Does the β-Blocker Nebivolol Increase Coronary Flow Reserve?

Introduction: Nebivolol, a highly selective β1-adrenergic receptor-blocker, increases basal and stimulated endothelial nitric oxide (NO)-release. It is unknown, whether coronary perfusion is improved by the increase in NO availability. Therefore, we sought to evaluate the effect of nebivolol on coronary flow reserve (CFR) and collateral flow. Methods: Doppler-flow wire derived coronary flow velocity measurements were obtained in ten controls and eight patients with coronary artery disease (CAD) at rest and after intracoronary nebivolol. CFR was defined as maximal flow during adenosine-induced hyperemia divided by resting flow. In the CAD group, collateral flow was determined after dilatation of a flow-limiting coronary stenosis. Collateral flow index (CFI) was defined as the ratio of flow velocity during balloon inflation divided by resting flow. Results: CFR at rest was 3.0 ± 0.6 in controls and 2.1 ± 0.4 in CAD patients. After intracoronary doses of 0.1, 0.25, and 0.5mg nebivolol, CFR increased to 3.4 ± 0.7, 3.9 ± 0.9, and 4.0 ± 0.1 (p < 0.01) in controls, and to 2.3 ± 0.7, 2.6 ± 0.9, and 2.6 ± 0.5 (p < 0.05) in CAD patients. CFI decreased significantly with intracoronary nebivolol and correlated to changes in heart rate (r = 0.75, p < 0.001) and rate-pressure product (r = 0.59, p = 0.001). Discussion: Intracoronary nebivolol is associated with a significant increase in CFR due to reduction in resting flow (controls), or due to an increase in maximal coronary flow (CAD patients). CFI decreased with nebivolol parallel to the reduction in myocardial oxygen consumptio

Does the beta-blocker nebivolol increase coronary flow reserve?

INTRODUCTION: Nebivolol, a highly selective beta1-adrenergic receptor-blocker, increases basal and stimulated endothelial nitric oxide (NO)-release. It is unknown, whether coronary perfusion is improved by the increase in NO availability. Therefore, we sought to evaluate the effect of nebivolol on coronary flow reserve (CFR) and collateral flow. METHODS: Doppler-flow wire derived coronary flow velocity measurements were obtained in ten controls and eight patients with coronary artery disease (CAD) at rest and after intracoronary nebivolol. CFR was defined as maximal flow during adenosine-induced hyperemia divided by resting flow. In the CAD group, collateral flow was determined after dilatation of a flow-limiting coronary stenosis. Collateral flow index (CFI) was defined as the ratio of flow velocity during balloon inflation divided by resting flow. RESULTS: CFR at rest was 3.0+/-0.6 in controls and 2.1+/-0.4 in CAD patients. After intracoronary doses of 0.1, 0.25, and 0.5 mg nebivolol, CFR increased to 3.4+/-0.7, 3.9+/-0.9, and 4.0+/-0.1 (p<0.01) in controls, and to 2.3+/-0.7, 2.6+/-0.9, and 2.6+/-0.5 (p<0.05) in CAD patients. CFI decreased significantly with intracoronary nebivolol and correlated to changes in heart rate (r=0.75, p<0.001) and rate-pressure product (r=0.59, p=0.001). DISCUSSION: Intracoronary nebivolol is associated with a significant increase in CFR due to reduction in resting flow (controls), or due to an increase in maximal coronary flow (CAD patients). CFI decreased with nebivolol parallel to the reduction in myocardial oxygen consumption

Crop Updates 2008 - Cereals

This session covers twenty four papers from different authors: WHEAT AGRONOMY 1. Wheat variety performance in the Northern Agricultural Region in 2007, Christine Zaicou, Department of Agriculture and Food 2. Wheat variety performance on the Central Agricultural Region in 2007, Shahajahan Miyan, Department of Agriculture and Food 3. Response of wheat varieties to sowing time in the Great Southern and Lakes Region in 2007, Brenda Shackley and Steve Penny, Department of Agriculture and Food 4. Wheat variety performance in the South Coastal Region in 2007, Sarah Ellis, Department of Agriculture and Food 5. Flowering dates of wheat varieties in Western Australia in 2007, Darshan Sharma, Brenda Shackley and Christine Zaicou, Department of Agriculture and Food BARLEY AGRONOMY 6. Barley variety options for Western Australia, Blakely Paynter, Andrea Hills and Jeff Russell, Department of Agriculture and Food 7. Vlaming A – the newest malting barley variety, Blakely Paynter, Jeff Russell and Andrea Hills, Department of Agriculture and Food 8. Barley yields higher in wide rows with stubble retained in a very dry season at Merredin, Glen Riethmuller, Bill Bowden and Paul Blackwell, Department of Agriculture and Food HERBICIDE TOLERANCE 9. Herbicide tolerance of current/new wheat varieties, Dr Harmohinder Dhammu, Department of Agriculture and Food 10. Herbicide tolerance of new oat varieties, Dr Harmohinder Dhammu, Vince Lambert, and Chris Roberts,Department of Agriculture and Food NUTRITION 11. Managing nitrogen inputs in malting barley, Andrea Hills and Blakely Paynter, Department of Agriculture and Food 12. Decision tools for optimal N on cereal crops, David and Sally Cox, Jeremy Lemon* and Andrea Hills*, *Department of Agriculture and Food 13. Wheat varieties respond differently to potassium application on potassium responsive soils, Paul Damon and Zed Rengel, Faculty of Natural and Agricultural Sciences, University of Western Australia DISEASES 14. Leaf disease management in continuous barley in the northern and central grainbelt of WA, Geoff Thomas, Ciara Beard, Anne Smith, Kith Jayasena and Sean Kelly, Department of Agriculture and Food 15. Temperature and moisture requirements of leaf, stem and stripe rusts of wheat, Geoff Thomas, Rob Loughman and Bill MacLeod, Department of Agriculture and Food 16. Fungicide options for controlling diseases in oats, Raj Malik and Blakely Paynter, Department of Agriculture and Food 17. Survey of wheat root diseases under intensive cereal production in Western Australia during 2005-2007, Ravjit Khangura, William MacLeod, Vivien Vanstone, Colin Hanbury, Mehreteab Aberra, Gordon MacNish and Robert Loughman, Department of Agriculture and Food 18. Epidemiology studies on Wheat Streak Mosaic Virus in 2007, Brenda Coutts, Geoff Strickland, Monica Kehoe, Dustin Severtson and Roger Jones, Department of Agriculture and Food 19. Bacterial diseases that affect WA export hay quality, Dominie Wright and Megan Jordan, Department of Agriculture and Food SOIL 20. Hardpan penetration ability of drought-stressed wheat under pot and field conditions, Xinhua He1, Eli Manyol1, Song-Ai Nio1, Imran Malik1, Tina Botwright-Acuña1,2and Len Wade1,3,1School of Plant Biology, University of Western Australia, 2Tasmanian Institute of Agricultural Research, University of Tasmania, TAS, 3E.H. Graham Centre, Charles Sturt University, NSW HARVEST MANAGEMENT 21. Calculating the risk – the SEPWA Harvest Calculator, Nigel Metz, South East Premium Wheat Growers Association 22. The relationship between grain moisture and atmospheric conditions in cereal crop harvesting on the South Coast of WA, Nigel Metz, South East Premium Wheat Growers Association (SEPWA) MARKETS 23. Varietal accreditation for Australian Barley, Linda Price, Barley Australia STATISTICAL METHODS 24. Applying data mining tools to improve grain quality for growers, Dean Diepeveen1, Leisa Armstrong2, Peter Clarke1, Doug Abrecht1, Rudi Appels2 and Matthew Bellgard3,1Department of Agriculture and Food, Western Australia 2Edith Cowan University, Western Australia, 3Centre of Comparative Genomics, Murdoch Universit

A randomised determination of the effect of fluvastatin and atorvastatin on top of dual antiplatelet treatment on platelet aggregation after implantation of coronary drug-eluting stents. The EFA-Trial

Drug-drug interaction between statins metabolised by cytochrome P450 3A4 and clopidogrel have been claimed to attenuate the inhibitory effect of clopidogrel. However, published data regarding this drug-drug interaction are controversial. We aimed to determine the effect of fluvastatin and atorvastatin on the inhibitory effect of dual antiplatelet therapy with acetylsalicylic acid (ASA) and clopidogrel. One hundred one patients with symptomatic stable coronary artery disease undergoing percutaneous coronary intervention and drug-eluting stent implantation were enrolled in this prospective randomised study. After an interval of two weeks under dual antiplatelet therapy with ASA and clopidogrel, without any lipid-lowering drug, 87 patients were randomised to receive a treatment with either fluvastatin 80 mg daily or atorvastatin 40 mg daily in addition to the dual antiplatelet therapy for one month. Platelet aggregation was assessed using light transmission aggregometry and whole blood impedance platelet aggregometry prior to randomisation and after one month of receiving assigned statin and dual antiplatelet treatment. Platelet function assessment after one month of statin and dual antiplatelet therapy did not show a significant change in platelet aggregation from 1st to 2nd assessment for either statin group. There was also no difference between atorvastatin and fluvastatin treatment arms. In conclusion, neither atorvastatin 40 mg daily nor fluvastatin 80 mg daily administered in combination with standard dual antiplatelet therapy following coronary drug-eluting stent implantation significantly interfere with the antiaggregatory effect of ASA and clopidogrel

Early and late coronary stent thrombosis of sirolimus-eluting and paclitaxel-eluting stents in routine clinical practice: data from a large two-institutional cohort study

BACKGROUND: Stent thrombosis is a safety concern associated with use of drug-eluting stents. Little is known about occurrence of stent thrombosis more than 1 year after implantation of such stents. METHODS: Between April, 2002, and Dec, 2005, 8146 patients underwent percutaneous coronary intervention with sirolimus-eluting stents (SES; n=3823) or paclitaxel-eluting stents (PES; n=4323) at two academic hospitals. We assessed data from this group to ascertain the incidence, time course, and correlates of stent thrombosis, and the differences between early (0-30 days) and late (>30 days) stent thrombosis and between SES and PES. FINDINGS: Angiographically documented stent thrombosis occurred in 152 patients (incidence density 1.3 per 100 person-years; cumulative incidence at 3 years 2.9%). Early stent thrombosis was noted in 91 (60%) patients, and late stent thrombosis in 61 (40%) patients. Late stent thrombosis occurred steadily at a constant rate of 0.6% per year up to 3 years after stent implantation. Incidence of early stent thrombosis was similar for SES (1.1%) and PES (1.3%), but late stent thrombosis was more frequent with PES (1.8%) than with SES (1.4%; p=0.031). At the time of stent thrombosis, dual antiplatelet therapy was being taken by 87% (early) and 23% (late) of patients (p<0.0001). Independent predictors of overall stent thrombosis were acute coronary syndrome at presentation (hazard ratio 2.28, 95% CI 1.29-4.03) and diabetes (2.03, 1.07-3.83). INTERPRETATION: Late stent thrombosis was encountered steadily with no evidence of diminution up to 3 years of follow-up. Early and late stent thrombosis were observed with SES and with PES. Acute coronary syndrome at presentation and diabetes were independent predictors of stent thrombosis