number and duration of acute admissions of patients suffering from refractory angina pectoris. The aim of this study was to examine the costs involved in order to establish if this reduction could lead to recovery of the initial outlay of the SCS unit - approximately £6 000. Methods: We compared admissions in 19 patients implanted with SCS devices between 1989 to 1997. Admissions post-CABG up until SCS implantation were compared to admissions post-SCS up until the end of 1997. Ward and investigations were costed using local figures, otherwise national average costs were used. Results: There were a total of 87.13 patient years post CABG and 52.84 post SCS. Post CABG annual admission rate was 0.97 v. 0.27 post SCS (p=0.02), with a mean admission lasting 8.3 days post CABG v. 2.6 post SCS (p=0.04). Ward costs include ECG, CXR & blood tests. Cost of revascularisations and SCS have NOT been included. These results allowed us to generate the following mean costs: Mean post CABG Mean post SCS Admission £253 £253 CCU @ 24 hours £487 £487 Ward @ 7.3 v 1.6 days £1 654 £267 TOTAL £2 395 £1 007 Per patient per year (0.97 v 0.27) £2 323 £272 Conclusions: Based upon a mean admission to our hospital, we calculated that SCS could save an average of £2 051 per patient treated per year. This would lead to the cost of the implant itself being recovered within 3 years. We conclude that SCS is a cost effective therapy.
Sorensen M, Ong P, Webb C, et al., 2000, Measurement of endothelium-dependent and endothelium-independent vascular function by cardiovascular magnetic resonance, JOURNAL OF PHYSIOLOGY-LONDON, Vol: 525, Pages: 11P-11P, ISSN: 0022-3751
Figtree GA, Griffiths H, Liu YQ, et al., 2000, Plant-derived estrogens relax coronary arteries in vitro by a calcium antagonistic mechanism, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 35, Pages: 1977-1985, ISSN: 0735-1097
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- Citations: 108
Hayward CS, Kelly RP, Collins P, 2000, The roles of gender, the menopause and hormone replacement on cardiovascular function, CARDIOVASCULAR RESEARCH, Vol: 46, Pages: 28-49, ISSN: 0008-6363
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- Citations: 227
Ong PJL, Linardou H, Graham H, et al., 2000, Tamoxifen is not detrimental to endothelial function in women with breast cancer, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 35, Pages: 254A-255A, ISSN: 0735-1097
Murray S, Collins PD, James MA, 2000, Neurostimulation treatment for angina pectoris., Heart, Vol: 83, Pages: 217-220, ISSN: 1355-6037
Ong PJL, Patrizi G, Chong WCF, et al., 2000, Testosterone enhances flow-mediated brachial artery reactivity in men with coronary artery disease, AMERICAN JOURNAL OF CARDIOLOGY, Vol: 85, Pages: 269-272, ISSN: 0002-9149
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- Citations: 110
Ong PJL, Dean TS, Hayward CS, et al., 1999, Effect of fat and carbohydrate consumption on endothelial function, LANCET, Vol: 354, Pages: 2134-2134, ISSN: 0140-6736
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- Citations: 74
Collins P, Webb C, 1999, Cell membrane estrogen receptors resurface -: <i>Collins and Webb reply</i>, NATURE MEDICINE, Vol: 5, Pages: 1330-1330, ISSN: 1078-8956
Chong WC, Collins P, Hayward CS, et al., 1999, Radial artery versus saphenous vein patency (RSVP) study: A prospective, randomised surgical trial, CIRCULATION, Vol: 100, Pages: 96-96, ISSN: 0009-7322
Soresen MB, Ong PJ, Hayward CS, et al., 1999, Gradient echo magnetic resonance imaging of the brachial artery: A novel method far assessing vascular reactivity, CIRCULATION, Vol: 100, Pages: 49-49, ISSN: 0009-7322
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- Citations: 1
Webb CM, McNeill JG, Hayward CS, et al., 1999, Effects of testosterone on coronary vasomotor regulation in men with coronary heart disease, CIRCULATION, Vol: 100, Pages: 1690-1696, ISSN: 0009-7322
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- Citations: 353
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