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136 results on '"Canepa-Anson, R."'

4. Cardiac troponins

Author

Collinson, P O, Canepa-Anson, R, and Joseph, S

Published
1998

7. Efficacy and safety of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin: the ASSENT-3 randomised trial in acute myocardial infarction

Author

Van de Werf, F., Armstrong, P. W., Granger, C., Wallentin, L., Adgey, A. A. J., Aylward, P., Binbrek, A. S., Califf, R., Cassim, S., Diaz, R., Fanebust, R., Fioretti, P. M., Huber, K., Husted, S., Lindahl, B., Lopez-Sendon, J. L., Makijarvi, M., Meyer, J., Navarro Robles, J., Pfisterer, M., Seabra-Gomes, R., Soares-Piegas, L., Sugrue, D., Tendera, M., Theroux, P., Toutouzas, P., Vahanian, A., Verheugt, F., Sarelin, H., Goetz, G., Bluhmki, E., Daclin, V., Danays, T., Houbracken, K., Kaye, J., Reilly, P., Hacke, W., von Kummer, R., Lesaffre, E., Bogaerts, K., Peeters, C., Fox, K. A. A., Brower, R., Hirsh, J., Maggioni, A., Tijssen, J., Weaver, D., Beernaert, A., Beysen, N., Broos, K., De Prins, E., D'Hollander, K., Dupon, L., Fomyna, N., Fransen, A., Genesse, D., Goffin, L., Hendrickx, R., Jansen, B., Jorissen, F., Luys, C., Luyten, A., Marschal, C., Moreira, M., Munsters, K., Salerno, R., Schoovaerts, C., Sinnaeve, P., Schildermans, C., Vandenberghe, K., Vandeschoot, K., Van Gucht, H., Van Rompaey, P., Vlassak, S., Watzeels, M., Wittockx, H., Galan, K., Humeniuk, L., Seidel, A., Molina, M., Hafley, G., Alexander, J., Pascual, A., Bestilny, S., Temple, T., Ahuad Guerrero, R., Albisu, J. P., Bassani Arrieta, C. A., Bono, J., Caccavo, A., Cagnolatti, A., Cartasegna, L. R., Castellanos, R., Chekerdemian, S., Covelli, G., Cuello, J. L., Cuneo, C. A., Fernandez, A., Ferrara, C., Ferro-Queirel, E., Gambarte, A., Garcia-Duran, R., Hasbani, E., Hrabar, A., Keller, L., Lobo Marquez, L. L., Luciardi, H., Macin, S. M., Marinig, A., Marzetti, E., Muntaner, J., Nordaby, R., Orlandini, A. D., Piombo, A. C., Pomposiello, J. C., Quijano, R. A., Amerena, J., Aroney, G., Buckmaster, N., Carroll, P., Fitzpatrick, M., Newman, R., Rowe, M., Singh, B., Thomson, A., Winter, C., Eber, B., Gaul, G. B., Klein, W., Leisch, F., Mayr, H., Mlczoch, J., Niessner, H., Pachinger, O., Pall, H., Pichler, M., Roggla, G., Schaflinger, E., Schreiber, W., Slany, J., Traindl, O., Zenker, G., Beckers, J., Bekaert, I., Berthe, C., Bodur, G., Carlier, B., Carlier, M., Carpentier, J., Celen, H., Charlier, F., Clement, A., Coenen, A., Crochelet, L., De Keyser, F., De Man, F., de Meester, A., Dendale, P., Dhondt, E., Dhooghe, G., El Allaf, D., Elshot, S., Emmerechts, C., Foret, F., Gatera, E., Geraedts, J., Gerardy, A. C., Gysbrechts, M., Hallemans, R., Hellemans, S., Herssens, H., Huygens, L., Janssens, L., Lalmand, J., Maamar, R., Marechal, P., Mertens, D., Michel, P., Morandini, E., Nannan, M., Nguyen, D., Odeurs, W., Peerenboom, P., Pirenne, B., Quinonez, M., Raymenants, E., Renard, M., Silance, P. G., Standaert, A. M., Striekwold, H., Thiels, H., Valadi, D., van Brabandt, H., Van Dormael, M., Van Iseghem, P., Van Walleghem, U., Vanden Bosch, H., Vandenbossche, J. L., Vermylen, J., Verstraete, S., Vo Ngoc, P., Willems, P., Zenner, R., Campos de Albuquerque, D., Coutinho, M., de Camargo Carvalho, A. C., Fernandes Manenti, E. R., Ferreira Azevedo, A., Golin, V., Gun, C., Marin Neto, J. A., Marino, R. L., Miranda Abrantes, J. A., Nicolau, J. C., Porto Alegre Dancini, E. M., Rabelo, A., Ramos, R. F., Rizzi Coelho, O., Alexander, D., Bata, I. R., Bhargava, R. K., Bogaty, P., D'Amours, G., Darcel, I., Finnie, K. J. C., Fowlis, R., Gupta, M. K., Henderson, M., Howlett, M. K., Javier, J. J., Kieu, C. V., Kumar, G., Lebouthillier, P., Leduc, F., Lepage, S., Mcavinue, T., Mcgillen, J. E., Mcmeekin, J. D., Morse, J. W., Pistawka, K., Raimondo, E. F., Sandrin, F., Smith, H., Smylie, P. C., Tran, K., Turabian, M., Wagner, K. R., Winkler, L. H., Woo, K. S., Falstie-Jensen, N., Lind Rasmussen, S., Lomholt, P., Markenvard, J., Nielsen, H., Petersen, J., Romer, F., Ahonen, J., Huttunen, M., Kokkonen, L., Luukkonen, J., Mantyla, P., Melin, J., Mustonen, J., Valli, J., Voutilainen, S., Agraou, B., Allam, S., Baradat, G., Battistella, P., Bazin, P., Bouvier, J. -M., Destrac, S., Fouche, R., Fournier, P. -Y., Funck, F., Garnier, H., Grall, J. -Y., Gully, C., Lallement, P. -Y., Loiselet, P., Mycinsky, C., Page, A., Parisot, M., Range, G., Rocher, R., Tafani, C., Thisse, J. -Y., Tibi, T., Tissot, M., Wahl, P., Backenkohler, U., Bavastro, P., Beckmann-Hiss, H., Behnke, M., Bermes, M., Bernsmeier, R., Bethge, K. P., Bethge, H., Block, M., Burkhardt, W., Cieslinski, G., Claus, G., Deetjen, A., Diefenbach, A., Diehm, C., Dietz, A., Dippold, W. G., Eichner, A., Erckenbrecht, J. F., Gawlick, L., Gerber, V., Goppel, L., Gottwik, M., Grosch, B., Hammer, B., Hanheide, M., Hanrath, P., Haspel, J., Hennersdorf, F., Hermanns, M., Hoffmeister, H. M., Holzapfel, P., Hubner, H., Jansen, W., Jung, S., Kaddatz, J., Kienbock, H., Klein, H. H., Konz, K. H., Kulschbach, M., Leschke, M., Liebau, G., Linnartz, M., Lockert, G., Loesbrock, R., Lollgen, H., Ludwig, N., Mudra, H., Munzer, K., Nebel, B., Nellessen, U., Neu, C., Olbrich, H. G., Pfeffer, A., Pfeiffer, P., Plate, V., Pollock, B., Rapp, H., Rommele, U., Sauer, K., Scheffler, N., Schlotterbeck, K., Schmidt-Salzmann, A., Schnitzler, G., Schumann, H., Schuster, C. J., Schuster, P., Schweizer, P., Seitz, K., Simon, R., Spes, C., Szabo, S., Terhardt-Kasten, E., Theuerkauf, B., Tigges, R., Tinnappel, J., Topp, H., Trockel, P., Unland, N., Veth, V., Vom Dahl, J., Vossbeck, G., Weindel, K., Weib, D., Wiewel, D., Wirtz, P., Zipp, C., Apostolou, T., Chalkidis, C., Exadaktylos, N., Foussas, S., Hatseras, D., Karas, S., Karydis, K., Lambrou, S., Louridas, G., Manolis, A., Nanas, J., Novas, I., Panagiotidou, T., Papadopoulos, C., Papakonstantinou, D., Papasteriadis, E., Pavlidis, P., Pyrgakis, V., Skoufas, P., Stavrati, A., Tyrologos, A., Vardas, P., Vrouchos, G., Zacharoulis, A., Zarifis, J., Brown, A., Daly, K., Fennell, W., Horgan, J., Mccann, H., Mcdonald, K., O'Reilly, M., Sullivan, P., Altamura, G., Ambrosio, G., Auteri, A., Aveta, P., Azzarito, M., Badano, L. P., Barbiero, M., Barletta, C., Biscosi, C., Boccanelli, A., Bottero, M., Brizio, E., Brunazzi, M. C., Brunelli, C., Bugatti, U., Capozi, A., Capucci, A., Carfora, A., Caronna, A., Carrone, M., Casazza, F., Cauticci, A., Ceci, V., Ciconte, V., Circo, A., Ciricugno, S., Comito, F., Cornacchia, D., Corsini, G., D'Andrea, F., De Rosa, P., De Simone, M., Del Citerna, F., Del Pinto, M., Dell'Ali, C., Della Casa, S., Della Monica, R., Delogu, G., Di Biase, M., Di Chiara, A., Di Guardo, G., Di Marco, S., Di Mario, F., Di Napoli, T., Di Palma, F., Fadin, B. M., Fazzari, M., Ferraiuolo, G., Fiaschetti, R., Fontanelli, A., Fresco, C., Gambelli, G., Gasbarri, F., Gemelli, M., Giani, P., Gigantino, A., Giomi, A., Giorgi, G., Greco, C., Gregorio, G., Guagnozzi, G., Guiducci, U., Guzzardi, G., Izzo, A., La Rosa, A., Leone, F., Leone, G., Lo Bianco, F., Locuratolo, N., Maggiolini, S., Malinconico, M., Mancone, C., Mangiameli, S., Marchi, S. M., Maresta, A., Mauri, F., Mazzini, C. A., Michisanti, M., Miracapillo, G., Modena, M. G., Morgagni, G. L., Mossuti, E., Nascimbeni, F., Negrelli, M., Notaristefano, A., Pardi, S., Peci, P., Pettinati, G., Pietropaolo, F., Pirelli, S., Pretolani, M., Prinzi, D., Proietti, F., Raganelli, L., Rapino, S., Re, F., Ricci, R., Rinaldi, G., Rusticali, G., Severi, S., Spallarossa, P., Tartagni, F., Terrosu, P., Tortorella, G., Tota, F., Tritto, I., Tuccilo, B., Turco, V., Uscio, G., Valagussa, F., Vergoni, W., Verzuri, M. S., Vetrano, A., Villani, R., Zanini, R., Boisante, L., Niclou, R., Alcocer, L., Castro, A., Fragoso, J., Gonzalez, V., Gonzalez-Pacheco, H., Hernandez-Santamaria, I., Huerta, R., Huerta, D., Martinez, A., Mendoza, M., Moguel, R., Navarro, J., Portos, J. M., Rodriguez, I., Sierra, L., Valencia, S., Vazquez, A., Arnold, A. E. R., Boehmer, A. G., de Graaf, J. J., Funke Kupper, A. J., Gobel, E. J. A. M., Janus, C. L., Linssen, G. C. M., Sedney, M. I., Slegers, L. C., Spierenburg, H. A. M., Strikwerda, S., Tans, J. G. M., Twisk, S. P. M., van der Heijden, R., van Kalmthout, P. M., Verheugt, F. W. A., Holt, E., Skogsholm, A., Thorshaug, R., Thybo, N. K., Wang, H., Maciejewicz, J., Piotrowski, W., Pluta, W., Ruminski, W., Skura, M., Smielak-Korombel, W., Carranca, J., Carvalho, M., Catarino, C., Cunha, D., Ferreira, D., Ferreira, J., Ferreira da Costa, A. F., Lopes de Carvalho, J., Martins, L., Mourao, L., Oliveira Carrageta, M., Prazeres de Sa, E., Puig, J., Ramalho Dos Santos, M. J. J., Resende, M., Seabra Gomes, R., Baig, M. M. E., Bayat, J., Benjamin, J. D., Ranjith, N., Routier, R., Wittmer, H., Abizanda Campos, R., Alonso Garcia, M. A., Amaro Cendon, A., Arboleda Sanchez, J. A., Blanco Varela, J., Bruguera I Cortada, J., Carpintero Avellaneda, J. L., Caturla Such, J., Civeira Murillo, E., Fernandez Aviles, F., Fernandez Fernandez, R., Figueras Bellot, J., Fiol Sala, M., Froufe Sanchez, J., Garcia Calabozo, R., Garcia Palacios, J. L., Gonzalez Maqueda, I., Kallmeyer Martin, C., Lopez Sendon, J. L., Manzano Ramirez, A., Marine Rebull, J., Monton Rodriguez, A., Pique Gilart, M., Reina Toral, A., Rodriguez Llorian, A., Ruano Marco, M., Sanchez Miralles, A., Sanjose Garagarza, J. M., Santalo Bel, M., Torres Ruiz, J. M., Valentin Segura, V., Ahlstrom, P., Ahremark, U., Bandh, S., Bellinetto, A., Dahlberg, A., Hansen, O., Hurtig, U., Jonasson, L., Karlsson, J. E., Larsson, L. E., Moller, B., Ohlin, H., Persson, H., Sandstedt, L., Soderberg, S., Svennberg, L., Swahn, E., Tygesen, H., Broccard, A. F., Estlinbaum, W., Follath, F., Frutiger, A., Hess, N., Maggiorini, M., Marti, D., Muller, P., Rickenbacher, P., Schaller, M. D., Weinbacher, M., Abdulali, S., Ahmad, G., George, S., Ghazi, A., Rao, K. N., Bishop, A., Bridges, A., Canepa-Anson, R., Cave, M., Clarck, R., Cooper, I., de Belder, A., Farrer, M., Kendall, J. M., Ludman, P., Mattu, R., Mcglinchey, P., Moriarty, A. J., Muthusamy, S., Nee, P. A., Nolan, J., Papouchado, M., Rose, E. L., Shahi, M., Stephens, J., Trevelyan, J., Abdul-Karim, A., Adler, L., Arunasalam, S., Avington, D., Baron, S., Beel, T., Bellamy, B., Bennett, J., Berndt, T., Berrick, A., Bersin, R. M., Bethala, V., Bharath, S., Bouchard, A., Boulet, J. E., Bowerman, R., Boyek, T., Brar, R. S., Brodell, G., Bryant, B., Buckner, J. K., Cage, J., Cannon, J. D., Carducci, B., Carr, K., Chang, M., Chelliah, N., Chin, W. L., Chin, J., Church, D. H., Clark, R., Coulis, L., Dadkhah, S., Dearing, B., Defranco, A., Dharawat, M., Dharawat, R., Dhruva, N., Dicola, J., Dykstra, G., Eisenberg, S., El-Bialy, A., Fera, S., Ford, K., Foreman, R. D., Friedman, S., Friedman, V., Garibian, G., Gelormini, J., Geninatti, M. R., Genovese, R., Ghazi, F., Gilchrist, I., Gitler, B., Glover, R., Gonzalez, J., Goulah, R., Graham, B., Gray, R., Grodman, R., Habib, G. B., Hack, T., Hamroff, G., Hanna, G., Hart, M., Haught, H., Hawkins, J., Hempel, R., Hiremath, Y., Hiser, W., Holland, E., Jaffe, N., Jamal, N., James, K. F., Kalla, S., Kates, M., Kemper, A. J., Kennedy, J. J., Kerut, E. K., Killpack, M., King, J., T. Y., Ko, Kollar, K., Kontos, M., Kugelmassluu, A., Kumar, A., Kutscher, A. H., Lambrecht, C., Lancaster, L., Layden, J., Lazar, A., Lebow, M., Lee, C., Lee, A. B., Lehr, J., Levin, F. L., Levitt, R., Levy, R. M., Lieberman, A., Litman, G. I., Lui, H., Luu, M. Q., Macdonald, G., Madyoon, H., Mancherje, C., Marmulstein, M., Mclaurin, B. T., Mcnellis, M., Mendelson, R., Micale, P. J., Miller, M. J., Miller, M. S., Miller, J., Millman, A., Millsaps, R., Minor, S., Modica, J., Morse, H., Moskovits, N., Nester, B. A., Newton, A. S., Niazi, I., Niederman, A., Oatfield, R., Painter, J. A., Pamfilis, S. M., Pamulapati, K. M., Patel, N., Payne, R., Pearson, C., Peizner, D. S., Petrovich, L., Piriz, J., Pollack, M., Pollock, S., Popkave, A., Puma, J. A., Quesada, R., Quigley-Malcolm, D., Raby, K., Ravindran, K., Rees, A. P., Reiner, J., Rivera, E., Rogers, F., Rosenthal, A., Rowe, W. W., Ryan, P. F., Ryman, K., Salacata, A., Santolin, C., Saucedo, J., Savage, R., Savage, W., Schumacher, R., Segarra, S., Sharkey, S., Shonkoff, D., Silver, M., Silver, S. L., Singh, G., Sinyard, R. D., Sporn, D., Srivastava, N. K., Stomel, R., Suresh, D. P., Tallman, M., Togioka, T., Varma, S., Verant, R. P., Wallach, R., Weinberg, M., Weinberg, D., Weinstein, J. M., Wesley, G., Westerman, J. H., Wheeling, J., Whitaker, J., Widmer, M., Yasin, M., and Zakrzewski, M. J.

Subjects
Male, medicine.medical_specialty, Abciximab, Ischemia, Myocardial Infarction, Tenecteplase, Injections, Immunoglobulin Fab Fragments, Reperfusion therapy, Fibrinolytic Agents, Recurrence, Internal medicine, medicine, Humans, Myocardial infarction, Enoxaparin, Aged, Intention-to-treat analysis, Chi-Square Distribution, business.industry, Heparin, Antibodies, Monoclonal, General Medicine, Middle Aged, medicine.disease, Survival Analysis, Regimen, Treatment Outcome, Anesthesia, Tissue Plasminogen Activator, Cardiology, Drug Therapy, Combination, Female, business, Platelet Aggregation Inhibitors, medicine.drug
Abstract

BACKGROUND: Current fibrinolytic therapies fail to achieve optimum reperfusion in many patients. Low-molecular-weight heparins and platelet glycoprotein IIb/IIIa inhibitors have shown the potential to improve pharmacological reperfusion therapy. We did a randomised, open-label trial to compare the efficacy and safety of tenecteplase plus enoxaparin or abciximab, with that of tenecteplase plus weight-adjusted unfractionated heparin in patients with acute myocardial infarction. METHODS: 6095 patients with acute myocardial infarction of less than 6 h were randomly assigned one of three regimens: full-dose tenecteplase and enoxaparin for a maximum of 7 days (enoxaparin group; n=2040), half-dose tenecteplase with weight-adjusted low-dose unfractionated heparin and a 12-h infusion of abciximab (abciximab group; n=2017), or full-dose tenecteplase with weight-adjusted unfractionated heparin for 48 h (unfractionated heparin group; n=2038). The primary endpoints were the composites of 30-day mortality, in-hospital reinfarction, or in-hospital refractory ischaemia (efficacy endpoint), and the above endpoint plus in-hospital intracranial haemorrhage or in-hospital major bleeding complications (efficacy plus safety endpoint). Analysis was by intention to treat. FINDINGS: There were significantly fewer efficacy endpoints in the enoxaparin and abciximab groups than in the unfractionated heparin group: 233/2037 (11.4%) versus 315/2038 (15.4%; relative risk 0.74 [95% CI 0.63-0.87], p=0.0002) for enoxaparin, and 223/2017 (11.1%) versus 315/2038 (15.4%; 0.72 [0.61-0.84], p

Published
2001

15. Differences between acute and long-term metabolic and endocrine effects of oral beta-adrenoceptor agonist therapy with pirbuterol for cardiac failure.

Author

Canepa-Anson, R, Dawson, JR, Kuan, P, Poole-Wilson, PA, Sutton, GC, Cockrill, B, and Reuben, SR

Abstract

The metabolic, hormonal and haemodynamic effects of oral pirbuterol, a new beta 2-adrenoceptor agonist, were studied acutely (n = 19) and after 3 months treatment (n = 11) in patients with severe heart failure receiving chronic frusemide therapy. In the acute study fasted patients (n = 10) showed reductions in plasma K+ (P less than 0.005) and cortisol (P less than 0.01) and increases in plasma glucose (P less than 0.005), insulin (P less than 0.01), lactate (P less than 0.005) and pyruvate (P less than 0.0025). These acute changes were less in unfasted subjects (n = 9). Maximal increase in stroke volume occurred at approximately half the plasma pirbuterol concentration required for maximal effect on plasma insulin. Treatment with pirbuterol for 3 months was associated with sustained increases in stroke volume and fasting plasma glucose and insulin, but there was loss of all other acute metabolic effects. Despite concurrent frusemide and digoxin therapy acute hypokalaemia caused no adverse effects. Hypokalaemia did not occur with chronic pirbuterol administration. [ABSTRACT FROM AUTHOR]

Published
1987
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16. Continuous recording of coronary sinus oxygen saturation during atrial pacing in patients with coronary artery disease or with syndrome X.

Author

Crake, T, Canepa-Anson, R, Shapiro, L, and Poole-Wilson, P A

Abstract

Coronary sinus oxygen saturation was measured continuously during incremental atrial pacing in 34 patients undergoing cardiac catheterisation. In eleven patients with normal coronary arteriograms, negative exercise tests, and no ST segment depression on the electrocardiogram, an increase in the rate of atrial pacing transiently decreased coronary sinus oxygen saturation but within 20 s oxygen saturation returned to the control value. In six patients with coronary artery disease ST segment depression developed during atrial pacing. The coronary sinus oxygen saturation fell and remained reduced until pacing was discontinued. The size of the fall of coronary sinus oxygen saturation increased with increasing heart rate. In seven patients with coronary artery disease the ST segments were unaltered during atrial pacing and coronary sinus oxygen saturation did not fall. Ten patients with syndrome X were studied. In six ST segment depression developed on atrial pacing. In five, three of whom developed ST segment depression, the changes in coronary sinus oxygen saturation during atrial pacing were similar to those observed in patients without any evidence of coronary artery disease. In three, all of whom developed ST segment depression, coronary sinus oxygen saturation gradually increased throughout the period of atrial pacing. In two patients coronary sinus oxygen saturation fell in a manner similar to that observed in patients with obstructive coronary artery disease who developed ST segment depression on pacing. Thus regulation of coronary blood flow in normal persons in response to an increase of heart rate is rapid. Oxygen extraction across the coronary bed can increase by up to 30% and a persistent increase in oxygen extraction is an indicator of myocardial ischaemia. The term "syndrome X" does not describe a homogeneous group of patients but in the majority coronary sinus oxygen saturation does not fall despite symptoms and changes on the electrocardiogram, indicating that inadequate coronary blood flow is not the dominant mechanism. [ABSTRACT FROM PUBLISHER]

Published
1988
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17. Untreated heart failure: clinical and neuroendocrine effects of introducing diuretics.

Author

Bayliss, J, Norell, M, Canepa-Anson, R, Sutton, G, and Poole-Wilson, P

Abstract

The clinical and neuroendocrine response to diuretic treatment was assessed at rest and on exercise in 12 patients with heart failure. Before treatment all patients were limited by breathlessness on exercise; one was oedematous. Plasma renin activity and aldosterone were normal but plasma noradrenaline was raised both at rest and on exercise. After one month's treatment with frusemide (40 mg) and amiloride (5 mg) weight was significantly reduced by a mean of 3.5 kg and exercise capacity had doubled. Plasma noradrenaline fell to normal at rest but remained abnormally raised on exercise. Plasma renin activity and aldosterone increased significantly both at rest and on exercise. Diuretics bring about a considerable clinical improvement in patients with chronic heart failure but they stimulate the renin-angiotensin system. Activation of the renin-angiotensin system in moderate heart failure occurs as a response to diuretic treatment rather than as a result of the disease process itself. [ABSTRACT FROM PUBLISHER]

Published
1987
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18. Factors determining symptoms in heart failure: comparison of fast and slow exercise tests.

Author

Lipkin, D P, Canepa-Anson, R, Stephens, M R, and Poole-Wilson, P A

Abstract

Factors determining the symptoms of breathlessness and fatigue in patients with congestive heart failure were investigated by comparing the response to slow and fast exercise. Symptom limited oxygen consumption (maximal); minute ventilation, mean pulmonary capillary wedge pressure; and arterial blood gases, pH, and lactate concentrations were measured during treadmill exercise using a slow protocol in 25 men (age 34-67 years) with congestive heart failure (New York Heart Association class II-III). Ten of these patients were also exercised according to a rapid protocol. Exercise was terminated by fatigue in 23/25 patients after the slow test and by breathlessness in all patients after the rapid test. Exercise capacity (maximal oxygen consumption and exercise duration) was not related to resting or exercise pulmonary capillary wedge pressure or the change in pulmonary capillary wedge pressure during exercise, nor was there any difference in pulmonary capillary wedge pressure at the end of exercise within individuals between the fast and slow tests. Minute ventilation was greater (51 vs 43 1/min), peak exercise lactate concentration higher (3.7 vs 2.2 mmol/l), and the change in pH from the resting state was greater (0.06 vs 0.02) during the rapid test than during the slow test. The sensation of breathlessness in congestive heart failure is not simply related to raised pulmonary capillary wedge pressure, but may in part be due to stimulation of peripheral chemoreceptors in response to metabolic acidosis. [ABSTRACT FROM PUBLISHER]

Published
1986
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19. Vasodilatation with captopril and prazosin in chronic heart failure: double blind study at rest and on exercise.

Author

Bayliss, J, Canepa-Anson, R, Norell, M S, Poole-Wilson, P, and Sutton, G

Abstract

A double blind cross over study was performed to compare the long term hormonal, haemodynamic, and clinical responses to specific inhibition of the renin-angiotensin-aldosterone system (captopril) and of the alpha 1 adrenoceptors of the sympathetic system (prazosin) both at rest and during upright exercise in patients with chronic heart failure. Sixteen patients completed one month's treatment with each drug. During conventional diuretic treatment (control) plasma renin activity, aldosterone, and noradrenaline were increased at rest and on exercise. Control left ventricular filling pressures were raised, and correlated significantly with plasma renin activity both at rest and on exercise. Systemic vascular resistance was increased at rest, and its reduction during exercise correlated inversely with the increase in plasma renin activity and plasma noradrenaline. After one month's treatment with captopril there were reductions in plasma aldosterone, weight, left ventricular filling pressure, and systemic vascular resistance at rest and on exercise. Dyspnoea was relieved and exercise capacity increased. The greater fall in systemic vascular resistance on exercise no longer correlated with the increase in plasma renin activity. During treatment with prazosin there were increases in plasma noradrenaline and, transiently, in plasma aldosterone. Fluid retention occurred, and left ventricular filling pressure was unchanged. Compared with control values systemic vascular resistance was reduced at rest but not on exercise. Dyspnoea and exercise capacity did not improve. In chronic heart failure, vasodilatation by inhibition of the alpha adrenergic system with prazosin causes compensatory stimulation of the renin-angiotensin-aldosterone system and does not result in clinical benefit. Inhibition of the renin-angiotensin-aldosterone system with captopril causes secondary vasodilatation at rest and on exercise and results in improvement in symptoms and exercise capacity. [ABSTRACT FROM PUBLISHER]

Published
1986
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20. Symptoms, haemodynamics, and exercise capacity during long term treatment of chronic heart failure. Experience with pirbuterol.

Author

Dawson, J R, Canepa-Anson, R, Kuan, P, Reuben, S R, Poole-Wilson, P A, and Sutton, G C

Abstract

An open study of long term treatment with an oral beta 2 agonist (pirbuterol 20 mg three times daily) was undertaken in 63 patients with severe chronic heart failure. During three months of treatment 20 (32%) patients died, of whom 16 were taking the drug at the time of death. Mortality was related to initial functional class (New York Heart Association classification: 23% in grade III and 75% in grade IV). Concomitant treatment with digoxin did not affect mortality. The drug was well tolerated by most patients but unwanted side effects necessitated withdrawal of the drug in six (10%). Thirty-five patients were continuing to take the drug after three months, of whom 22 reported symptomatic improvement and only four deterioration. There was a relation between symptomatic improvement and increase in exercise capacity. At initial haemodynamic assessment a single dose of pirbuterol increased the cardiac index by 34% and the stroke index by 21%. Left ventricular filling pressure fell by 23% and systemic vascular resistance by 22%. Haemodynamic reassessment after three months of continuous treatment in 29 patients showed maintained improvement in the group as a whole, although individual variation was considerable. There was no apparent relation between haemodynamic improvement and improvement in exercise duration and symptoms. Severe heart failure has a poor prognosis. Identification of those patients who may derive benefit from treatment with a particular drug is not yet possible. [ABSTRACT FROM PUBLISHER]

Published
1983
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21. Acute haemodynamic comparison of amrinone and pirbuterol in chronic heart failure. Additional effects of isosorbide dinitrate.

Author

Bayliss, J, Norell, M, Canepa-Anson, R, Reuben, S R, Poole-Wilson, P A, and Sutton, G C

Abstract

A randomised, within patient comparison was made in patients with severe chronic heart failure, to study the acute haemodynamic effects of oral agents which have inotropic and vasodilator properties. A non-glycosidic non-adrenergic positive inotropic agent with vasodilator properties (amrinone) was compared with a beta-agonist which has vasodilator and positive inotropic effects (pirbuterol). To assess whether combined treatment with a venodilator might be advantageous, the effect of adding isosorbide dinitrate was studied. Oral amrinone or pirbuterol were given in random order to each of 13 patients, on successive days, and oral isosorbide dinitrate was added after two-and-a-half hours. Control values before amrinone or pirbuterol were similar, and both drugs increased cardiac index while reducing left ventricular filling pressure, right atrial pressure, and systemic vascular resistance. Heart rate and blood pressure were unchanged. The magnitude of the changes caused by amrinone and pirbuterol were not significantly different. The addition of isosorbide dinitrate caused further falls in left ventricular filling pressure and right atrial pressures, and a fall in heart rate with each drug. Other measurements remained unchanged. Although amrinone and pirbuterol have different pharmacological properties, their acute haemodynamic effects in patients with chronic heart failure are indistinguishable. [ABSTRACT FROM PUBLISHER]

Published
1983
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22. Influence of R wave analysis upon diagnostic accuracy of exercise testing in women.

Author

Ilsley, C, Canepa-Anson, R, Westgate, C, Webb, S, Rickards, A, and Poole-Wilson, P

Abstract

Exercise electrocardiography in women with chest pain is associated with a high incidence of false positive ST segment depression. The recent observation that changes in R wave amplitude during exercise can also be used diagnostically may improve the value of stress testing in women. The results of 12 lead treadmill exercise and coronary angiography were reviewed in 62 women, mean age 51 years, presenting with "angina" without previous myocardial infarction. These were compared with exercise results in 14 healthy asymptomatic volunteers with a mean age of 26 years. In addition to conventional ST analysis, R wave amplitude changes during exercise, measured in leads II, III, a VF, and V4 to 6, were examined. While the sensitivity and specificity of ST and R wave changes were similar at about 67%, their combined interpretation was helpful. If both ST and R wave criteria were negative the predictive accuracy for normal coronary angiography was 94% (17/18). Alternatively, in tests showing both ST depression and an abnormal R wave response, coronary angiography was always abnormal (13/13). None of the normal volunteers developed ST segment depression and 93% (13/14) had a normal R wave response. If both were positive, however, coronary angiography was always abnormal (13/13). Although stress test interpretation in women is difficult, R wave analysis is a useful adjunct to ST change and can improve the predictive accuracy of the test in a significant number of patients. [ABSTRACT FROM PUBLISHER]

Published
1982
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23. Elective aortic and mitral valve surgery in patients over 70 years of age.

Author

Canepa-Anson, R and Emanuel, R W

Abstract

The results of elective cardiac surgery carried out between 1970 and 1975 on 29 patients over 70 years of age are reported. Operative mortality was 10%, late cardiac mortality 14%, with 72% survival at a mean follow-up of 38.6 months. Before operation 96% were in functional classes 3 and 4. After operation 90.5% of late survivors were in functional classes 1 and 2 at a mean follow-up of 43.5 months. These results compare favourably with those in younger patients. Complication rate and length of hospital stay were unremarkable. The risks of neurological damage and of long-term anticoagulation are not increased. Emergency surgery carries a very high risk in this age group. The importance of biological youth and good left ventricular function is emphasised. For aortic stenosis at least prognosis is improved by surgery. [ABSTRACT FROM PUBLISHER]

Published
1979
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24. The renal response to neuroendocrine inhibition in chronic heart failure: double-blind comparison of captopril and prazosin.

Author

BAYLISS, J., CANEPA-ANSON, R., NORELL, M., POOLE-WILSON, P., and SUTTON, G.

Abstract

Activation of the renin–angiotensin and sympathetic systems in chronic heart failure causes important renal vasoconstriction. In a double-blind cross-over study, treatment with captopril for one month reduced systemic and renal vascular resistance by 14% and 25%, increased renal blood flow by 12%, and increased the percentage of the cardiac output perfusion to the kidney by 13%. Treatment with prazosin for one month also reduced systemic vascular resistance by 8%, renal vascular resistance increased by 20%, and renal blood flow and the percentage of the cardiac output going to the kidney fell by 14% and 26%. During captopril treatment, plasma aldosterone concentration was reduced to normal, but during prazosin treatment there was an initial increase in aldosterone of 45%, and a sustained increase in plasma noradrenaline concentration of 26%. Body weight decreased by 1.7kg on captopril, but increased by 3.0 kg on prazosin, correlating inversely with the changes in renal blood flow. Sympathetic inhibition with prazosin causes systemic vasodilatation which diverts blood from the kidney and may result in fluid retention. Inhibition of the renin system with captopril causes preferential renal vasodilatation and can improve renal perfusion in chronic heart failure. [ABSTRACT FROM PUBLISHER]

Published
1986
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25. Clinical importance of the renin-angiotensin system in chronic heart failure: double blind comparison of captopril and prazosin

Author

Canepa-Anson R, Philip A. Poole-Wilson, C Reid, J Bayliss, M Norell, and G C Sutton

Subjects
Male, medicine.medical_specialty, Captopril, Time Factors, Proline, Heart disease, Coronary Disease, Plasma renin activity, Renin-Angiotensin System, Norepinephrine, Double-Blind Method, Internal medicine, Renin–angiotensin system, Prazosin, Humans, Medicine, Aged, General Environmental Science, Clinical Trials as Topic, biology, business.industry, Hemodynamics, General Engineering, Angiotensin-converting enzyme, General Medicine, Middle Aged, medicine.disease, Crossover study, Endocrinology, Heart failure, Chronic Disease, Quinazolines, Cardiology, biology.protein, General Earth and Planetary Sciences, Female, business, Research Article, medicine.drug
Abstract

Nineteen patients with chronic heart failure participated in a double blind crossover trial of captopril and prazosin--two drugs with differing neuroendocrine effects--to determine whether neuroendocrine changes could explain clinical and haemodynamic responses to treatment. Patients were assessed before and after acute and long term (four weeks') treatment with each drug given in random order. Sixteen patients completed the study. During captopril haemodynamic improvement was maintained by inhibition of the renin-angiotensin system. Breathlessness was relieved in 15 patients and exercise capacity increased. During prazosin a reduction in systemic vascular resistance was maintained, but plasma renin activity and aldosterone and noradrenaline concentrations increased, fluid retention developed, and clinical benefit did not occur. These results suggest that clinical and haemodynamic responses to long term vasodilator treatment for chronic heart failure are related to neuroendocrine changes. In patients with chronic heart failure inhibition of the renin-angiotensin system results in clinical benefit, whereas inhibition of the alpha adrenergic system does not.

Published
1985
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26. Differences between acute and long-term metabolic and endocrine effects of oral beta-adrenoceptor agonist therapy with pirbuterol for cardiac failure

Author

G C Sutton, Canepa-Anson R, P Kuan, J R Dawson, P A Poole-Wilson, S R Reuben, and Barbara A. Cockrill

Subjects
Adult, Blood Glucose, Male, medicine.medical_specialty, Hydrocortisone, Digoxin, medicine.medical_treatment, Fatty Acids, Nonesterified, Oral administration, Internal medicine, medicine, Humans, Pharmacology (medical), Aged, Heart Failure, Pharmacology, business.industry, Insulin, Hemodynamics, Furosemide, Fasting, Stroke volume, Middle Aged, medicine.disease, Endocrinology, Ethanolamines, Heart failure, Lactates, Female, business, Pirbuterol, Research Article, medicine.drug
Abstract

The metabolic, hormonal and haemodynamic effects of oral pirbuterol, a new beta 2-adrenoceptor agonist, were studied acutely (n = 19) and after 3 months treatment (n = 11) in patients with severe heart failure receiving chronic frusemide therapy. In the acute study fasted patients (n = 10) showed reductions in plasma K+ (P less than 0.005) and cortisol (P less than 0.01) and increases in plasma glucose (P less than 0.005), insulin (P less than 0.01), lactate (P less than 0.005) and pyruvate (P less than 0.0025). These acute changes were less in unfasted subjects (n = 9). Maximal increase in stroke volume occurred at approximately half the plasma pirbuterol concentration required for maximal effect on plasma insulin. Treatment with pirbuterol for 3 months was associated with sustained increases in stroke volume and fasting plasma glucose and insulin, but there was loss of all other acute metabolic effects. Despite concurrent frusemide and digoxin therapy acute hypokalaemia caused no adverse effects. Hypokalaemia did not occur with chronic pirbuterol administration.

Published
1987
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27. Atrial natriuretic peptide released by rapid ventricular pacing in dogs does not cause a natriuresis

Author

Walsh, K. P., Williams, T. D. M., Canepa-Anson, R., Roe, P., Pitts, E., Lightman, S. L., and Sutton, R.

Abstract

1. The relationships between the haemodynamic, renal and endocrine changes induced by rapid ventricular pacing were studied in ten chloralose-anaesthetized dogs paced from the right ventricular apex for 60 min at 250 beats/min. 2. Pacing increased mean right atrial and mean pulmonary wedge pressure (P < 0.05), and decreased cardiac output and mean arterial pressure (P < 0.05). 3. Coronary sinus atrial natriuretic peptide (ANP) concentrations were approximately fourfold greater than arterial concentrations; both increased markedly during pacing (P < 0.01). Plasma concentrations of arginine vasopressin and plasma renin activity did not change signficantly. 4. Urine flow and free water clearance increased during the latter 30 min of pacing (P < 0.05). There was no significant change in sodium clearance despite high sustained concentrations of ANP. 5. Without the availability of specific inhibitors of ANP release or action, we are unable to exclude the possibility that ANP may have prevented sodium clearance from otherwise decreasing during rapid ventricular pacing. Nevertheless, the dissociation between elevated ANP concentrations and natriuresis in this study indicates that a rise in ANP concentrations per se is not sufficient to produce a natriuresis.

Published
1988
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28. The renal response to neuroendocrine inhibition in chronic heart failure: double-blind comparison of captopril and prazosin

Author

Philip A. Poole-Wilson, J. Bayliss, Canepa-Anson R, M Norell, and George C. Sutton

Subjects
Cardiomyopathy, Dilated, Male, medicine.medical_specialty, Captopril, Myocardial Infarction, Coronary Disease, Renal Circulation, chemistry.chemical_compound, Norepinephrine, Random Allocation, Double-Blind Method, Internal medicine, Renin, medicine, Prazosin, Humans, Cardiac Output, Aldosterone, Aged, Kidney, business.industry, Middle Aged, medicine.disease, medicine.anatomical_structure, Endocrinology, chemistry, Renal blood flow, Heart failure, Vascular resistance, Cardiology, Female, Vascular Resistance, medicine.symptom, Cardiology and Cardiovascular Medicine, business, Vasoconstriction, medicine.drug, Glomerular Filtration Rate
Abstract

Activation of the renin-angiotensin and sympathetic systems in chronic heart failure causes important renal vasoconstriction. In a double-blind cross-over study, treatment with captopril for one month reduced systemic and renal vascular resistance by 14% and 25%, increased renal blood flow by 12%, and increased the percentage of the cardiac output perfusion to the kidney by 13%. Treatment with prazosin for one month also reduced systemic vascular resistance by 8%, renal vascular resistance increased by 20%, and renal blood flow and the percentage of the cardiac output going to the kidney fell by 14% and 26%. During captopril treatment, plasma aldosterone concentration was reduced to normal, but during prazosin treatment there was an initial increase in aldosterone of 45%, and a sustained increase in plasma noradrenaline concentration of 26%. Body weight decreased by 1.7 kg on captopril, but increased by 3.0 kg on prazosin, correlating inversely with the changes in renal blood flow. Sympathetic inhibition with prazosin causes systemic vasodilatation which diverts blood from the kidney and may result in fluid retention. Inhibition of the renin system with captopril causes preferential renal vasodilatation and can improve renal perfusion in chronic heart failure.

Published
1986

29. Treatment of chronic heart failure with pirbuterol: acute haemodynamic responses

Author

J Carnie, J. R. Dawson, G C Sutton, Canepa-Anson R, Philip A. Poole-Wilson, P Kuan, S R Reuben, N H Whitaker, and C Warnes

Subjects
Inotrope, Adult, Male, medicine.medical_specialty, Haemodynamic response, Heart Ventricles, Hemodynamics, Administration, Oral, Internal medicine, Heart rate, Medicine, Humans, General Environmental Science, Aged, Heart Failure, business.industry, General Engineering, Heart, General Medicine, Adrenergic beta-Agonists, Middle Aged, medicine.disease, medicine.anatomical_structure, Blood pressure, Ethanolamines, Heart failure, Anesthesia, Chronic Disease, Vascular resistance, Cardiology, General Earth and Planetary Sciences, Female, business, Pirbuterol, medicine.drug, Research Article
Abstract

Fifty-nine patients with severe chronic heart failure were given pirbuterol, a beta agonist with vasodilator and positive inotropic properties. The acute haemodynamic responses to both single (20 patients) and incremental doses (39 patients) were measured. Pirbuterol increased cardiac index and reduced left ventricular filling pressure and systemic vascular resistance with only small changes in heart rate and blood pressure. Maximal effects were observed at an average of 170 minutes after a single oral dose of pirbuterol. In the incremental dose studies the plasma pirbuterol concentration was found to increase with increasing doses and was related to the magnitude of the haemodynamic response. Pirbuterol was well tolerated, and no drug-related side effects were recorded. Oral pirbuterol clearly improved pump performance in these patients, the haemodynamic changes being consistent with vasodilatation as the dominant mechanism rather than a direct inotropic effect.

Published
1981

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