189 results on '"Wodniecki J"'
Search Results
2. Oxidative stress and hemodynamic parameters in heart failure patients with dilated cardiomyopathy: 3
- Author
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Jacheć, W., Wojciechowska, C., Skrzep-Poloczek, B., Romuk, E., Kozielska, E., Birkner, E., and Wodniecki, J.
- Published
- 2008
3. Serum concentrations of acute phase proteins as the markers of inflammation in patients with heart failure: 8
- Author
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Wojciechowska, C., Wodniecki, J., Nowalany-Kozielska, E., Wojnicz, R., Jacheć, W., Tomasik, A., Skrzep-Poloczek, B., and Romuk, E.
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- 2006
4. Lymphocytes T subpopulations in coronary heart disease patients: 7
- Author
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Romuk, E., Skrzep-Poloczek, B., Birkner, E, Mazur, B., Wojciechowska, C., Tomasik, A., Jachć, W., and Wodniecki, J.
- Published
- 2006
5. Circulating electronegatively charged low-density lipoprotein in patients with angiographically documented coronary artery disease
- Author
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TOMASIK, A, JACHEĆ, W, SKRZEP-POLOCZEK, B, WIDERA-ROMUK, E, WODNIECKI, J, and WOJCIECHOWSKA, C
- Published
- 2003
6. Selectin-P and interleukin-8 plasma levels in coronary heart disease patients
- Author
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Romuk, E., Skrzep-Poloczek, B., Wojciechowska, C., Tomasik, A., Birkner, E., Wodniecki, J., Gabrylewicz, B., Ochala, A., and Tendera, M.
- Published
- 2002
7. The additional value of patient-reported health status in predicting 1-year mortality after invasive coronary procedures: a report from the Euro Heart Survey on Coronary Revascularisation
- Author
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Lenzen M. J., Scholte Op Reimer W. J. M., Pedersen S. S., Boersma E., Maier W., Widimsky P., Simoons M. L., Mercado N. F., Wijns W., Bertrand M., Meier B., Sechtem U., Sergeant P., Stahle E., Unger F., Manini M., Bramley C., Laforest V., Taylor C., Del Gaiso S., Huber K., De Backer G., Sirakova V., Cerbak R., Thayssen P., Lehto S., Blanc J. -J., Delahaye F., Kobulia B., Zeymer U., Cokkinos D., Karlocai K., Graham I., Shelley E., Behar S., Maggioni A., Grabauskiene V., Deckers J., Asmussen I., Stepinska J., Goncalves L., Mareev V., Riecansky I., Kenda M. F., Alonso A., Lopez-Sendon J. L., Rosengren A., Buser P., Okay T., Sychov O., Fox K., Wood D., Crijns H., McGregor K., Mulder B., Priori S., Ryden L., Tavazzi L., Vahanian A., Vardas P., Sarkisyan K., Glogar H. D., Frick M., Pachinger O., Zwick R., Vrints C., Van Hertbruggen E., Vercammen M., Sysmans T., Schroeder E., Domange J., De Pril H., De Vriese J., Van Hecke T., Legrand V., Gillon M. -F., Richardy M., Doneux P., Petrov I., Jorgova J., Starcevic B., Eeckhout E., Berger A., Prudent V., Camenzind E., Masson N., Zambartas C., Kleanthous H., Stellova B., Aschermann M., Simek S., Kautzner J., Karmazin V., Svab P., Indrak J., Branny M., Hladilova K., Kala P., Cappelen H., Jensen L. O., Gitt A., Gehrke K., am Rhein L., Erbel R., Gutersohn A., Eggebrecht H., Al Khani M., Rosenberger A., Vogelsberg H., Klepzig H., Schmidt A., Silber S., Mau B., Leuner C., Czyborra K., Reuschling C., Muno E., Nauheim B., Kleber F., Rux S., Saad A., Elabady M., Beiras A. C., Fernandez J. S., del Arno F. N., Romo A. I., Fernandez J. M. C., Mayoreal A. R., Rebanal F. J. R., de la Borbolla M. G., Chaparro M., Brotons C., Miralda C. P., Vila i Perez S. I., Moris C., Aviles F. F., de la Fuente Galan L., Vinuela P. T., de Torres F. M., Mora J., Rodriguez I. S., Bustamante I. P., Fernandez P. L. S., Torrent J. L. D., Diez Gil J. L., Perpinan J., Motilla V. P., Juango M. S. A., Berjon-Reyero J., Moreno R. M., Guerrero J. C. F., Savolainen K., Syvanne M., Cohen-Solal A., Oboa A. -S., Bassand J. P., Espinosa D. P., Jouet V., Cedex B., Montalescot G., Gallois V., Daubert J. C., Clerc J. M., Machecourt J., Cottin Y., Walker D., Holland F., Prosser J., Muir L., Barber K., Cleland J. G. F., Cook J., Chapichadze Z., Christos I. S. A., Tsiavou N., Chrysohoou C., Manginas A., Terrovitis J., Kanakakis J., Vavuranakis M., Drakos S., Farmakis T., Samara C., Papakosta C., Bourantas C., Michalis L. K., Christos M., Foussas S., Adamopoulou E., Vardas P. E., Marketou M., Alotti N., Basa A. M., Vigh A., Preda I., Csoti E., Keltai M., Kerkovits G., Hendler A., Blatt A., Yakov B., Beyar R., Shefer A., Halon D., Bentzvi M., Avramovitch N., Bakst A., Saba K., Cafri C., Grosbard A., Sheva B., Margolis B., Suleiman K., Banai S., Meerkin D., Mosseri M., Guita P., Jabara R., Jafari J., Shitrit D. B., Ghasan Salameh, Brezins M., van den Akker-Berman L., Guetta V., Hashomer T., Rozenman Y., Biagini A., Berti S., Ferrero M., Colombo A., Roccaforte R., Milici C., Scarpino L., Salvi A., Desideri A., Sabbadin D., Veneto C., Galassi A., Giuffrida G., Rognoni A., Vassanelli C., Paffoni P., Cioppa A., Rubino P., de Carlo M., Petronio A. S., Naccarella F., Saia F., Marzocchi A., Maranga S. S., Presbitero P., Valsecchi F., Piscione F., Esposito G., Santini N. M., Tubaro M., Erglis A., Narbute I., Kavoliuniene A., Zaliunas R., Navickas R., Luckute D., Subkovas E., Wagner D., Vermeer F., Lousberg A., Fransen H., Breeman A., Tebbe H., De Boer M. J., van der Wal M., Vos J., Leenders C. M., Veerhoek M. J., Jansen C., Bijl M., Koppelaar C., den Linden V., Brons R., Widdershofen J. W. M. G., Broers H., Kontny F., Jonzon M., Wodniecki J., Tomasik A., Trusz-Gluza M., Nowak S., Ruzyllo W., Deptuch T., Marques J., Matias F., Madeira H., Oliveira J., Sargento L., Ionac A., Dragulescu I. S., Mut-Vitcu B., Maximov D., Dorobantu M., Apetrei E., Niculescu R., Petrescu V., Bucsa A., Deleanu D., Bucharest, Benedek I. S., Hintea T., Aronov D., Tikhomirova E., Kranjec I., Prokselj K., Kanic V., Sepetoglu A., Aytekin S., Aytekin V., Catakoglu A. B., Parlar H., Tufekcioglu S., Ozyedek Z., Baltali M., Kiziltan D., Vukovic M., Neskovic A. N., Cardiology, Lenzen, M. J., Scholte Op Reimer, W. J. M., Pedersen, S. S., Boersma, E., Maier, W., Widimsky, P., Simoons, M. L., Mercado, N. F., Wijns, W., Bertrand, M., Meier, B., Sechtem, U., Sergeant, P., Stahle, E., Unger, F., Manini, M., Bramley, C., Laforest, V., Taylor, C., Del Gaiso, S., Huber, K., De Backer, G., Sirakova, V., Cerbak, R., Thayssen, P., Lehto, S., Blanc, J. -J., Delahaye, F., Kobulia, B., Zeymer, U., Cokkinos, D., Karlocai, K., Graham, I., Shelley, E., Behar, S., Maggioni, A., Grabauskiene, V., Deckers, J., Asmussen, I., Stepinska, J., Goncalves, L., Mareev, V., Riecansky, I., Kenda, M. F., Alonso, A., Lopez-Sendon, J. L., Rosengren, A., Buser, P., Okay, T., Sychov, O., Fox, K., Wood, D., Crijns, H., Mcgregor, K., Mulder, B., Priori, S., Ryden, L., Tavazzi, L., Vahanian, A., Vardas, P., Sarkisyan, K., Glogar, H. D., Frick, M., Pachinger, O., Zwick, R., Vrints, C., Van Hertbruggen, E., Vercammen, M., Sysmans, T., Schroeder, E., Domange, J., De Pril, H., De Vriese, J., Van Hecke, T., Legrand, V., Gillon, M. -F., Richardy, M., Doneux, P., Petrov, I., Jorgova, J., Starcevic, B., Eeckhout, E., Berger, A., Prudent, V., Camenzind, E., Masson, N., Zambartas, C., Kleanthous, H., Stellova, B., Aschermann, M., Simek, S., Kautzner, J., Karmazin, V., Svab, P., Indrak, J., Branny, M., Hladilova, K., Kala, P., Cappelen, H., Jensen, L. O., Gitt, A., Gehrke, K., am Rhein, L., Erbel, R., Gutersohn, A., Eggebrecht, H., Al Khani, M., Rosenberger, A., Vogelsberg, H., Klepzig, H., Schmidt, A., Silber, S., Mau, B., Leuner, C., Czyborra, K., Reuschling, C., Muno, E., Nauheim, B., Kleber, F., Rux, S., Saad, A., Elabady, M., Beiras, A. C., Fernandez, J. S., del Arno, F. N., Romo, A. I., Fernandez, J. M. C., Mayoreal, A. R., Rebanal, F. J. R., de la Borbolla, M. G., Chaparro, M., Brotons, C., Miralda, C. P., Vila i Perez, S. I., Moris, C., Aviles, F. F., de la Fuente Galan, L., Vinuela, P. T., de Torres, F. M., Mora, J., Rodriguez, I. S., Bustamante, I. P., Fernandez, P. L. S., Torrent, J. L. D., Diez Gil, J. L., Perpinan, J., Motilla, V. P., Juango, M. S. A., Berjon-Reyero, J., Moreno, R. M., Guerrero, J. C. F., Savolainen, K., Syvanne, M., Cohen-Solal, A., Oboa, A. -S., Bassand, J. P., Espinosa, D. P., Jouet, V., Cedex, B., Montalescot, G., Gallois, V., Daubert, J. C., Clerc, J. M., Machecourt, J., Cottin, Y., Walker, D., Holland, F., Prosser, J., Muir, L., Barber, K., Cleland, J. G. F., Cook, J., Chapichadze, Z., Christos, I. S. A., Tsiavou, N., Chrysohoou, C., Manginas, A., Terrovitis, J., Kanakakis, J., Vavuranakis, M., Drakos, S., Farmakis, T., Samara, C., Papakosta, C., Bourantas, C., Michalis, L. K., Christos, M., Foussas, S., Adamopoulou, E., Vardas, P. E., Marketou, M., Alotti, N., Basa, A. M., Vigh, A., Preda, I., Csoti, E., Keltai, M., Kerkovits, G., Hendler, A., Blatt, A., Yakov, B., Beyar, R., Shefer, A., Halon, D., Bentzvi, M., Avramovitch, N., Bakst, A., Saba, K., Cafri, C., Grosbard, A., Sheva, B., Margolis, B., Suleiman, K., Banai, S., Meerkin, D., Mosseri, M., Guita, P., Jabara, R., Jafari, J., Shitrit, D. B., Ghasan, Salameh, Brezins, M., van den Akker-Berman, L., Guetta, V., Hashomer, T., Rozenman, Y., Biagini, A., Berti, S., Ferrero, M., Colombo, A., Roccaforte, R., Milici, C., Scarpino, L., Salvi, A., Desideri, A., Sabbadin, D., Veneto, C., Galassi, A., Giuffrida, G., Rognoni, A., Vassanelli, C., Paffoni, P., Cioppa, A., Rubino, P., de Carlo, M., Petronio, A. S., Naccarella, F., Saia, F., Marzocchi, A., Maranga, S. S., Presbitero, P., Valsecchi, F., Piscione, F., Esposito, G., Santini, N. M., Tubaro, M., Erglis, A., Narbute, I., Kavoliuniene, A., Zaliunas, R., Navickas, R., Luckute, D., Subkovas, E., Wagner, D., Vermeer, F., Lousberg, A., Fransen, H., Breeman, A., Tebbe, H., De Boer, M. J., van der Wal, M., Vos, J., Leenders, C. M., Veerhoek, M. J., Jansen, C., Bijl, M., Koppelaar, C., den Linden, V., Brons, R., Widdershofen, J. W. M. G., Broers, H., Kontny, F., Jonzon, M., Wodniecki, J., Tomasik, A., Trusz-Gluza, M., Nowak, S., Ruzyllo, W., Deptuch, T., Marques, J., Matias, F., Madeira, H., Oliveira, J., Sargento, L., Ionac, A., Dragulescu, I. S., Mut-Vitcu, B., Maximov, D., Dorobantu, M., Apetrei, E., Niculescu, R., Petrescu, V., Bucsa, A., Deleanu, D., Bucharest, Benedek, I. S., Hintea, T., Aronov, D., Tikhomirova, E., Kranjec, I., Prokselj, K., Kanic, V., Sepetoglu, A., Aytekin, S., Aytekin, V., Catakoglu, A. B., Parlar, H., Tufekcioglu, S., Ozyedek, Z., Baltali, M., Kiziltan, D., Vukovic, M., and Neskovic, A. N.
- Subjects
Male ,medicine.medical_specialty ,Epidemiology ,medicine.medical_treatment ,Health Status ,Coronary Artery Disease ,Revascularization ,Coronary artery disease ,Cohort Studies ,Risk Factors ,Surveys and Questionnaires ,medicine ,Myocardial Revascularization ,Surveys and Questionnaire ,Humans ,Prospective Studies ,Prospective cohort study ,Aged ,business.industry ,Risk Factor ,Mortality rate ,Confounding ,Middle Aged ,medicine.disease ,Surgery ,Europe ,Prospective Studie ,Treatment Outcome ,Emergency medicine ,Population study ,Female ,Cohort Studie ,Cardiology and Cardiovascular Medicine ,business ,Human ,Cohort study - Abstract
Objective: Self-perceived health status may be helpful in identifying patients at high risk for adverse outcomes. The Euro Heart Survey on Coronary Revascularization (EHS-CR) provided an opportunity to explore whether impaired health status was a predictor of 1-year mortality in patients with coronary artery disease (CAD) undergoing angiographic procedures. Methods: Data from the EHS-CR that included 5619 patients from 31 member countries of the European Society of Cardiology were used. Inclusion criteria for the current study were completion of a self-report measure of health status, the EuroQol Questionnaire (EQ-5D) at discharge and information on 1-year follow-up, resulting in a study population of 3786 patients. Results: The 1-year mortality was 3.2% (n = 120). Survivors reported fewer problems on the five dimensions of the EQ-5D as compared with non-survivors. A broad range of potential confounders were adjusted for, which reached a p
- Published
- 2006
8. Patients enrolled in coronary intervention trials are not representative of patients in clinical practice: results from the Euro Heart Survey on Coronary Revascularization
- Author
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Hordijk-Trion M., Lenzen M., Wijns W., De Jaegere P., Simoons M. L., Scholte Op Reimer W. J. M., Bertrand M. E., Mercado N., Boersma E., Maier W., Meier B., Moris C., Piscione F., Sechtem U., Sergeant P., Stahle E., Vos J., Widimsky P., Unger F., Manini M., Bramley C., Laforest V., Taylor C., Del Gaiso S., Huber K., De Backer G., Sirakova V., Cerbak R., Thayssen P., Lehto S., Blanc J. -J., Delahaye F., Kobulia B., Zeymer U., Cokkinos D., Karlocai K., Graham I., Shelley E., Behar S., Maggioni A., Grabauskiene V., Deckers J., Asmussen I., Stepinska J., Goncalves L., Mareev V., Riecansky I., Kenda M. F., Alonso A., Lopez-Sendon J. L., Rosengren A., Buser P., Okay T., Sychov O., Fox K., Wood D., Crijns H., McGregor K., Mulder B., Priori S., Ryden L., Tavazzi L., Vahanian A., Vardas P., Sarkisyan K., Glogar H. D., Frick M., Pachinger O., Zwick R., Vrints C., Van Hertbruggen E., Vercammen M., Sysmans T., Schroeder E., Domange J., De Pril H., De Vriese J., Van Hecke T., Legrand V., Gillon M. -F., Richardy M., Doneux P., Petrov I., Jorgova J., Starcevic B., Eeckhout E., Berger A., Prudent V., Camenzind E., Masson N., Zambartas C., Kleanthous H., Stellova B., Aschermann M., Simek S., Kautzner J., Karmazin V., Svab P., Indrak J., Branny M., Hladilova K., Kala P., Cappelen H., Jensen L. O., Gitt A., Gehrke K., am Rhein L., Erbel R., Gutersohn A., Eggebrecht H., Al Khani M., Rosenberger A., Vogelsberg H., Klepzig H., Schmidt A., Silber S., Mau B., Leuner C., Czyborra K., Reuschling C., Muno E., Nauheim B., Kleber F., Rux S., Saad A., Elabady M., Beiras A. C., Fernandez J. S., del Arno F. N., Romo A. I., Fernandez J. M. C., Mayoreal A. R., Rebanal F. J. R., de la Borbolla M. G., Chaparro M., Brotons C., Miralda C. P., Vila i Perez S. I., Aviles F. F., de la Fuente Galan L., Vinuela P. T., de Torres F. M., Mora J., Rodriguez I. S., Bustamante I. P., Fernandez P. L. S., Torrent J. L. D., Gil J. L. D., Perpinan J., Motilla V. P., Juango M. S. A., Berjon-Reyero J., Moreno R. M., Guerrero J. C. F., Savolainen K., Syvanne M., Cohen-Solal A., Oboa A. -S., Bassand J. P., Espinosa D. P., Jouet V., Cedex B., Montalescot G., Gallois V., Daubert J. C., Clerc J. M., Machecourt J., Cottin Y., Walker D., Holland F., Prosser J., Muir L., Barber K., Cleland J. G. F., Cook J., Chapichadze Z., Christos I. S. A., Tsiavou N., Chrysohoou C., Manginas A., Terrovitis J., Kanakakis J., Vavuranakis M., Drakos S., Farmakis T., Samara C., Papakosta C., Bourantas C., Michalis L. K., Christos M., Foussas S., Adamopoulou E., Marketou M., Alotti N., Basa A. M., Vigh A., Preda I., Csoti E., Keltai M., Kerkovits G., Hendler A., Blatt A., Yakov B., Beyar R., Shefer A., Halon D., Bentzvi M., Avramovitch N., Bakst A., Saba K., Cafri C., Grosbard A., Sheva B., Margolis B., Suleiman K., Banai S., Meerkin D., Mosseri M., Guita P., Jabara R., Jafari J., Shitrit D. B., Ghasan D., Salameh D., Brezins M., van den Akker-Berman L., Guetta V., Hashomer T., Rozenman Y., Biagini A., Berti S., Ferrero M., Colombo A., Roccaforte R., Milici C., Scarpino L., Salvi A., Desideri A., Sabbadin D., Veneto C., Galassi A., Giuffrida G., Rognoni A., Vassanelli C., Paffoni P., Cioppa A., Rubino P., de Carlo M., Petronio A. S., Naccarella F., Saia F., Marzocchi A., Maranga S. S., Presbitero P., Valsecchi F., Esposito G., Santini N. M., Tubaro M., Erglis A., Narbute I., Kavoliuniene A., Zaliunas R., Navickas R., Luckute D., Subkovas E., Wagner D., Vermeer F., Lousberg A., Fransen H., Breeman A., Tebbe H., De Boer M. J., van der Wal M., Leenders C. M., Veerhoek M. J., Jansen C., Bijl M., Koppelaar C., den Linden V., Brons R., Widdershofen J. W. M. G., Broers H., Kontny F., Jonzon M., Wodniecki J., Tomasik A., Trusz-Gluza M., Nowak S., Ruzyllo W., Deptuch T., Marques J., Matias F., Madeira H., Oliveira J., Sargento L., Ionac A., Dragulescu I. S., Mut-Vitcu B., Maximov D., Dorobantu M., Apetrei E., Niculescu R., Petrescu V., Bucsa A., Deleanu D., Bucharest, Benedek I. S., Hintea T., Aronov D., Tikhomirova E., Kranjec I., Prokselj K., Kanic V., Sepetoglu A., Aytekin S., Aytekin V., Catakoglu A. B., Parlar H., Tufekcioglu S., Ozyedek Z., Baltali M., Kiziltan, Vukovic M., Neskovic A. N., Cardiology, Hordijk-Trion, M., Lenzen, M., Wijns, W., De Jaegere, P., Simoons, M. L., Scholte Op Reimer, W. J. M., Bertrand, M. E., Mercado, N., Boersma, E., Maier, W., Meier, B., Moris, C., Piscione, F., Sechtem, U., Sergeant, P., Stahle, E., Vos, J., Widimsky, P., Unger, F., Manini, M., Bramley, C., Laforest, V., Taylor, C., Del Gaiso, S., Huber, K., De Backer, G., Sirakova, V., Cerbak, R., Thayssen, P., Lehto, S., Blanc, J. -J., Delahaye, F., Kobulia, B., Zeymer, U., Cokkinos, D., Karlocai, K., Graham, I., Shelley, E., Behar, S., Maggioni, A., Grabauskiene, V., Deckers, J., Asmussen, I., Stepinska, J., Goncalves, L., Mareev, V., Riecansky, I., Kenda, M. F., Alonso, A., Lopez-Sendon, J. L., Rosengren, A., Buser, P., Okay, T., Sychov, O., Fox, K., Wood, D., Crijns, H., Mcgregor, K., Mulder, B., Priori, S., Ryden, L., Tavazzi, L., Vahanian, A., Vardas, P., Sarkisyan, K., Glogar, H. D., Frick, M., Pachinger, O., Zwick, R., Vrints, C., Van Hertbruggen, E., Vercammen, M., Sysmans, T., Schroeder, E., Domange, J., De Pril, H., De Vriese, J., Van Hecke, T., Legrand, V., Gillon, M. -F., Richardy, M., Doneux, P., Petrov, I., Jorgova, J., Starcevic, B., Eeckhout, E., Berger, A., Prudent, V., Camenzind, E., Masson, N., Zambartas, C., Kleanthous, H., Stellova, B., Aschermann, M., Simek, S., Kautzner, J., Karmazin, V., Svab, P., Indrak, J., Branny, M., Hladilova, K., Kala, P., Cappelen, H., Jensen, L. O., Gitt, A., Gehrke, K., am Rhein, L., Erbel, R., Gutersohn, A., Eggebrecht, H., Al Khani, M., Rosenberger, A., Vogelsberg, H., Klepzig, H., Schmidt, A., Silber, S., Mau, B., Leuner, C., Czyborra, K., Reuschling, C., Muno, E., Nauheim, B., Kleber, F., Rux, S., Saad, A., Elabady, M., Beiras, A. C., Fernandez, J. S., del Arno, F. N., Romo, A. I., Fernandez, J. M. C., Mayoreal, A. R., Rebanal, F. J. R., de la Borbolla, M. G., Chaparro, M., Brotons, C., Miralda, C. P., Vila i Perez, S. I., Aviles, F. F., de la Fuente Galan, L., Vinuela, P. T., de Torres, F. M., Mora, J., Rodriguez, I. S., Bustamante, I. P., Fernandez, P. L. S., Torrent, J. L. D., Gil, J. L. D., Perpinan, J., Motilla, V. P., Juango, M. S. A., Berjon-Reyero, J., Moreno, R. M., Guerrero, J. C. F., Savolainen, K., Syvanne, M., Cohen-Solal, A., Oboa, A. -S., Bassand, J. P., Espinosa, D. P., Jouet, V., Cedex, B., Montalescot, G., Gallois, V., Daubert, J. C., Clerc, J. M., Machecourt, J., Cottin, Y., Walker, D., Holland, F., Prosser, J., Muir, L., Barber, K., Cleland, J. G. F., Cook, J., Chapichadze, Z., Christos, I. S. A., Tsiavou, N., Chrysohoou, C., Manginas, A., Terrovitis, J., Kanakakis, J., Vavuranakis, M., Drakos, S., Farmakis, T., Samara, C., Papakosta, C., Bourantas, C., Michalis, L. K., Christos, M., Foussas, S., Adamopoulou, E., Marketou, M., Alotti, N., Basa, A. M., Vigh, A., Preda, I., Csoti, E., Keltai, M., Kerkovits, G., Hendler, A., Blatt, A., Yakov, B., Beyar, R., Shefer, A., Halon, D., Bentzvi, M., Avramovitch, N., Bakst, A., Saba, K., Cafri, C., Grosbard, A., Sheva, B., Margolis, B., Suleiman, K., Banai, S., Meerkin, D., Mosseri, M., Guita, P., Jabara, R., Jafari, J., Shitrit, D. B., Ghasan, D., Salameh, D., Brezins, M., van den Akker-Berman, L., Guetta, V., Hashomer, T., Rozenman, Y., Biagini, A., Berti, S., Ferrero, M., Colombo, A., Roccaforte, R., Milici, C., Scarpino, L., Salvi, A., Desideri, A., Sabbadin, D., Veneto, C., Galassi, A., Giuffrida, G., Rognoni, A., Vassanelli, C., Paffoni, P., Cioppa, A., Rubino, P., de Carlo, M., Petronio, A. S., Naccarella, F., Saia, F., Marzocchi, A., Maranga, S. S., Presbitero, P., Valsecchi, F., Esposito, G., Santini, N. M., Tubaro, M., Erglis, A., Narbute, I., Kavoliuniene, A., Zaliunas, R., Navickas, R., Luckute, D., Subkovas, E., Wagner, D., Vermeer, F., Lousberg, A., Fransen, H., Breeman, A., Tebbe, H., De Boer, M. J., van der Wal, M., Leenders, C. M., Veerhoek, M. J., Jansen, C., Bijl, M., Koppelaar, C., den Linden, V., Brons, R., Widdershofen, J. W. M. G., Broers, H., Kontny, F., Jonzon, M., Wodniecki, J., Tomasik, A., Trusz-Gluza, M., Nowak, S., Ruzyllo, W., Deptuch, T., Marques, J., Matias, F., Madeira, H., Oliveira, J., Sargento, L., Ionac, A., Dragulescu, I. S., Mut-Vitcu, B., Maximov, D., Dorobantu, M., Apetrei, E., Niculescu, R., Petrescu, V., Bucsa, A., Deleanu, D., Bucharest, Benedek, I. S., Hintea, T., Aronov, D., Tikhomirova, E., Kranjec, I., Prokselj, K., Kanic, V., Sepetoglu, A., Aytekin, S., Aytekin, V., Catakoglu, A. B., Parlar, H., Tufekcioglu, S., Ozyedek, Z., Baltali, M., Kiziltan, Vukovic, M., and Neskovic, A. N.
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Male ,medicine.medical_specialty ,Randomization ,medicine.medical_treatment ,Euro Heart Survey ,Coronary Artery Disease ,Revascularization ,law.invention ,Coronary artery disease ,Randomized controlled trial ,law ,Internal medicine ,Angioplasty ,medicine ,Humans ,cardiovascular diseases ,Angioplasty, Balloon, Coronary ,Coronary Artery Bypass ,CABG ,Aged ,Randomized Controlled Trials as Topic ,business.industry ,Coronary Artery Bypa ,Patient Selection ,PCI ,Health Survey ,Middle Aged ,medicine.disease ,Health Surveys ,Surgery ,Clinical trial ,Stenosis ,surgical procedures, operative ,Clinical Trials, Phase III as Topic ,Conventional PCI ,Female ,Cardiology and Cardiovascular Medicine ,business ,Human - Abstract
Aims: Revascularization in patients with coronary artery disease changed over the last two decades, favouring the number of patients treated by means of percutaneous coronary interventions (PCI) when compared with coronary artery bypass grafting (CABG). Many randomized controlled trials (RCTs) have been performed to compare these two competing revascularization techniques. Because of the strict enrolment criteria of RCTs in which highly selected patients are recruited, the applicability of the results may be limited in clinical practice. The current study evaluates to what extent patients in clinical practice were similar to those who participated in RCTs comparing PCI with CABG. Methods and results: Clinical characteristics and 1-year outcome of 4713 patients enrolled in the Euro Heart Survey on Coronary Revascularization were compared with 8647 patients who participated in 14 major RCTs, comparing PCI with CABG. In addition, we analysed which proportion of survey patients would have disqualified for trial participation (n = 3033, 64%), aiming at identifying differences between trial-eligible and trial-ineligible survey patients. In general, important differences were observed between trial participants and survey patients. Patients in clinical practice were older, more often had comorbid conditions, single-vessel disease, and left main stem stenosis when compared with trial participants. Almost identical differences were observed between trial-eligible and trial-ineligible survey patients. In clinical practice, PCI was the treatment of choice, even in patients who were trial-ineligible (46% PCI, 26% CABG, 28% medical). PCI remained the preferred treatment option in patients with multi-vessel disease (57% in trial-eligible and 40% in trial-ineligible patients, respectively, P < 0.001); yet, the risk profile of patients treated by PCI was better than that for patients treated either by CABG or by medical therapy. In the RCTs, there was no mortality difference between PCI and CABG. In clinical practice, however, we observed 1-year unadjusted survival benefit for PCI vs. CABG (2.9 vs. 5.4%, P < 0.001). Survival benefit was only observed in trial-ineligible patients (3.3 vs. 6.2%, P < 0.001). Conclusion: Many patients in clinical practice were not represented in RCTs. Moreover, only 36% of these patients were considered eligible for participating in a trial comparing PCI with CABG. We demonstrated that RCTs included younger patients with a better cardiovascular risk profile when compared with patients in everyday clinical practice. This study highlights the disparity between patients in clinical practice and patients in whom the studies that provide the evidence for treatment guidelines are performed. © The European Society of Cardiology 2006. All rights reserved.
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- 2006
9. Reduced costs with bisoprolol treatment for heart failure - An economic analysis of the second Cardiac Insufficiency Bisoprolol Study (CIBIS-II)
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Bacquet, P, Levy, E, Mcguire, A, Mcmurray, J, Merot, Jl, Paschen, B, Remme, Wj, Szucs, Td, Klein, W, Brunhuber, W, Hofmann, R, Kuhn, P, Nesser, Hj, Slany, J, Weihs, W, Wiedermann, C, Wimmer, H, van Mieghem, W, Boland, J, Chaudron, Jm, Jordaens, L, Melchior, Jp, Aschermann, M, Bruthansl, J, Hradec, M, Kolbel, F, Semrad, B, Haghfelt, T, Hansen, Jf, Goetzsche, Co, Hildebrandt, P, Kassis, E, Rasmussen, V, Rokkedal, J, Thomassen, A, Groundstroem, K, Uusimaa, P, Le Heuzey JY, Aumont, Mc, Aupetit, Jf, Baille, N, Baudouy, P, Belin, A, Bonneau, A, Bonneric, G, Bousser, Jp, Citron, B, Dary, P, Decoulx, E, De Groote, P, Denolle, T, Dievart, F, Duriez, P, Eicher, Jc, Enjuto, G, Ferriere, M, Fournier, E, Garandeau, M, Gauthier, J, Genest, M, Gerbe, A, Godenir, Jp, Guillot, B, Guillot, Jp, Guillot, P, Heno, P, D'Ivernois, C, Jean, M, Kacet, S, Kalle, R, Komajda, M, Lacroix, A, Lallemand, R, Lardoux, H, Marquet, M, Martin, M, Martin, O, Mery, D, Mossaz, R, Mothes, P, Olive, T, Ostorero, M, Paganelli, F, Page, E, Pauly Laubry, C, Puel, J, Rousseau, Jf, Roux, Jj, Schenowitz, A, Sourdais, K, Tremel, F, Verdun, A, Witchiz, S, Wolf, Je, Hombach, V, Assmann, I, Beyer, T, Bischoff, Ko, Darius, H, Ertl, G, Fleck, E, Forster, K, Freytag, F, Gleichmann, U, Haasis, R, Henssge, R, Hey, D, Hesse, P, Hofs, T, Keck, M, Klein, H, Kromer, Et, Kruls Munch, J, Luderitz, B, Maisch, B, Mitrovic, V, Neubauer, S, Osterziel, Kj, Simon, H, Spitzer, Sg, Stohring, R, Taubert, G, Teichmann, W, Theisen, K, Wende, W, Wieser, H, Zotz, R, Bridges, A, Adgey, J, Ambepitiya, G, Boon, N, Boyle, Rm, Cowley, Aj, Cripps, T, Davies, Mk, Dunn, F, Findlay, J, Forsey, P, Fyfe, T, Gould, B, Greenwood, Tw, Hubner, P, Khan, S, Lewis, P, Mackay, A, Maltz, M, Mcarthur, J, Mcleod, A, Mcleod, D, Metcalfe, M, Millar Craig, M, Mills, P, Nelson, Jk, Nicholls, D, Oakley, Gd, Patterson, Dlh, Pohl, Jef, Ray, S, Silke, B, Wilkinson, Pr, Preda, I, Csanady, M, Cserhalmi, L, Edes, I, Gesztesi, T, Karpati, P, Simon, K, Tarjan, J, Fogari, R, Tramarin, R, Galie, N, Giani, P, Milanese, U, Scalvini, S, Scrutinio, D, Sechi, Leonardo Alberto, Tettamanti, F, De Vito, F, Crean, P, Mccann, H, Mulcahy, D, Sugrue, D, van Hoogenhuyze DCA, van der Burgh PH, Ciampricotti, R, van Dantzig JM, Denhartog, Fr, Henneman, Ja, van Kesteren HAM, Kragten, Ja, Liem, Kl, Limburg, A, van der Linde MR, Linssen, Gcm, Pasteuning, H, Penn, Hjam, Van Rossum, P, Schaafsma, Hj, Schelling, A, Sloos, R, Wesdorp, Jcl, Korewicki, J, Achremczyk, P, Czestockowska, E, Dowgird, M, Dyduszynski, A, Gorski, J, Ilmurzynska, K, Janicki, K, Kornacewicz Jach, Z, Kraska, T, Krzeminska Pakula, M, Kuch, J, Nartowicz, E, Petelenz, T, Piwowarska, W, Rawczynska Englert, I, Ruzyllo, W, Swiatecka, G, Tendera, M, Wierzchowiecki, M, Wodniecki, J, Wojciechowoski, D, Wrabec, K, Wysocki, H, Gomes, Rs, Ceia, Mf, Lousada, N, Campos, Jmm, Providencia, La, de Moura ALZC, Marejev, Vj, Aronov, Dm, Arutjunov, Gp, Bart, Bj, Basechikin, Ss, Belenkov, Jn, Beloussov, Jb, Bokeria, Oa, Charchogljan, Ra, Doschytsin, V, Fedorova, Ta, Glezer, Mg, Gorbachenkov, A, Gorshkov, Gospodarenko, Al, Ivashkin, Vt, Ivleva, Aj, Kyrichenko, Aa, Lavrov, Aa, Lazebnik, Lb, Marynov, A, Mazaev, Vp, Polejev, Nr, Shpektor, Sidorenko, Ba, Sobolev, Ke, Starodoubtsev, Ak, Storozhakhov, Gi, Syrkin, Al, Zodionchenko, Vs, Zvereva, Tv, Murin, J, Kaliska, G, Rybar, R, Valle, V, Artaza, M, Conthe, P, Cruz, Jm, Garcia Moll, M, Lopez Sendon JL, Martinez, A, Monzon, F, Ribas, M, Roig, E, Roldan, I, Hoglund, C, Ekdahl, S, Hjelmaeus, L, Lindberg, K, Lofdahl, P, Ulvenstam, G, Warselius, L, Follath, F, Anghern, W, Dubach, P, Erne, P, Gallino, A, Moccetti, T, Jmouro, Av, Dargie, Hj, Erdmann, E, Lechat, P, Sendon, Jll, Mareyev, V, Sadowski, Z, Seabra Gomes RJ, Zannad, F, Wehrlen Grandjean, M, Funck Brentano, C, Hansen, S, Hohnloser, S, Vanoli, E, Jaillon, P, De Baker, G, Dahlstrom, U, Hill, C, Leizorovicz, A, Burgnard, F, Rolland, C, Wiemann, H, Verkenne, P, Arab, T, Cussac, N, Dussous, V, Haise, S, and Funck Brentano, C.
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H Social Sciences (General) ,medicine.medical_specialty ,Cost-Benefit Analysis ,Adrenergic beta-Antagonists ,METOPROLOL ,Placebo ,THERAPY ,Indirect costs ,Pharmacoeconomics ,Pharmacotherapy ,RANDOMIZED INTERVENTION TRIAL ,PHARMACOECONOMICS ,Germany ,Health care ,Bisoprolol ,Humans ,Medicine ,Outpatient clinic ,Prospective Studies ,Intensive care medicine ,health care economics and organizations ,Heart Failure ,CARVEDILOL ,business.industry ,MORTALITY ,Diagnosis-related group ,United Kingdom ,Chemotherapy, Adjuvant ,MERIT-HF ,HOSPITALIZATION ,MINIMIZATION ,INHIBITORS ,France ,Quality-Adjusted Life Years ,Cardiology and Cardiovascular Medicine ,business ,medicine.drug - Abstract
Background Beta-blockers, used as an adjunctive to diuretics, digoxin and angiotensin converting enzyme inhibitors, improve survival in chronic heart failure. We report a prospectively planned economic analysis of the cost of adjunctive beta-blocker therapy in the second Cardiac Insufficiency BIsoprolol Study (CIBIS II). Methods Resource utilization data (drug therapy, number of hospital admissions, length of hospital stay, ward type) were collected prospectively in all patients in CIBIS . These data were used to determine the additional direct costs incurred, and savings made, with bisoprolol therapy. As well as the cost of the drug, additional costs related to bisoprolol therapy were added to cover the supervision of treatment initiation and titration (four outpatient clinic/office visits). Per them (hospital bed day) costings were carried out for France, Germany and the U.K. Diagnosis related group costings were performed for France and the U.K. Our analyses took the perspective of a third party payer in France and Germany and the National Health Service in the U.K. Results Overall, fewer patients were hospitalized in the bisoprolol group, there were fewer hospital admissions perpatient hospitalized, fewer hospital admissions overall, fewer days spent in hospital and fewer days spent in the most expensive type of ward. As a consequence the cost of care in the bisoprolol group was 5-10% less in all three countries, in the per them analysis, even taking into account the cost of bisoprolol and the extra initiation/up-titration visits. The cost per patient treated in the placebo and bisoprolol groups was FF35 009 vs FF31 762 in France, DM11 563 vs DM10 784 in Germany and pound 4987 vs pound 4722 in the U.K. The diagnosis related group analysis gave similar results. Interpretation Not only did bisoprolol increase survival and reduce hospital admissions in CIBIS II, it also cut the cost of care in so doing. This `win-win' situation of positive health benefits associated with cost savings is Favourable from the point of view of both the patient and health care systems. These findings add further support for the use of beta-blockers in chronic heart failure.
- Published
- 2001
10. [Troponin T--is it a marker of restenosis after transluminal percutaneous angioplasty in unstable angina patients?]
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Wodniecki J, Wojciech Jachec, Szczurek-Katański K, Wilczek K, Kawecki D, Tarnawski R, and Tomasik A
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Male ,Troponin T ,Recurrence ,Humans ,Coronary Disease ,Female ,Angina, Unstable ,Angioplasty, Balloon, Coronary ,Middle Aged ,Biomarkers ,Follow-Up Studies - Abstract
Troponin T (TpT) is a protein implicated in skeletal muscle contractions, including myocardium. It was shown that the presence of troponin TpT in unstable angina patients' blood is associated with poor prognosis. In the present study amongst 25 patients with unstable angina 12 were found to have TpT present in their blood. TpT concentration was higher in patients with III and IVo CCS symptoms in comparison with class I and IIo CCS symptoms: 0.207 +/- 0.275 and 0.144 +/- 0.186 ng/mL respectively (p = 0.053; nonparametric Kolmogorow-Smirnov test). Patients were subjected to percutaneous transluminal coronary angioplasty (PTCA). After 3 months of follow up 17 patients (the rest of them dropped out) were assigned to two groups: A (n = 8)--without and B (n = 9)--with clinical and electrocardiographic signs of restenosis. Retrospective analysis revealed the presence of TpT before PTCA in 6 group B patients and 2 group A patients. Relative risk of stenocardia recurrence was calculated as 2.25. TpT was present in the blood of 20 patients in the first 24 hours after PTCA, and group B patients had higher mean TpT concentration; that could result from reperfusion of more ischaemic myocardium. It seems that the presence of TpT in unstable angina patients' blood may be an important factor characterizing patients with more serious prognosis.
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- 1999
11. The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial
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Lechat, P, Brunhuber, Kw, Hofmann, R, Kuhn, P, Nesser, Hj, Slany, J, Weihs, W, Wiedermann, C, Wimmer, H, van Mieghem, W, Boland, J, Chaudron, Jm, Jordaens, L, Melchior, Jp, Aschermann, M, Bruthansl, J, Hradec, M, Kolbel, F, Semrad, B, Haghfelt, T, Fischer Hansen, J, Goetzsche, Co, Hildebrandt, P, Kassis, E, Rasmussen, V, Rokkedal, J, Thomassen, A, Groundstroem, K, Uusimaa, P, Le Heuzey JY, Aumont, Mc, Aupetit, Jf, Baille, N, Baudouy, P, Belin, A, Bonneau, A, Bonneric, G, Bousser, Jp, Citron, B, Dary, P, Decoulx, E, De Groote, P, Denolle, T, Dievart, F, Duriez, P, Eicher, Jc, Enjuto, G, Ferriere, M, Fournier, E, Garandeau, M, Gauthier, J, Genest, M, Gerbe, A, Godenir, Jp, Guillot, B, Guillot, Jp, Guillot, P, Heno, P, D'Ivernois, C, Jean, M, Kacet, S, Kalle, R, Komajda, M, Lacroix, A, Lallemand, R, Lardoux, H, Marquet, M, Martin, M, Martin, O, Mery, D, Mossaz, R, Mothes, P, Olive, T, Ostorero, M, Paganelli, F, Page, E, Pauly Laubry, C, Puel, J, Rousseau, Jf, Roux, Jj, Schenowitz, A, Sourdais, K, Tremel, F, Verdun, A, Witchiz, S, Wolf, Je, Hombach, V, Assmann, I, Beyer, T, Bischoff, Ko, Darius, H, Ertl, G, Fleck, E, Forster, K, Freytag, F, Gleichmann, U, Haasis, R, Henssge, R, Hey, D, Hesse, P, Hofs, T, Keck, M, Klein, H, Kromer, Et, Kruls Munch, J, Luderitz, B, Maisch, B, Mitrovic, V, Neubauer, S, Osterziel, Kj, Simon, H, Spitzer, Sg, Stohring, R, Taubert, G, Teichmann, W, Theisen, K, Wende, W, Wieser, H, Zotz, R, Preda, I, Csanady, M, Cserhalmi, L, Edes, I, Gesztesi, T, Karpati, P, Simon, K, Tarjan, J, Fogari, R, Tramarin, R, Galie, N, Giani, P, Milanese, U, Scalvini, S, Scrutinio, D, Sechi, Leonardo Alberto, Tettamanti, F, De Vito, F, Crean, P, Mccann, H, Mulcahy, D, Sugrue, D, van Hoogenhuyze DCA, van der Burgh PH, Ciampricotti, R, van Dantzig JM, Denhartog, Fr, Henneman, Ja, van Kesteren HAM, Kragten, Ja, Liem, Kl, Limburg, A, van der Linde MR, Linssen, Gcm, Pasteuning, H, Penn, Hjam, Van Rossum, P, Schaafsma, Hj, Schelling, A, Sloos, R, Wesdorp, Jcl, Korewicki, J, Achremczyk, P, Czestockowska, E, Dowgird, M, Dyduszynski, A, Gorski, J, Ilmurzynska, K, Janicki, K, Kornacewicz Jach, Z, Kraska, T, Krzeminska Pakula, M, Kuch, J, Nartowicz, E, Petelenz, T, Piwowarska, W, Rawczynska Englert, I, Ruzyllo, W, Swiatecka, G, Tendera, M, Wierzchowiecki, M, Wodniecki, J, Wojciechowoski, D, Wrabec, K, Wysocki, H, Gomes, Rs, Ceia, Mf, Lousada, N, Campos, Jmm, Providencia, La, de Moura ALZC, Marejev, Vj, Aronov, Dm, Arutjunov, Gp, Bart, Bj, Basechikin, Ss, Belenkov, Jn, Beloussov, Jb, Bokeria, Oa, Charchogljan, Ra, Doschytsin, V, Fedorova, Ta, Glezer, Mg, Gorbachenkov, A, Gorshkov, Va, Gospodarenko, Al, Ivashkin, Vt, Ivleva, Aj, Kyrichenko, Aa, Lavrov, Aa, Lazebnik, Lb, Marynov, A, Mazaev, Vp, Polejev, Nr, Shpektor, A, Sidorenko, Ba, Sobolev, Ke, Starodoubtsev, Ak, Storozhakhov, Gi, Syrkin, Al, Zodionchenko, Vs, Zvereva, Tv, Murin, J, Kaliska, G, Rybar, R, Valle, V, Artaza, M, Conthe, P, Cruz, Jm, Garcia Moll, M, Lopez Sendon JL, Martinez, A, Monzon, F, Ribas, M, Roig, E, Roldan, I, Hoglund, C, Ekdahl, S, Hjelmaeus, L, Lindberg, K, Lofdahl, P, Ulvenstam, G, Warselius, L, Follath, F, Anghern, W, Dubach, P, Erne, P, Gallino, A, Moccetti, T, Bridges, A, Adgey, J, Ambepitiya, G, Boon, N, Boyle, Rm, Cowley, Aj, Cripps, T, Davies, Mk, Dunn, F, Findlay, J, Forsey, P, Fyfe, T, Gould, B, Greenwood, Tw, Hubner, P, Khan, S, Lewis, P, Mackay, A, Maltz, M, Mcarthur, J, Mcleod, A, Mcleod, D, Metcalfe, M, Millar Craig, M, Mills, P, Nelson, Jk, Nicholls, D, Oakley, Gd, Patterson, Dlh, Pohl, Jef, Ray, S, Silke, B, Wilkinson, Pr, and Jmouro, Av
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- 1999
12. [Early results and many years of observing treatment of unstable angina]
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Adamowicz-Czoch E, Wojciech Jachec, Wantrych M, Szyguła E, Poloński L, Tendera M, and Wodniecki J
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Adult ,Male ,Stroke Volume ,Middle Aged ,Coronary Angiography ,Prognosis ,Ventricular Function, Left ,Survival Rate ,Treatment Outcome ,Recurrence ,Humans ,Female ,Angina, Unstable ,Angioplasty, Balloon, Coronary ,Coronary Artery Bypass ,Aged ,Follow-Up Studies - Abstract
Immediate effect of PTCA and CABG for unstable angina then followed-up for PTCA and CABG several years are analyzed in 112 patients selected out of 204 unstable angina patients hospitalized from 1990 to 1991. Fifty three patients, aged 25-68 (mean 51) were assigned to PTCA, fifty nine aged 33-69 (mean 53) were subjected to CABG. Both groups comprised of 72% and 83% males respectively. Nine patients with de novo angina, forty with crescendo angina and four with prolonged stenocardia were assigned to PTCA. 28% of patients have had myocardial infarction. Nine patients with de novo angina and fifty with crescendo angina were assigned to CABG. 56% of them have had myocardial infarction. Left ventricular ejection fraction (LVEF) less than 40% was found in 8 (15%) PTCA patients and in 18 (31%) patients who underwent CABG. Full revascularization was achieved in 38 (73%) patients treated with PTCA and 46 (78%) CABG patients. In 9/17% patients only critical stenosis in multivessel disease was subjected to PTCA. Four cases of myocardial infarction underwent intervention and all of these patients died: one (2%) after PTCA, and three (5%) after CABG. Fifty two patients after PTCA and fifty six after CABG were followed for one to four (mean 3) years. Thirty one percent of patients after PTCA and 41% after CABG were asymptomatic, 61% and 54% respectively had little to moderate symptoms. Left ventricular systolic function improved in most patients, predominantly in those with LVEF less than 40% (p0.05) treated with PTCA. Hospitalization due to anginal pain was needed in 46% of patients after PTCA and 15% after CABG (p0.05). Coronary artery restenosis after PTCA was successfully treated with re-PTCA or CABG in 9 (17%) patients. Venous graft stenoses were dilated in two cases. Myocardial infarction occurred in 3 (6%) patients after PTCA and 2 (4%) patients after CABG. One patient died after redilatation CABG treated patients required nonsignificantly less antianginal drugs. Four week survival rate in PTCA group and CABG group was 98% and 95% respectively; three year survival was 95% in both groups. We conclude, that unstable angina patients requiring either angioplasty or surgery may expect good procedural and long term prognosis. Remarkably good results may be expected in successfully revascularised patients with low ejection fraction.
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- 1995
13. Echocardiografic evaluation, physical capacity and NTproBNP concentration in dilated cardiomyopathy patients wit low and elevated trasnspulmonary gradient
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WOJCIECHOWSKA, C, primary, JACHEC, W, additional, IRLIK, G, additional, NOWALANYKOZIELSKA, E, additional, GLANOWSKA, G, additional, and WODNIECKI, J, additional
- Published
- 2008
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14. Evaluation of usefulness of combine nitroprusside, nitric oxide, sildenafil vasodilatative test in reversibility of pulmonary venous hypertension in dilated cardiomyopathy patients
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JACHEC, W, primary, WOJCIECHOWSKA, C, additional, NOWALANYKOZIELSKA, E, additional, IRLIK, G, additional, and WODNIECKI, J, additional
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- 2008
- Full Text
- View/download PDF
15. [Does the appearance of pro-arrhythmic response to anti-arrhythmic drugs have prognostic significance?]
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Trusz-Gluza M, Giec L, Dabrowski A, Kuch J, Piwowarska W, Pracka H, Sadowski Z, Wodniecki J, Filipecki A, and Krzysztof Szydło
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Male ,Risk Factors ,Electrocardiography, Ambulatory ,Humans ,Coronary Disease ,Middle Aged ,Prognosis ,Anti-Arrhythmia Agents ,Survival Analysis - Abstract
Study was undertaken to assess whether proarrhythmic response to antiarrhythmic drug is a risk factor for cardiac death in patients (pts) with ischaemic heart disease (IHD). In 782 pts with IHD and frequent and/or complex ventricular ectopic beats (VEB) 1041 drug tests guided by 24 hour Holter monitoring were conducted. The following drugs were assessed: propranolol, disopyramide, mexiletine, amiodarone. Pro-arrhythmia was defined according to Velebit: 1/greater than or equal to 4-fold increase in VEBs, 2/greater than or equal to 10-fold increase in repetitive forms of 3/new occurrence of ventricular tachycardia or ventricular fibrillation (VT/VF). Proarrhythmic effect was observed in 8.4% of pts and in 7.9% of drug tests. The frequency with individual drugs ranged from 5.7% to 9%. No drug was completely free of this type of reaction. Antiarrhythmic drugs inducing arrhythmogenic response were eliminated. Pts were followed-up for a mean of 22 months (range 1-49). Chronic antiarrhythmic treatment was conducted. Pts were discharged taking the agent deemed most effective for suppression of arrhythmia. Follow-up visits were made every 6-12 months. All cases of death were verified. In long-term observation cardiac death and sudden death occurred in 53 and 32 pts. With actuarial analysis (Kaplan-Meler method, log rank test) there was significant difference in cardiac death (p less than 0.05) of pro-arrhythmia (+) compared with ++pro-arrhythmia (-) pts at yr (11% v 4%, 7% v 3%) and 3 yr (24% x 11%, 16% v 7%). The relative importance of baseline clinical variables in predicting survival was assessed with a stepwise Cox regression.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1992
16. Plasma α-tocopherol is not the predictor of repeat revascularization in coronary artery disease patients
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Tomasik, A.R., primary, Jacheć, W., additional, Wodniecki, J., additional, Skrzep-Poloczek, B., additional, Wojciechowska, C., additional, Widera, E., additional, Tarnawski, R., additional, Szczurek-Katański, K., additional, Wȩgiel, A., additional, Borawska, E., additional, and Świtalska, I., additional
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- 2000
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17. Circulating electronegatively charged LDL (LDL-) in patients with angiographically evidenced coronary artery disease
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Tomasik, A., primary, Jacheć, W., additional, Skrzep-Poloczek, B., additional, Widera, E., additional, Wodniecki, J., additional, Tarnawski, R., additional, and Wojciechowska, C., additional
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- 1999
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18. Effect of four-week-long treatment with micronised fenofibrate on the amount of electronegatively charged LDL particles (LDL-)
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Widera, E., primary, Tomasik, A., additional, Skrzep-Poloczek, B., additional, Jacheć, W., additional, Wodniecki, J., additional, Tarnawski, R., additional, and Wojciechowska, C., additional
- Published
- 1999
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- View/download PDF
19. The acute response of left ventricular filling dynamics to intravenous verapamil predicts the changes in exercise tolerance after oral verapamil therapy in patients with hypertrophic cardiomyopathy
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TENDERA, M., primary, SCHNEEWEISS, A., additional, BARTOSZEWSKI, A., additional, POLONSKI, L., additional, WODNIECKI, J., additional, and SALAMON, A., additional
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- 1993
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20. Prognostic value of QT dispersion in patients with diabetes mellitus type 2 after acute coronary syndrome.
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Switalska-Janiczek I, Tomasik A, Kawecki D, Wodniecki J, Foremny A, Fudal M, and Bajor M
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- 2006
21. Randomized, placebo-controlled study for immunosuppressive treatment of inflammatory dilated cardiomyopathy: two-year follow-up results.
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Wojnicz, R, Nowalany-Kozielska, E, Wojciechowska, C, Glanowska, G, Wilczewski, P, Niklewski, T, Zembala, M, Polonski, L, Rozek, M M, and Wodniecki, J
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- 2001
22. Immunohistological diagnosis of myocarditis.
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Wojnicz, R., Nowalany-Kozielska, E., Wodniecki, J., Szczurek-Katański, K., Nożyński, J., Zembala, M., and Rozek, M.M.
- Abstract
Aims The aim of this study was to characterize the up-regulation of major histocompatibility complex antigens class I (HLA-A, B, C) and class II (HLA-DR), and inter-cellular adhesion molecule-1 with special emphasis on de novo induction of these molecules on cardiac myocytes in patients with suspected myocarditis.Methods Endomyocardial biopsy specimens were obtained from 83 consecutive patients. Specimens were subdivided into two groups according to clinical presentation of the disease: Group A, 58 patients with idiopathic congestive heart failure and Group B, 25 patients without heart failure. In group A, 15% of patients had active myocarditis, 36% had borderline and 48% no myocarditis according to Dallas criteria. In group B, myocarditis distribution was 12%, 36% and 52%, respectively. The major histocompatibility complex was considered to be positive when the immunoreactivity index was ≥3+; intercellular adhesion molecules were considered positive when the score was ≥2+.Results We observed two characteristic staining patterns of the HLA molecules on cardiac myocytes: (i) multifocal sarcolemmal staining at the sites of mononuclear inflam-matory infiltration, (ii) linear sarcolemmal staining with otherwise normal endomyocardium. Positive immunoreactivity was observed in 60% of patients in group A, and in 44% of patients in group B. We found no correlation between a histopathological diagnosis of myocarditis or left ventricular systolic function and positive immunoreactivity.Conclusion The lack of correlation between immuno-histological signs of active inflammation and clinical symptoms in patients with myocarditis may indicate independence of an immunological mechanism. The lack of correlation between immunoreactivity and histopathological diagnosis of myocarditis may suggest low sensitivity of traditional histological evaluation. In our opinion, the induction of major histocompatibility and intercellular adhesion molecules on cardiac myocytes may indicate an autoimmune inflammatory response in patients with inflammatory myocardial disease. Immunohisto-chemical methods may be helpful in selecting patients for immunosuppressive therapy. [ABSTRACT FROM PUBLISHER]
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- 1998
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23. Thermoluminescence dosimetry in evaluation of liquid 32P sources for intravascular brachytherapy
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Bilski, P. l., Ochab, E., Petelenz, B., Walichiewicz, P., and Wodniecki, J.
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- 2000
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24. Assessment of the intracardiac left to right shunts with a single scintillation probe.
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Tendera, M., Bartoszewski, A., Foremny, J., Salamon, A., Wodniecki, J., and Malecka-Tendera, E.
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- 1989
- Full Text
- View/download PDF
25. Sildenafil citrate therapy for pulmonary arterial hypertension (vol 353, pg 2148, 2005)
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Manes, A., Seeger, W., Fijalkowska, A., Kramer, M. R., Peacock, A. J., Sitbon, O., Al-Hiti, H., Pulido, T., Ben-Dov, I., Frost, A. E., Zwicke, D. L., Shapiro, S. M., Keogh, A., Ickinger, C., Frantz, R. P., Hill, N. S., Ouduz, R. J., Karlocai, K., Yu, C. M., Boonstra, A., Gomez-Sanchez, M. A., Rubenfire, M., Barbera, J. A., Channick, R. N., Naeije, R., Marini, C., Berman-Rosenzweig, E., Robbins, I. M., Girgis, R. E., Tapson, V. F., Delcroix, M., Kiely, D. G., Wodniecki, J., Schauer, J., Hoeper, M., Lim, S. T., Tack, S. J., Reuter, H., Carlsen, J., Lang, C. C., Roman, A., Benza, R. L., Williams, T. J., Corris, P. A., Zaba, J. P., Apro, D., Ghali, J. K., Badesch, D. B., Rich, S., Ross, D. J., Schulze-Neick, I., Martensson, G., Antonio Augusto Lopes, Andreassen, A. K., and Super Study Grp
26. [Interventional treatment of myocardial infarction. Own experience]
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Kawecki D, Szczurek-Katański K, Jacheć W, Szyguła J, Walichiewicz P, Andrzej Tomasik, Wilczewski P, Fudal M, Rybczyk R, Glanowska G, and Wodniecki J
27. Statistical dependence of clinical data on the chosen treatment of patients with a multivessel coronary artery disease
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Walichiewicz P, Wodniecki J, Szczurek-Katański K, Wojciech Jachec, Nowalany-Kozielska E, Trzeciak P, and Janik J
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Heart Failure ,Analysis of Variance ,Chi-Square Distribution ,Hemodynamics ,Discriminant Analysis ,Coronary Disease ,Coronary Artery Disease ,Coronary Vessels ,Ventricular Function, Left ,Treatment Outcome ,Echocardiography ,Dobutamine ,Exercise Test ,Humans ,Angioplasty, Balloon, Coronary ,Coronary Artery Bypass ,Retrospective Studies - Abstract
In this study we tried to check which clinical data are connected with the choice of treatment in patients with a multivessel coronary artery disease.The data of 137 patients with a multivessel coronary artery disease, were analysed retrospectively. The patients were divided into three groups: treated conservatively, CABG and PTCA. Multivessel coronary artery disease was recognised when there were atherosclerotic changes in more a 2 vessels with a not less a 2 mm in diameter. Patients with previous CABG or a left main coronary artery disease were excluded. The data were analysed by means of several methods, variance analysis, correlation analysis, discriminant functions, chi-square test and T-Student test.For treatment decision making in multivessel coronary artery disease of statistical significance were: the state of the left anterior descendent artery below the first diagonal branch, the state of the first diagonal branch and peripheral parts of the left anterior descendent artery and right coronary artery, the systolic function of the antero-lateral, apical and phrenic segments of the left ventricle, the global left ventricular ejection fraction in angiography and echocardiography, local systolic disturbances of the left ventricular observed in echocardiography, the coexistence of symptoms of heart failure as well as unstable angina.Treatment decision making will always depend not only on diagnostic procedures but also on all the clinical data about the patient and the experience of coworking cardiology and surgery centres.
28. [Coenzyme Q--clinical significance]
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Wojciech Jachec, Wodniecki J, and Kamiński K
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Cardiovascular Diseases ,Ubiquinone ,Diabetes Mellitus ,Humans ,Musculoskeletal Diseases ,Obesity ,Endocrine System Diseases - Abstract
In the paper the clinical importance is presented of the use of coenzyme Q (ubiquinone) preparation. On the basis of available literature the participation of coenzyme Q was determined in the pathogenesis and aetiology of a number of diseases, e.g. diseases of the circulatory system, locomotor system, diabetes mellitus, obesity or endocrine system diseases.
29. Effect of metoprolol CR XL in chronic heart failure: Metoprolol CR XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF)
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Hjalmarson, A., Goldstein, S., Fagerberg, B., Wedel, H., Waagstein, F., Kjekshus, J., Wikstrand, J., Westergren, G., Hassle, A., Thimell, M., El Allaf, D., Vitovec, J., Aldershvile, J., Halinen, M., Dietz, R., Neuhaus, Kl, Janosi, A., Thorgeirsson, G., Dunselman, P., Gullestad, L., Kuch, J., Herlitz, J., Rickenbacher, P., Ball, S., Gottlieb, S., Deedwania, P., Vandenhoven, G., Novakova, I., Danker, S., Lundstrom, M., Meyer-Sabellek, W., Balla, I., Sveinsdottir, M., Dorhout, B., Hildebrandt, A., Szczurko, I., Larsson, C., Bucher, E., Scott, E., Dwyer, D., Julian, Dg, Demets, Dl, Chatterjee, K., Feyzi, J., Lehto, S., Karpati, P., Motz, W., Samuelsson, O., Viersma, Jw, Andersson, B., Berthe, C., Boutefeu, Jm, Boxho, G., Decroly, P., Derbaudrenghien, Jp, Pirlet, J., Henry, P., Heyndrickx, G., Missault, L., Nannan, M., Timmermans, P., Vachiery, Jl, Mieghem, W., Vandenbossche, Jl, Dvorak, K., Herold, M., Hradec, J., Kana, A., Petr, P., Rybka, J., Smid, J., Svitil, P., Toman, J., Agner, E., Amtorp, O., Egstrup, K., Eliasen, P., Gotzsche, Co, Hildebrandt, P., Johannesen, A., Kaiser-Nielsen, P., Nielsen, H., Nielsen, Pe, Pedersen, F., Nielsen, Jr, Skagen, K., Honkanen, T., Hussi, E., Juvonen, J., Jaaskelainen, H., Rinne, J., Salonen, T., Andresen, D., Berwing, H., Forster, A., Hauf, Gf, Krosse, B., Luderitz, B., Olshausen, Ke, Schmailzl, Kjg, Schwimmbeck, Pl, Sigmund, M., Voller, H., Czuriga, I., Hetey, M., Katona, A., Lengyel, M., Nyaradi, A., Rednik, A., Sandori, K., Szabo, P., Tarjan, J., Tenczer, J., Timar, S., Valyi, P., Veress, G., Zamolyi, K., Oze, B., Bernink, Pjlm, Bredero, Ac, Breedveld, Rw, Breuls, Pnwm, Bucx, Jjj, jan cornel, Milliano, Par, Dunselman, Phjm, Hamer, Bjb, Holwerda, Nl, Hoogsteen, J., Hoorntje, Jca, Kragten, Ja, Liem, Ah, Linssen, Gcm, Michels, Hr, Misier, Arr, Schaafsma, Hj, Sijbring, P., Taverne, Rjt, Kempen, Lhj, Stralen, R., Veldhuisen, Dj, Veerhoek, Mj, Werter, Cjpj, Wesdorp, Jcl, Willems, Ar, Withagen, Ajam, Zwart, Pag, Bjornerheim, R., Dahle, M., Dickstein, K., Froland, Gs, Gundersen, T., Hofsoy, K., Hole, Tl, Johansen, T., Mannsverk, J., Nesje, P., Omland, Tm, Sjodin, C., Smith, P., Tjonndal, Ha, Vikesdal, O., Waage, K., Jaworska, K., Kolodziej, P., Kornacewicz-Jach, Z., Krzeminska-Pakula, M., Piotrowski, Jw, Piwowarska, W., Stogowski, A., Wodniecki, J., Wrabec, K., Ahlstrom, P., Ekdahl, S., Hemmingson, Lo, Holmberg, L., Lernfelt, B., Nilsson, H., Widgren, B., Angman, K., Erne, P., Mohacsi, P., Polikar, R., Schlapfer, H., Batin, P., Berkin, Ke, Callaghan, Ts, Forfar, J., Frenneaux, M., Greenbaum, Ra, Maltz, M., Murdoch, D., Reynolds, G., Stephens, J., Struthers, A., Swan, J., Tildesley, G., Abbasi, A., Alagona, P., Alderman, J., Alipour, M., Anderson, Jl, Ansari, Z., Ashraf, M., Beanblossom, Bt, Bennett, S., Benvenuti, D., Berk, MR, Bhalla, R., Bilazarian, Sd, Browne, Kf, Buchter, Cm, Carlson, R., Carlson, Cj, Danisa, K., Dauber, I., Dewood, Ma, Dennish, G., Denny, Dm, Dibianco, R., Diller, Pm, Dunlap, M., Dowd, K., Edmiston, A., El Shahawy, M., Elkayam, U., Farnham, J., Fenster, P., Friedman, S., Heywood, T., Galichia, Jp, Geller, M., Ghali, Jk, Gheorghiade, M., Giles, T., Gillespe, R., Goldberg, G., Goldberg, Mc, Goldscher, Da, Gooden, Gp, Goodman, M., Goodman, L., Gorwit, J., Gottlieb, Ss, Gradman, A., Grech, D., Hack, T., Hall, Jh, Hattenhauer, Mt, Higginbotham, Mb, Hutchins, S., Imburgia, M., Iteld, Bj, Jackson, B., Jafri, S., Jauch, W., Jennison, S., Kahn, Bh, Kao, W., Kaplan, K., Karlsberg, R., Kennedy, Hl, Kennedy, Jj, Kirkegaard, L., Kraus, Dh, Labresh, K., Lalonde, L., Lesser, Mf, Levites, R., Levy, M., Lewis, Rk, Loh, Ik, Madyoon, H., Maislos, F., Mann, D., Maurice, Gl, Nisar, A., Old, W., Pappas, Jd, Phadke, K., Promisloff, S., Rashkow, Am, Reeves, B., Rosen, Jh, Rotman, M., Saleem, T., Savran, Sv, Shah, R., Shalev, Y., Shanes, Jg, O Shaughnessy, M., Silverman, B., Steingart, Rm, Swenson, L., Syed, K., Thadani, U., Thorsen, Rd, Tonkon, Mj, Touchon, R., Uhl, G., Vaska, Kj, Wagner, Sg, Weaver, Cj, Weiss, Rj, Wickemeyer, Wj, Willens, Hj, Wilson, Jr, Wright, R., and Yellen, L.
30. Expression of TGF-beta1 and its receptor genes (TbetaR I, TbetaR II, and TbetaR III-betaglycan) in peripheral blood leucocytes in patients with idiopathic pulmonary arterial hypertension and Eisenmenger's syndrome
- Author
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Wojciech Jachec, Foremny A, Domal-Kwiatkowska D, Smolik S, Tomasik A, Mazurek U, and Wodniecki J
31. [Statistical analysis of decision making in the treatment in two-vessel coronary artery disease]
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Walichiewicz P, Kawecki D, Szczurek-Katański K, Wojciech Jachec, Glanowska G, and Wodniecki J
- Subjects
Male ,Decision Making ,Humans ,Female ,Coronary Artery Disease ,Middle Aged ,Attitude to Health ,Choice Behavior - Abstract
The objective of this paper was to analyze the choice of treatment in two-vessel coronary artery disease and to evaluate the effectiveness of the chosen treatment. The data of sixty-five patients with two-vessel coronary artery disease was analyzed. Two-vessel coronary artery disease was recognized when critical stenoses were present in two arteries with a diameter no less than 2 mm across. Patients who had a CABG were excluded. Patients were divided into three groups according to their treatment: those treated with CABG (29 patients), those treated with coronary angioplasty (20 patients), and those treated conservatively (16 patients). The mean follow-up was 29.3 months (12-48 mo). There were two groups of data collected. The first group consisted of data which might have influenced the decision-making and state of the patients after they had been introduced to the selected treatment. The second group consisted of data necessary to evaluate the state of the patients during the follow-up period. The statistical analysis was divided into three stages. In the first stage, clinical data connected to the selected treatments was studied. In the second, the effects of the chosen treatment were examined. During the third stage of analysis, variables which influenced the effectiveness of the specific treatment were evaluated. Decision-making in patients with two-vessel coronary artery disease depended on the co-existence of hypertension, diabetes, lower-limb ischemia and earlier-performed coronary angioplasty. The only statistically important angiographic feature was the condition of the proximal LAD. Objective improvements in the states of patients (evaluated by exercise tests) were frequently connected to CABG treatment. Subjective improvements in the states of patients were more often connected to conservative treatment. Elevated cholesterol levels were connected to the progression of the disease both in those treated conservatively and interventionally.
32. Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo-controlled, multicentre trial (the EUROPA study)
- Author
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Fox, K. M., Bertrand, M., Ferrari, Roberto, Remme, W. J., Simoons, M. L., Simoons, M., Bassand, J. P., Aldershvile, J., Hildebrandt, P., Cokkinos, D., Toutouzas, P., Eha, J., Erhardt, L., Erikssen, J., Grybauskas, P., Kalnins, U., Karsch, K., Sechtem, U., Keltai, M., Klein, W., Luscher, T., Mulcahy, D., Nieminen, M., Oto, A., Ozsaruhan, O., Paulus, W., Providencia, L., Riecansky, I., Ruzyllo, W., Ferrari, R., Santini, U., Tavazzi, L., Soler Soler, J., Widimsky, P., Julian, D., Dargie, H., Murray, G., Kubler, W., Thygesen, K., Duprez, D., Steg, G., Drexel, H., Gombotz, G., Heyndrickx, G. H., Legrand, V., Materne, P., Van Mieghem, W., Bocek, P., Branny, M., Cech, M., Charouzek, J., Drazka, J., Fabik, L., Florian, J., Francek, L., Groch, L., Havranek, P., Hradec, J., Jansky, P., Jirmar, R., Jokl, I., Krejcova, H., Kvasnak, M., Maratka, T., Marcinek, G., Moravcova, J., Nedbal, P., Peterka, K., Povolny, J., Rosolova, H., Semrad, B., Sochor, K., Spacek, R., Spinar, J., Stipal, R., Stuchlik, K., Sulda, M., Ulman, J., Vaclavicek, A., Vojtisek, P., Bjerregaard Andersen, H., Kristensen, K., Madsen, J. K., Markenvard, J., Meibom, J., Norgaard, A., Scheibel, M., Leht, A., Teesalu, R., Vahula, V., Itkonen, A., Juvonen, J., Karmakoski, J., Kilkki, E., Koskela, E., Melin, J., Nieminen, M. S., Savola, R., Terho, T., Voipio Pulkki, L. M., Apffel, F., Attali, P., Barjhoux, C., Baron, B., Berthier, Y., Dambrine, P., Decoulx, E., Deshayes, P., Fouche, R., Genest, M., Godard, S., Guillot, J. P., Hanania, G., Khattar, P., Leroy, F., Mansourati, J., Piquemal, R., Quiret, J. C., Raynaud, P., Rondepierre, D., Roynard, J. L., Sudhibhasilp, S., Van Belle, E., Bilbal, A., Lauer, B., Rettig Sturmer, G., Riessen, R., Rutsch, W., Sigel, H. A., Simon, R., Von Schacky, C., Winkelmann, B. R., Avgeropoulou, C., Christakos, S., Feggos, S., Floros, S., Fotiadis, I., Goudevenos, I., Kardara, D., Karidis, C., Koliopoulos, N., Kremastinos, D., Lekakis, I., Manolis, A., Pyrgakis, V., Papanikolaou, C., Papasteriadis, E., Skoufas, P., Stravrati, A., Stavridis, A., Syribeis, S., Vardas, P., Vassiliadis, I., Voudris, V., Zobolos, S., Berenyi, I., Edes, I., Janosi, A., Kalo, E., Karpati, P., Kornel, S., Pap, I., Polak, G., Reiber, I., Rusznak, M., Tarjan, J., Timar, S., Toth, K., Barton, J., Crean, P., Daly, K., Kearney, P., Meany, T. B., Quigley, P., Antolini, R., Azzolini, P., Bellone, E., Branzi, A., Brunelli, C., Capponi, E., Capucci, A., Casaccia, M., Cecchetti, E., Ceci, V., Celegon, L., Colombo, A., Corsini, G., Cucchini, F., Dalla Volta, S., De Caterina, R., De Luca, I., De Servi, S., Di Donato, M., Di Giacomo, U., Di Pasquale, G., Fiorentini, C., Gaddi, O., Giannetto, M., Giannuzzi, P., Giordano, A., Giovannini, E., Guarnierio, M., Iacono, A., Inama, G., Leghissa, R., Lorusso, R., Marinoni, G., Marzilli, M., Mauri, F., Mosele, G. M., Papi, S., Pela, G., Pettinati, G., Polimeni, M. R., Portaluppi, Francesco, Proto, C., Renaldini, E., Riva, S., Sanguinetti, M., Santini, M., Severi, S., Sinagra, G., Tantalo, L., Vajola, S. F., Volterrani, M., Ansmite, B., Gailiss, E., Gersamija, A., Ozolina, M. A., Baubiniene, A., Berukstis, E., Grigoniene, L., Kibarskis, A., Kirkutis, A., Marcinkus, R., Milvidaite, I., Vasiliauskas, D., Aalders, J. C. A., Bruggeling, W. A. J., De Feyter, P. J., De Leeuw, M. J., De Waard, D. E. P., De Weerd, G. J., De Zwaan, C., Dijkgraaf, R., Droste, H. T., Freericks, M. P., Hagoort Kok, A. W., Hillebrand, F., Jap, W. T. J., Jochemsen, G. M., Kiemeney, F., Kuijer, P. J. P., Mannaerts, H. F. J., Piek, J. J., Saelman, J. P. M., Slob, F. D., Smits, W. C. G., Suttorp, M. J., Tan, T. B., Van Beek, G. J., Van den Merkhof, L. F. M., Van der Heyden, R., Van Hessen, M. W. J., Van Langeveld, R. A. M., Van Nierop, P. R., Van Rey, F. J. W., Van Straalen, M. J., Vos, J., Werner, H. A., Westendorp, J. J. C., Achremczyk, P., Adamus, J., Baska, J., Bolinska Soltysiak, H., Bubinski, R., Ceremuzynski, L., Cieslinski, A., Dariusz, D., Drozdowski, P., Dubiel, J. S., Galewicz, M., Halawa, B., Janion, M., Jaworska, K., Kaszewska, I., Kleinrok, A., Kornacewicz Jach, Z., Krawczyk, W., Krynicki, R., Krzciuk, M., Krzeminska Pakula, M., Kuch, J., Kuzniar, J., Liszewska Pfejfer, D., Loboz Grudzien, K., Musial, W., Opolski, G., Pasyk, S., Piwowarska, W., Pulkowski, G., Rynkiewicz, A., Sinkiewicz, W., Skura, M., Slowinski, S., Smielak Korombel, W., Targonski, R., Templin, W., Tendera, M., Tracz, W., Trusz Gluza, M., Wodniecki, J., Zalewski, M., Zinka, E., Carrageta, M., Gil, J. C., Ferreira, R., Marques, A. L., Andrade, C. M. S., Seabra Gomes, R., Bada, V., Belicova, M., Dukat, A., Kaliska, G., Kamensky, G., Micko, K., Mikes, Z., Palinsky, M., Pella, D., Renker, B., Sefara, P., Sojka, G., Sulej, P., Szakacs, M., Salcedo, J. M. A., Orcajo, N. A., Garcia, P. A., Sanpera, J. M. A., Azcarate, J. A., Mayor, J. L. B., Martinez, V. B., Coronado, J. L. B., Ojeda, F. B., Caimari, R. B., Cortada, J. B., Valderrama, J. C., Ligorit, A. D., Caliani, J. S. E., Aviles, F. F., Guerrero, J. J. G., Lopez, D. G., Cocina, E. G., Urena, C. G., Lorente, L. J., Garcia Aranda, V. L., De Miguel, C. M., Montero, J. M., Romero, P. M., Benito, I. M., Lopez, F. N., Peiro, F. N., De Ros, J. O., Mas, J. O., Bermejo, M. A. P., Peralta, L. J. P., Padial, L. R., Sanz, A. S., Bonnin, J. S., Martin, E. S., Belsue, F. V., Ekdahl, S., Forslund, L., Ohlin, H., Pieper, M., Moccetti, T., Acarturk, E., Guzelsoy, D., Turkoglu, C., Adgey, A. A. J., Ahsan, A., Al Khafaji, M., Ball, S. G., Birkhead, J., Boon, N., Brack, M., Bridges, A., Buchalter, M., Calder, B., Cooke, R. A., Corr, L., Cowell, R., Curzen, N. P., Davidson, C., Davies, J., De Belder, M. A., Dhiya, L., Doig, J. C., Findlay, I. N., Francis, C. M., Glancy, J. M., Greenwood, T. W., Groves, P., Hall, A. S., Hamilton, G., Haq, I., Hillman, R., Hubbard, W., Hudson, I., Hutton, I., Ilsley, C., Innes, M., James, M., Jennings, K., Johnston, G., Jones, C. J. H., Joy, M., Keeling, P., Kooner, J., Lawson, C., Levy, R. D., Lip, G., Mclachlan, B., Montgomery, H. E., Morley, C. A., Murdoch, D. L., Muthusamy, R., Oakley, G. D. G., Penny, W., Percival, R., Purvis, J., Pye, M. P., Ramsdale, D., Roberts, D. H., Rozkovec, A., Salmassi, A. M., Saltissi, S., Sardar, S., Shapiro, L. M., Schofield, P. M., Stephens, J., Shakespeare, C., Srivastava, S., Swan, J. W., Tildesley, G., Travill, C., Wilkinson, P. R., Fratacci, M. D., Lerebours, G., and Deckers, J.
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Relative risk reduction ,Male ,medicine.medical_specialty ,Myocardial Infarction ,Angiotensin-Converting Enzyme Inhibitors ,Coronary Disease ,Coronary artery disease ,Double-Blind Method ,Internal medicine ,Cause of Death ,Clinical endpoint ,Perindopril ,Medicine ,Humans ,Myocardial infarction ,Heart Failure ,Ejection fraction ,business.industry ,General Medicine ,Middle Aged ,medicine.disease ,Heart Arrest ,Treatment Outcome ,Cardiovascular Diseases ,Heart failure ,ACE inhibitor ,Cardiology ,Female ,business ,circulatory and respiratory physiology ,medicine.drug ,Follow-Up Studies - Abstract
Background Treatment with angiotensin-converting-enzyme (ACE) inhibitors reduces the rate of cardiovascular events among patients with left-ventricular dysfunction and those at high risk of such events. We assessed whether the ACE inhibitor perindopril reduced cardiovascular risk in a low-risk population with stable coronary heart disease and no apparent heart failure. Methods We recruited patients from October, 1997, to June, 2000. 13655 patients were registered with previous myocardial infarction (64%), angiographic evidence of coronary artery disease (61%), coronary revascularisation (55%), or a positive stress test only (5%). After a run-in period of 4 weeks, in which all patients received perindopril, 12218 patients were randomly assigned perindopril 8 mg once daily (n=6110), or matching placebo (n=6108). The mean follow-up was 4.2 years, and the primary endpoint was cardiovascular death, myocardial infarction, or cardiac arrest. Analysis was by intention to treat. Findings Mean age of patients was 60 years (SD 9), 85% were male, 92% were taking platelet inhibitors, 62% beta blockers, and 58% lipid-lowering therapy. 603 (10%) placebo and 488 (8%) perindopril patients experienced the primary endpoint, which yields a 20% relative risk reduction (95% CI 9-29, p=0.0003) with perindopril. These benefits were consistent in all predefined subgroups and secondary endpoints. Perindopril was well tolerated. Interpretation Among patients with stable coronary heart disease without apparent heart failure, perindopril can significantly improve outcome. About 50 patients need to be treated for a period of 4 years to prevent one major cardiovascular event. Treatment with perindopril, on top of other preventive medications, should be considered in all patients with coronary heart disease.
33. Comparison of fondaparinux and enoxaparin in acute coronary syndromes
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Yusuf, S., Mehta, S. R., Bassand, J. P., Budaj, A., Chrolavicius, S., Fox, K. A. A., Granger, C. B., Joyner, C., Peters, R. J. G., Wallentin, L., Avezum, A., Boden, W., Cardona, E., Ceremuzynski, L., Col, J., Commerford, P. J., Diaz, R., Faxon, D., Flather, M., Fodor, G., Franzosi, M. G., Granger, C., Halon, D., Hunt, D., Karatzas, N., Keltai, M., Kenda, M., Kim, J. H., Lanas, F., Lau, C. P., Lewis, B. S., Morais, J., Moccetti, T., Pais, P., Paolasso, E., Parkhomenko, A., Petrauskiene, B., Piegas, L., Pipilis, A., Robaayah, D., Ruda, M., Rumboldt, Z., Rupprecht, H. J., Sitkei, E., Steg, P. G., Swahn, E., Theroux, P., Valentin, V., Varigos, J., Weitz, J., White, H., Widimsky, P., Xavier, D., Zhu, J. R., Ameriso, S., Bonilla, C., Braekken, S., Chan, Y. K., Chen, W., Chenniappan, M., Cohen, E., Cottin, Y., Csiba, L., Czepiel, A., Raedt, H., Finet, G., Gardinale, E., Gaxiola, E., Gorecki, A., Gregor, P., Happola, O., Heras, M., Himbert, D., Irkin, O., Isaaz, K., Iyengar, S. S., Kalvach, P., Kevers, L., Klosiewicz-Wasek, B., Laine, M., Leys, D., Lundstrom, E., Lusic, I., Lutay, Y., Maggioni, A., Massaro, A., Mayosi, B. M., Moulin, T., Narendra, J., Naslund, U., Peeters, A., Penicka, M., Perakis, A., Petersen, P., Polic, S., Radhakrishnan, S., Renkin, J., Stockins, B., Sundararajan, R., Thygesen, K., Turazza, F., Belle, E., Vik-Mo, H., Zaborski, J., Sleight, P., Anderson, J. L., Johnstone, D. E., Hirsh, J., Demets, D., Holmes, D. R., Meeks, B., Afzal, R., Pogue, J., Boccalon, S., Chrysler, K., Cracknell, B., Horsman, C., Hoskin, T., Jedrzejowski, B., Johnson, J., Kotlan, S., Lawrence, M., Smiley, M., Stevens, C., Yallup, R., Connolly, S., Demers, C., Devereaux, P. J., Healey, J., Lonn, E., Magloire, P., Mckelvie, R., Morillo, C., Natarajan, M., Rokoss, M., Teo, K., Valettas, N., Velianou, J., Albisu, J. P., Amuchastegui, M., Bello, F. A., Bluguermann, J. J., Bono, J. O., Caccavo, A., Carlevaro, O. O., Cassettari, A., Cuneo, C., Farras, H. A., Fuselli, J., Garrido, M., Guerrero, R., Hasbani, E., Hominal, M. A., Hrabar, A., Marquez, L. L., Luciardi, H. L., Riera, L. M., Marzetti, E. M., Memoli, R., Nordaby, R., Orlandini, A. D., Perez, M., Piasentin, J. A., Ramos, H. R., Risolo, A. M., Sala, J., Salomone, O., Schygiel, P. O., Ubaldini, J., Vico, M., Amerena, J., Arnolda, L., Aroney, G., Boyd, P., Cahill, P., Chew, D., Counsell, J. T., Cross, D., Edington, J., Fitzpatrick, D., Hicks, P., Horowitz, J. D., Horrigan, M. C. G., New, G., Owensby, D., Schoeman, M., Thompson, P., Tulloch, G., Waites, J., Whelan, A., Ziffer, R., Huber, K., Jordanova, N., Al Shawafi, K., Convens, C., Coussement, P., Meester, A., El Allaf, D., Janssens, L., Marcovitch, O., Muyldermans, L., Roosen, J., Soeur, F., Lierde, J., Vrolix, M., Leaes, P., Carvalho, A. C., Schramm, E. C., Mora, R. D., Amino, J. D., Dutra, O., Manenti, E. R. F., Gun, C., Saraiva, J. F. K., Hayashi, E. K., Lichter, A., Lima, A., Marin-Neto, J. A., Teixeira, S. P. M., Abrantes, J. A. M., Baracioli, L. M., Nicolau, J. C., Maia, L. N., Jaeger, C. P., Esteves, J. P., Rabelo, A., Ramos, R. F., Reis, G., Rossi, P., Dos Santos, F. R., Teixeira, M. S., Silveira, D. S., Lemos, Mabt, Timerman, A., Greque, G. V., Vaz, R., Bhargava, R., Brons, S., Colclough, M., Constance, C., Costi, P., Dacyk, A., Davies, T., Diodati, J., Dupuis, R., Elliott, H., Fell, D. A., Fung, A. Y., Gladstone, P. J. S., Gosselin, G., Grondin, F., Huynh, T., Janzen, I., Kalaparambath, T., Kornder, J., Kouz, S., Kuritzky, R., Labelle-Stimac, S., Lamothe, M., Lauzon, C., Lemay, M., Ma, P., Maccallum, G. C., Mccallum, A., Mitchell, D., Montigny, M., Nguyen, N., Pearce, M., Pistawka, K. J., Rebane, T., Roy, M., Senaratne, M., Smith, J., Stimac, J., Traboulsi, M., Vizel, S., Weeks, A., Zadra, R., Zimmerman, R. H., Alcaino, M. E., Castro, P., Chen, J., Chen, J. L., Fan, W., Ge, J., Hu, D., Huang, J., Jingxuan, G., Ke, Y., Ma, H., Wu, Y., Yingxian, S., Yu, B., Zhu, W., Bakula, M., Bergovec, M., Lukin, A., Milicevic, G., Padovan, M., Raguz, M., Aschermann, M., Belohlavek, J., Bocek, P., Branny, M., Budesinsky, T., Groch, L., Holm, F., Jansky, P., Jelinek, P., Jirka, V., Kaislerova, M., Konecny, P., Lisa, L., Maly, M., Marcinek, G., Oscipovsky, M., Stumar, J., Vacha, M., Nielsen, T., Vigholt, E., Laanmets, P., Soopold, U., Voitk, J., Naveri, H., Niemela, M., Peuhkurinen, K., Tuomainen, P., Ylitalo, A., Py, A., Amat, G., Bessede, G., Boschat, J., Carrie, D., Charbonnier, B., Coliet, J. P., Dambrine, P., Dubois-Rande, J. L., Ferrari, E., Fouche, R., Grollier, G., Jaboureck, O., Ketelers, R., Khalife, K., Leroy, F., Lognone, T., Macquin-Mavier, I., Montalescot, G., Pacouret, G., Poulard, J. E., Puel, J., Richard, M., Schiele, F., Bischoff, K. O., Buerke, M., Buerke, U., Dominick, K., Drexler, H., Feiler, A., Guelker, H., Haltern, G., Katus, H. A., Klauss, V., Klutmann, M., Koeth, O., Meinhardt, G., Muenzel, T. M., Nitschke, T., Offterdinger, M., Rieber, J., Schieffer, B., Stangl, K., Stangl, V., Vom Dahl, J., Witzenbichler, B., Zeymer, U., Alexopoulos, D., Blassopoulou, N., Christon, A., Fotiadis, I., Foussas, S., Grapsas, N., Moschos, N., Papasteriadis, E., Symeonidis, D., Tyrologos, A., Leung, W. S., Li, S. K., Arabadzisz, H., Csikazs, J., Dancs, T., Davidovits, Z., Edes, I., Farkas, E., Herczeg, B., Janos, S., Janosi, A., Kadar, A., Kis, E., Kristof, E., Lupkovics, G., Mark, L., Nagy, A., Nagy, L., Poor, F., Regos, L., Sebo, J., Tomcsanyi, J., Toth, K., Bharani, A., Chidambaram, N., Haridas, K. K., Jain, A., Jain, P. R. K., Jaison, T. M., Kerkar, P. G., Naik, S., Nambiar, A., Panwar, R. B., Parikh, K., Puri, V. K., Rajesh, T., Ramesh, M., Singh, B., Thanikachalam, S., Tongia, R. K., Varma, S., Barbiero, M., Bardelli, G., Bernardi, D., Bolognese, L., Capponi, L., Ferrari, G., Fanelli, R., Frediani, L., Galli, M., Izzo, A., Lombardi, A., Maresta, A., Martinoni, A., Melloni, C., Meneghetti, P., Mennuni, M., Moretti, L., Orlandi, M., Pancaldi, L. G., Petronzelli, S., Piovaccari, G., Salvioni, A., Severini, D., Terrosu, P., Zanini, R., Erglis, A., Kalnins, U., Verboenko, J., Zakke, I., Kugiene, R., Zaliunas, R., Bin Othman, A., Chee, K. H., Hian, S. K., Gutierrez, A. C., Diaz, A. C., Garcia-Castillo, A., Guerrero, M. C., Morales, C. L., Ramos-Lopez, G., Baldew, S. C., Basart, D. C. G., Clappers, N., Daniels, M. C. G., Weerd, G. J., Den Hartog, F. R., Hendriks, Ihgm, Herrman, J. P. R., Kofflard, M., Krasznai, K., Michels, H. R., Stoel, I., Ten Berg, J. M., Umans, Vawn, Beek, G. J., Daele, Merm, Den Berg, B. J., Hessen, M. W. J., Kalmthout, P. M., Rossum, P., Verheugt, F. W. A., Viergever, E. P., Withagen, Ajam, Achremczyk, P., Arasimowicz, P., Baranowska, T., Biegayto, J., Bronisz, M., Buszman, P., Dalkowski, M., Dluzniewski, M., Gessek, J., Goch, J. H., Janik, K., Janion, M., Kawecki, D., Kleinrok, A., Komorowski, P., Krasowski, W., Krauze-Wielicka, M., Malinowski, S., Nowak, T., Nowakowski, P., Ogorek, M., Piepiorka, M., Pluta, W., Puzio, E., Puzniak, M., Rekosz, J., Rybka, P., Sendrowski, D., Siminiak, T., Skura, M., Stopinski, M., Szetemej, R., Szolkiewicz, M., Szpajer, M., Trusz-Gluza, M., Waszyrowski, T., Wita, K., Wodniecki, J., Wojewoda, P., Zambrzycki, J., Zielinski, Z., Cardoso, P., Carrageta, D. M., Ferreira, D., Gomes, M. V., Santos, L., Arkhipov, M., Belousov, Y., Charchoglyan, R., Gordeev, I. G., Gratsiansky, N. A., Grinshtein, Y., Khrustalev, O., Kokorin, V. A., Komarov, A., Kozulin, V., Minushkina, L. O., Panchenko, E., Panov, A., Petrik, E. S., Shakhnovich, R. M., Shalaev, S. V., Sukhinina, T. S., Trifonov, I. R., Zateyshchikov, D. A., Khoo, B. C. H., Tan, H. C., Tan, R. S., Hricak, V., Motovska, Z., Poliacik, P., Kanic, V., Kovacic, D., Kranjec, I., Voga, G., Bayat, J., Essop, M. R., Maritz, F., Marx, J. D., Ntsekhe, M., Pretorius, M. P., Ranjith, N., Theron, H., Chae, I. H., Chae, S. C., Choe, K. H., Chung, N. S., Jeong, M. H., Kim, C. J., Kim, H. S., Kim, W., Rhim, C. Y., Shin, E. K., Shin, G. J., Alameda, M., Alonso-Orcajo, N., Bethencourt, A., Calvo, F., Avellaneda, J. L. C., Delgado, V., Diaz-Castro, O., Esplugas, E., Faus, R., Antonio Fernandez-Ortiz, Frutos, A., Goirena, P., Iglesias, F. C., Llorian, A. R., Macaya, C., Mancisidor, X., Melgares, R., Pascual, C., Ruiz-Nodar, J. M., Simon, J. M., Agewall, S., Ahlstrom, P., Ali, M., Andersson, L., Bandh, S., Digerfeldt, C., Ericsson, H., Forsgren, M., Jabro, J., Janzon, M., Joborn, H., Johnston, N., Karlsson, J. E., Larsson, L. E., Linderfalk, C., Lonnberg, I., Mooe, T., Oldgren, J., Pihl, E., Risenfors, M., Sjolund, E., Soderberg, I., Stjerna, A., Svennberg, L., Wodlin, P., Pagnamenta, A., Pieper, M., Rossi, M. G., Weber, K., Peng, M. C., Cheng, J. J., Chiang, F. T., Kuo, C. T., Tseng, C. D., Andreyeshcheva, I., Dzyak, G. V., Fedtchouk, L., Gontar, A., Karpenko, O., Kononenko, L., Koval, E. A., Kovalsky, I., Kraitz, I., Netiazhenko, V., Polyvoda, S., Prokopenko, Y., Prudkiy, I., Rudenko, L., Serediuk, N., Zolotaykina, V., Adgey, J., Ahsan, A., Brack, M., Bridges, A. B., Burton, J., Findlay, I., Fluck, D. S., Radford, L., Robson, R. H., Senior, R., Starkey, I. R., Alexander, J., Baber, Z., Campbell, M., Caputo, R., Chandna, H., Chandrashekhar, Y., Chu, A., Deraad, R. E., Druken, B., Goyal, A., Holly, D., Kemp, A., Kotlaba, D., Levine, M. J., Miller, G. P., Nygaard, T., Parikh, D. K., Ramos, C., Rivera, E., Rodriguez, R., Sangani, B., Walder, J. S., and Oasis
34. Impact of baseline level of 7-ketocholesterol on the rate of coronary reintervention in coronary artery disease patients--results of an observational study with questionnaire-based follow up
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Andrzej Tomasik, Jacheć W, Skrzep-Poloczek B, Wojciechowska C, Tarnawski R, Wodniecki J, Poloński L, and Szczurek-Katański K
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Male ,Superoxide Dismutase ,Models, Cardiovascular ,Coronary Disease ,Middle Aged ,Lipids ,Cross-Sectional Studies ,Case-Control Studies ,Surveys and Questionnaires ,Humans ,Female ,Angioplasty, Balloon, Coronary ,Ketocholesterols ,Biomarkers ,Aged ,Follow-Up Studies - Abstract
The aim of study was to assess the relation between plasma level of one of the oxysterols--7-ketocholesterol and angiographically evidenced coronary artery disease.We measured plasma level of 7-ketocholesterol, malondialdehyde, total cholesterol, HDL cholesterol, triglycerides, erythrocyte activity of superoxide dismutase in 233 patients who previously underwent coronary angiography for diagnosis of coronary artery disease. The follow-up of patients (28 months) was done on basis of questionnaires sent out to them.We found that the subgroup of patients with 7-ketocholesterol above the median value (62 ng/mL) has higher rate of coronary reintervention (8/54 pts vs. 5/43 pts in 7-ketocholesterol below 62 ng/mL respectively, p = 0.284 Log-rank test). The finding was more pronounced, yet insignificant, in the subgroup of patients who underwent primary PTCA (6/19 pts vs. 2/20 pts, p = 0.1 Log-rank test). There were 3 patients in high 7-ketocholesterol subgroup who entered the study with previously undergone primary coronary intervention. There were not such patients in low 7-ketocholesterol subgroup. 4 deaths were observed in high 7-ketocholesterol subgroup, and one in low 7-ketocholesterol subgroup (they were predominantly not of cardiovascular origin).We failed to find a significant relation between 7-ketocholesterol and coronary artery disease, though there is a trend of such relation in patients who undergo PTCA, evidenced by a slightly higher number of repeated revascularizations among patients with high 7-ketocholesterol. The study indicates the areas of further studies with agents capable of lowering oxysterols and assessing also other end points.
35. [Sildenafil reduces pressure and pulmonary resistance and increases susceptibility of pulmonary arteries to nitric oxide in primary pulmonary arterial hypertension]
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Wodniecki J, Jacheć W, Poloński L, Ar, Tomasik, Celina Wojciechowska, and Foremny A
36. Application of Fourier row as a method to analyze circadian heart rate course in patients with left ventricle ejection fraction impairement,Zastosowanie szeregu Fouriera do analizy dobowego przebiegu akcji serca u pacjentów z upośledzeniem frakcji wyrzutowej lewej komory serca
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Walichiewicz, P., Mrózek, A., Rozentryt, P., Wilczek, K., Wojciech Jacheć, Wodniecki, J., Szyguła, E., and Wantrych, M.
37. [Use of fourier row as a method for analyzing the course of circadian heart rate in patients with left ventricular ejection fraction impairment]
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Walichiewicz P, Mrózek A, Rozentryt P, Wilczek K, Wojciech Jachec, Wodniecki J, Szyguła E, and Wantrych M
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Adult ,Male ,Ventricular Dysfunction, Left ,Fourier Analysis ,Echocardiography ,Heart Rate ,Electrocardiography, Ambulatory ,Humans ,Female ,Stroke Volume ,Circadian Rhythm - Abstract
The circadian heart rate course was assessed in 3 groups of patients with left ventricular ejection fraction (LVEF) 10-15%, 20-25% and 30-35%. The study comprised 36 persons. In 9 patients heart failure was due to MI and in 17--to dilated cardiomyopathy. Those with atrial fibrillation, ventricular tachycardia, supraventricular tachycardia, diabetes, valvular heart diseases and with central system disorders were excluded from the study. Left ventricular ejection fraction was evaluated by echocardiography. Heart rate, calculated as a mean value every 5 minutes, was taken in patients during 24 hour recordings. For each patient separately, mean value of all measurement was calculated. Then a ratio of each actual value to the mean value was calculated. This ratio was defined as relative heart rate; [formula: see text] Circadian heart rate courses were approximated by Fourier row: [formula: see text]. The 24 harmonics were analyzed. Statistically significant differences in circadian courses were closed to amplitudes of 1st, 12th, 13th, 14th, 16th, 18th harmonics. Using test of variance homogeneity it has been demonstrated that variability of amplitudes of 12th and 17th harmonics as well as phase of 5th harmonic depend on left ventricular ejection fraction.
38. Gallium-67 scintigraphy as a valuable test in qualifying patients with clinically suspected myocarditis for myocardial biopsy
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Wojnicz, R, Nowalany-Kozielska, E, Szewczyk, M, Szczurek-Katański, K, Walichiewicz, P, Niklewski, T, Poloński, L, and Wodniecki, J
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- 1999
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39. Neopterin and beta-2 microglobulin relations to immunity and inflammatory status in nonischemic dilated cardiomyopathy patients.
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Wojciechowska C, Wodniecki J, Wojnicz R, Romuk E, Jacheć W, Tomasik A, Skrzep-Poloczek B, Spinczyk B, and Nowalany-Kozielska E
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- Adult, Female, HLA-A Antigens metabolism, HLA-B Antigens metabolism, HLA-C Antigens metabolism, HLA-DR Antigens metabolism, Humans, Immunity physiology, Inflammation blood, Inflammation metabolism, Male, Middle Aged, Myocardium metabolism, Cardiomyopathy, Dilated blood, Cardiomyopathy, Dilated immunology, Neopterin blood, Neopterin immunology, beta 2-Microglobulin metabolism
- Abstract
Background: The aim of the study was to assess the relationships among serum neopterin (NPT), β2-microglobulin (β2-M) levels, clinical status, and endomyocardial biopsy results of dilated cardiomyopathy patients (DCM)., Methods: Serum NPT and β-2 M were determined in 172 nonischaemic DCM patients who underwent right ventricular endomyocardial biopsy and 30 healthy subjects (ELISA test). The cryostat biopsy specimens were assessed using histology, immunohistology, and immunochemistry methods (HLA ABC, HLA DR expression, CD3 + lymphocytes, and macrophages counts)., Results: The strong increase of HLA ABC or HLA DR expression was detected in 27.2% patients-group A-being low in 72.8% patients-group B. Neopterin level was increased in patients in group A compared to healthy controls 8.11 (4.50-12.57) versus 4.99 (2.66-8.28) nmol/L (P < 0.05). β-2 microglobulin level was higher in DCM groups A (2.60 (1.71-3.58)) and B (2.52 (1.51-3.72)) than in the control group 1.75 (1.28-1.96) mg/L, P < 0.001. Neopterin correlated positively with the number of macrophages in biopsy specimens (P < 0.05) acute phase proteins: C-reactive proteins (P < 0.05); fibrinogen (P < 0.01); and NYHA functional class (P < 0.05) and negatively with left ventricular ejection fraction (P < 0.05)., Conclusions: Neopterin but not β-2 microglobulin concentration reflected immune response in biopsy specimens. Neopterin correlated with acute phase proteins and stage of heart failure and may indicate a general immune and inflammatory activation in heart failure.
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- 2014
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40. [Body mass index influence on aortic valve stenosis].
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Swierszcz J, Dubiel JS, Krzysiek J, Sztefko K, Galicka-Latała D, Pfitzner R, Podolec P, and Wodniecki J
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- Adult, Aged, C-Reactive Protein metabolism, Cholesterol blood, Cholesterol, HDL blood, Cholesterol, LDL blood, Disease Progression, Female, Humans, Lipoproteins blood, Male, Middle Aged, Triglycerides classification, Ultrasonography, Aortic Valve diagnostic imaging, Aortic Valve Stenosis diagnostic imaging, Aortic Valve Stenosis metabolism, Body Mass Index
- Abstract
Aim: The 12 months' observation of body mass index (BMI) influence on natural course of aortic valve stenosis (AVS)., Patients: 60 AVS patients who did not agree for operational treatment were divided into group A (n = 15) with BMI 20-25, group B (n = 27) with BMI 25,01-30 and group C BMI > 30., Methods: Plasma Lp(a), total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides and C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha) as well as titers of immunoglobulin (Ig) class G, A, M against chlamydia pneumoniae were measured every 12 months. Echo-cardiographic evaluation of aortic valve was also done every 12 months., Results: Means serum CRP at 12 month was the highest in group C. No differences in mean serum TNF-alpha and IL-6 levels as well as in Ig titers between groups A, B, C were found. At 12 month of observation HDL/total cholesterol ratio as well as HDL/LDL-cholesterol ratio were the lowest in group B. Left atrium diameter and right ventricle diameter were bigger in groups B and C compared to group A at the visit I and after 12 months of observation. Systolic intraventricular septum (IVS syst) thickness was the highest in group C at visit I. Diastolic left ventricle posterior wall thickness (LVPW) was the highest in group C during 12 months of observation., Conclusion: The increase in fat tissue mass may lead to increase in inflammatory process and cardiac muscle remodeling in AVS patients.
- Published
- 2011
41. [Comparison of echocardiographic findings in AVS patients with and without high IgG, IgM, IgA titers against Chlamydia pneumoniae during 12 months' observation of AVS natural course].
- Author
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Swierszcz J, Dubiel JS, Krzysiek J, Sztefko K, Galicka-Latała D, Roman P, Podolec P, and Wodniecki J
- Subjects
- Adult, Aged, Disease Progression, Echocardiography, Female, Humans, Male, Middle Aged, Aortic Valve Stenosis diagnostic imaging, Aortic Valve Stenosis immunology, Chlamydophila pneumoniae immunology, Immunoglobulin A blood, Immunoglobulin G blood, Immunoglobulin M blood
- Abstract
Aim: Comparison of echocardiographic findings in AVS patients with and without high IgG, IgM, IgA titers against Chlamydia pneumoniae during 12 months' observation of AVS natural course., Patients: 60 AVS patients who did not agree for operational treatment were divided into group A (30 patients with high IgG titer) group B (30 patients with low IgG titer), group C (22 patients with high IgA titer) group D (38 patients with low IgA titer), group E (7 patients with high IgM titer), group F (53 patients with low IgA titer) Antibodies titers and echocardiographic scans were carried out every 12 months., Results: There were more (p < 0.02) patients with AVS deterioration in group A compared to group B. Group A patients had lower left ventricle posteriori wall systolic diameter compared to group B. There were no differences in echocardiographic parameters between group C and D. Mean ejection fraction was lower and mean right atrium diameter was higher in group E compared to group F., Conclusion: The results may suggest link between Chlamydia pneumoniae and deterioration of AVS.
- Published
- 2011
42. [One year observation of natural course of aortic valve stenosis in patients with normal and abnormal lipoprotein (a) plasma level].
- Author
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Swierszcz J, Dubiel JS, Milewicz T, Sztefko K, Galicka-Latała D, Pfitzner R, Wodniecki J, and Krzysiek J
- Subjects
- Adult, Aged, C-Reactive Protein metabolism, Cholesterol blood, Cholesterol, HDL blood, Disease Progression, Female, Follow-Up Studies, Humans, Immunoglobulin A blood, Immunoglobulin G blood, Immunoglobulin M blood, Interleukin-6 blood, Male, Middle Aged, Risk Factors, Tumor Necrosis Factor-alpha blood, Aortic Valve Stenosis blood, Lipoprotein(a) blood
- Abstract
Aim: The observation of natural course of aortic valvae stenosis (AVS) in patients with high lipoprotein (a) [Lp(a)]., Patients: 60 AVS patients who did not agree for operational treatment were divided into group A (n = 19) with high serum Lp(a) level and into group B (n = 41) with normal plasma Lp(a) level., Methods: Plasma Lp(a), total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides and C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor (TNF-alpha) as well as titers of immunoglobulin (Ig) class G, A, M against chlamydia pneumoniae were measured every 12 months. Echocardiographic evaluation of aortic valve was also done every 12 months., Results: Means serum CRP at 12 month was higher in group A. Mean serum TNF-alpha level was also higher at visit I and at 12 month (visit II) in group A. Mean serum IL-6 level did not differ between groups. IgG titer was higher in group A at visit I and visit II. At 12 month of observation HDL-cholesterol plasma level was lower in group A. HDL/total cholesterol ratio as well as HDL/LDL-cholesterol ratio was laso lower in group A at 12 month of observation. No statistically significant differences in echocardiographic parameters were founf between groups., Conclusion: The results may suggest risk factors similarity of AVS and atherosclerosis.
- Published
- 2010
43. [Natural course of aortic valve stenosis in patients with normal and abnormal lipid profile].
- Author
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Swierszcz J, Dubiel JS, Milewicz T, Sztefko K, Galicka-Latała D, Pfitzner R, Wodniecki J, and Krzysiek J
- Subjects
- Adolescent, Adult, Aged, Child, Child, Preschool, Cholesterol metabolism, Cholesterol, HDL metabolism, Cholesterol, LDL metabolism, Disease Progression, Echocardiography, Female, Humans, Male, Metabolome, Middle Aged, Risk Factors, Young Adult, Aortic Valve Stenosis complications, Aortic Valve Stenosis diagnostic imaging, Aortic Valve Stenosis metabolism, Hypercholesterolemia complications, Lipid Metabolism
- Abstract
Aim: Comparison of echocardiographic findings in AVS patients with and without hypercholesterolemia during 12 months' observation of AVS natural course., Patients: 60 AVS patients who did not agree for operational treatment were divided into group A (n = 47) with high serum total cholesterol and into group B (n = 13) with normal plasma cholesterol., Methods: plasma total cholesterol, HDL-cholesterol, LDL-cholesterol, tri-glycerides and lipoprotein (a) were measured every 12 months and echocardiographic evaluation of aortic valve was also done every 12 months., Results: Means total cholesterol did not change in group A, while increased in group B. HDL-cholesterol decreased in group A and LDL-cholesterol increased in group B. Mean TG and Lp(a) levels did not change in both groups. Increase in AOG max and AOG mean as well as V max were found only group A. LVPW syst increase was found in group A. LA diameter increased and AVA decreased only in group A., Conclusion: The results may suggest risk factors similarity of AVS progression and atherosclerosis.
- Published
- 2010
44. Expression of TGF-beta1 and its receptor genes (TbetaR I, TbetaR II, and TbetaR III-betaglycan) in peripheral blood leucocytes in patients with idiopathic pulmonary arterial hypertension and Eisenmenger's syndrome.
- Author
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Jachec W, Foremny A, Domal-Kwiatkowska D, Smolik S, Tomasik A, Mazurek U, and Wodniecki J
- Subjects
- Adolescent, Adult, Aged, Child, Female, Hemodynamics, Humans, Leukocytes pathology, Male, Middle Aged, Protein Serine-Threonine Kinases genetics, Protein Serine-Threonine Kinases metabolism, Proteoglycans genetics, Proteoglycans metabolism, Pulmonary Artery pathology, Receptor, Transforming Growth Factor-beta Type I, Receptor, Transforming Growth Factor-beta Type II, Receptors, Transforming Growth Factor beta metabolism, Eisenmenger Complex genetics, Gene Expression Regulation, Hypertension, Pulmonary genetics, Leukocytes metabolism, Pulmonary Artery metabolism, Receptors, Transforming Growth Factor beta genetics, Transforming Growth Factor beta1 genetics
- Abstract
Idiopathic pulmonary arterial hypertension (IPAH) is characterized by smooth muscle cell, endothelial cell, and fibroblast hypertrophy and an increase in extracellular matrix volume in pulmonary precapillary arterioles. These features lead to a gradual increase of pulmonary vascular resistance, right-heart failure, and premature death. Bone morphogenetic protein receptor type 2 (BMPR-2) gene mutations have been identified to cause IPAH. BMPR-2 receptor mutation results in BMP signalling pathway termination and leads to disturbed growth and differentiation of pulmonary circulation cells. Transforming growth factor (TGF)-beta1 inhibits the migration and proliferation of endothelial and smooth muscle cells, and stimulates their differentiation, thus it has antiinflammatory and immunosuppressive properties, inhibiting vascular remodeling and is responsible for extracellular matrix production. The aim of this study was to analyse the profile of TGF-beta1 and the expression of its receptor (TbetaR I, TbetaR II and TbetaR III-betaglycan) genes in IPAH and in secondary forms of pulmonary arterial hypertension [Eisenmenger's syndrome (ES) patients]. Twenty-one patients with IPAH (2 men), 12 ES patients, and 10 healthy controls were enrolled in the study. QRT-PCR analysis of the transcriptive activity of TGF-beta1 and its receptor genes was performed with each patient. There were differences in receptor gene expression among the patient groups. The highest expression was observed in Eisenmenger syndrome patients (approximately 5-to 8-fold increase). There was a negative correlation between the gene expression of TGF-beta1 and that of its receptors, and a positive correlation between TbetaR II and TbetaR III in healthy controls. In IPAH patients a positive correlation between TGF-beta1 and TbetaR I was found. There was a difference in expression of TGF-beta1/receptor gene ratios and expression of receptor gene ratios between the examined groups. The differences in expression between IPAH and ES patients might suggest the role of these cytokines in IPAH pathogenesis. A disturbed proportion of expression of TGF-beta1 and receptor genes in IPAH patients might be one of the pathogenetic factors of the disease.
- Published
- 2008
45. [Familial hypertrophic cardiomyopathy--a case report].
- Author
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Domal-Kwiatkowska D, Glanowska G, Smolik S, Wilczewski P, Mazurek U, Nowalany-Kozielska E, Fudal M, and Wodniecki J
- Subjects
- Adult, Aged, DNA Mutational Analysis methods, Female, Genotype, Humans, Male, Pedigree, Phenotype, Polymorphism, Genetic, Cardiomyopathy, Hypertrophic, Familial diagnosis, Cardiomyopathy, Hypertrophic, Familial genetics, Genetic Predisposition to Disease, Ventricular Myosins genetics
- Abstract
Genetic profile od four-generation family with hypertrophic cardiomyopathy is presented. The alterations in the MYH7 gene sequences were identified. Genetic background of familial hypertrophic cardiomyopathy is reviewed and discussed.
- Published
- 2006
46. Adjunctive therapy with low-molecular-weight heparin in patients with chronic heart failure secondary to dilated cardiomyopathy: one-year follow-up results of the randomized trial.
- Author
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Wojnicz R, Nowak J, Szyguła-Jurkiewicz B, Wilczek K, Lekston A, Trzeciak P, Nowalany-Kozielska E, Zembala M, Wodniecki J, and Poloński L
- Subjects
- Adult, Anticoagulants administration & dosage, Anticoagulants adverse effects, Cardiac Output, Low diagnostic imaging, Cardiac Output, Low physiopathology, Cardiovascular Agents therapeutic use, Chronic Disease, Drug Administration Schedule, Drug Therapy, Combination, Echocardiography, Enoxaparin administration & dosage, Enoxaparin adverse effects, Female, Follow-Up Studies, Humans, Male, Middle Aged, Natriuretic Peptide, Brain blood, Peptide Fragments blood, Pilot Projects, Survival Analysis, Systole, Treatment Outcome, Ventricular Function, Left, Anticoagulants therapeutic use, Cardiac Output, Low drug therapy, Cardiac Output, Low etiology, Cardiomyopathy, Dilated complications, Enoxaparin therapeutic use
- Abstract
Background: Defective endothelial function has been shown in dilated cardiomyopathy. Therefore, improvement in endothelial function after low-molecular-weight heparin (LMWH) therapy may be clinically beneficial. Consequently, the effect of adjunct enoxaparin, a LMWH, on standard treatment of dilated cardiomyopathy was investigated., Methods: This was a randomized, standard treatment-controlled, 2-center pilot trial of 102 patients (52 receiving adjunctive therapy with enoxaparin at a dosage of 1.5 mg/kg daily for 3 months and 50 receiving standard therapy with angiotensin-converting enzyme inhibitors, beta-blockers, and diuretics alone) with stable chronic heart failure secondary to dilated cardiomyopathy (New York Heart Association [NYHA] class II and III; left ventricular [LV] ejection fraction, < or = 40%). All patients underwent coronary angiography and endomyocardial biopsy and were clinically stable for at least 6 months before enrollment. The combined primary end point included mortality, urgent heart transplantation, and readmission to hospital due to heart failure progression. The secondary end point was to determine the severity of heart failure (serum level of N-terminal brain natriuretic peptide), cardiac function (LV ejection fraction by radionuclide ventriculography), LV diameters by echocardiography, exercise capacity (changes in NYHA class, changes in peak oxygen consumption), and changes in quality of life (Minnesota Living with Heart Failure questionnaire). The clinical outcome was assessed after 6 and 12 months of therapy., Results: Baseline characteristics were comparable in both groups. Five patients dropped out during 12 months of the study. Twelve patients achieved primary end point (8 in the control group and 4 in the LMWH group). The free survival rate was 94% for the LMWH group and 90% for the controls (not statistically significant). After the 12-month period, in the LMWH group, N-terminal brain natriuretic peptide level and LV diameters decreased significantly (P < .001 and P = .006, respectively), whereas LV systolic function increased (P < .001). Changes in exercise capacity and subjective improvement did not differentiate the groups (nonsignificant). Adverse reactions to the enoxaparin therapy were minor and transient., Conclusions: In patients with chronic heart failure due to dilated cardiomyopathy, adjunct long-term enoxaparin therapy may offer additional clinical benefit without deleterious effects on major cardiac events.
- Published
- 2006
- Full Text
- View/download PDF
47. Usefulness of atorvastatin in patients with heart failure due to inflammatory dilated cardiomyopathy and elevated cholesterol levels.
- Author
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Wojnicz R, Wilczek K, Nowalany-Kozielska E, Szyguła-Jurkiewicz B, Nowak J, Poloński L, Dyrbuś K, Badziński A, Mercik G, Zembala M, Wodniecki J, and Rozek MM
- Subjects
- Adult, Atorvastatin, Cardiomyopathy, Dilated drug therapy, Cholesterol, LDL drug effects, Drug Therapy, Combination, Endpoint Determination, Evaluation Studies as Topic, Female, Heart Failure drug therapy, Humans, Hypercholesterolemia complications, Immunohistochemistry, Male, Myocardium pathology, Quality of Life, Treatment Outcome, Ventricular Function, Left drug effects, Cardiomyopathy, Dilated complications, Cholesterol, LDL blood, Heart Failure etiology, Heptanoic Acids therapeutic use, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Hypercholesterolemia drug therapy, Pyrroles therapeutic use
- Abstract
This study evaluated the safety, tolerability, and efficacy of statin therapy in patients with heart failure secondary to inflammatory dilated cardiomyopathy and moderately elevated low-density lipoprotein cholesterol levels. Seventy-four patients were randomized to receive atorvastatin 40 mg/day or conventional treatment for heart failure. After 6 months of therapy, the predefined primary efficacy end point (an increase of >5% in the absolute left ventricular ejection fraction and > or =2 selected criteria by echocardiography and a decrease in New York Heart Association functional class) was significant in the statin-treated patients (p = 0.004). Among secondary efficacy parameters, the quality-of-life index showed a trend suggesting the benefit of statin therapy (p = 0.055). In conclusion, the results of this study demonstrate that treatment with atorvastatin in addition to standard therapy for heart failure may significantly improve clinical outcomes in this cohort of patients.
- Published
- 2006
- Full Text
- View/download PDF
48. Familial hypertrophic cardiomyopathy. Insertion-deletion polymorphism of angiotensin-converting enzyme and angiotensin II receptor.
- Author
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Gilanowska G, Domal-Kwiatkowska D, Smolik S, Wilczewski P, Szarek J, Nowalany-Kozielska E, Mazurek U, Wodniecki J, and Wilczok T
- Subjects
- Adolescent, Adult, Aged, Female, Genotype, Humans, Male, Middle Aged, Pedigree, Phenotype, Receptor, Angiotensin, Type 1 genetics, Cardiomyopathy, Hypertrophic, Familial genetics, Gene Deletion, Peptidyl-Dipeptidase A genetics, Polymorphism, Genetic, Receptors, Angiotensin genetics
- Abstract
Background: Hypertrophic cardiomyopathy (HCM) is a genetic-based disease. Several gene mutations leading to HCM development have been described., Aim: Detailed examination of phenotype and genotype of a family with HCM., Methods: Clinical and genetic examinations were performed in a family with HCM, in which 3 sick persons with different disease phenotype were found., Results: In all sick persons the same molecular substitution G->A (AGG->AAG) was noticed. It led to substitution Arg780-Lys in exon 21 beta-myosin heavy chain gene, which was responsible for the development of the disease. Insertion- deletion polymorphism analysis in ACE gene revealed D/D (deletion/deletion) genotype in proband and D/I (deletion/ insertion) phenotype in his mother and sister, who were heterozygous. Polymorphism A1166C analysis in AT1 gene revealed the presence of genotype A/A in proband and A/C in his mother and sister. In proband and his sister a very similar phenotype was observed, whereas they had different polymorphism for ACE gene and angiotensin 1 receptor gene. In sick proband's mother, who had phenotype different to her children, the same polymorphism as in his daughter was noticed., Conclusions: In the described family with HCM, different phenotype and polymorphism of ACE and AT1 genes were found.
- Published
- 2005
49. [Sildenafil reduces pressure and pulmonary resistance and increases susceptibility of pulmonary arteries to nitric oxide in primary pulmonary arterial hypertension].
- Author
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Wodniecki J, Jacheć W, Poloński L, Tomasik AR, Wojciechowska C, and Foremny A
- Subjects
- Electrocardiography, Female, Humans, Hypertension, Pulmonary diagnosis, Hypertension, Pulmonary metabolism, Hypertension, Pulmonary physiopathology, Purines, Sildenafil Citrate, Sulfones, Treatment Outcome, Hypertension, Pulmonary drug therapy, Nitric Oxide metabolism, Piperazines pharmacology, Pulmonary Artery drug effects, Vasodilator Agents pharmacology
- Abstract
Primary pulmonary arterial hypertension (PPH) is a rare disease of undetermined origin and fatal prognosis. A better prognosis is associated with at least 20% reduction of either pulmonary artery pressure or pulmonary vascular resistance ("responders") in acute vasodilatory trials. Prostacycline (PGI2) or nitric oxide (NO) administration promises valuable results. NO is one of the most powerful vasodilating agents, endogenously produced by endothelial cells. It migrates from these cells to smooth muscle cells and stimulates production of cGMP, that induces smooth muscle relaxation. cGMP is hydrolyzed by 5-phopshodiesterase (PDE-5). Several papers documenting hypotensive effect in pulmonary circulation of specific PDE5 inhibitor--sildenafil (Viagra--Pfizer) have been published recently. We present a case report of a 26 year old female patient with PPH--"nonresponder" in a trial with NO--and NO responder after sildenafil administration. Initial values were: mean pulmonary artery pressure (mPAP) was 58 mmHg, pulmonary vascular resistance was 10.9 Wood's units. mPAP and PVR during NO inhalation (40 ppm) decrease from 62 to 54 mmHg and from 11.4 to 10.3 Wood's units, respectively. Measurements performed 60 minutes after 50 mg of sildenafil orally disclosed a 19% reduction of mPAP and 21% reduction of PVR. NO inhalation caused further decrease of both parameters: mPAP was decreased for additional 28% and PVR for additional 36% in comparison to initial results. Neither peripheral hypotension nor other side effects were observed. A month-long administration of sildenafil in a dose 2 x 25 mg daily reduced mPAP and PVR to values reported for the acute trial. Physical capability improved also. It was assessed as increased distance in a six-minute-walk test (280 vs. 400 m in the first week of treatment, and 330 m in a fourth week of treatment). Echocardiography showed moderate decrease of right ventricle and right atrium diameters, along with decrease of the degree of relative tricuspid regurgitation with unchanged maximal velocity of regurgitant wave. Specific PDE-5 inhibitors might be an attractive alternative in the treatment of pulmonary hypertension in case the above noted observations are confirmed.
- Published
- 2005
50. Function of heart muscle in people chronically exposed to lead.
- Author
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Kasperczyk S, Przywara-Chowaniec B, Kasperczyk A, Rykaczewska-Czerwińska M, Wodniecki J, Birkner E, Dziwisz M, and Krauze-Wielicka M
- Subjects
- Adult, Case-Control Studies, Chronic Disease, Comorbidity, Electrocardiography, Ambulatory methods, Female, Humans, Hypertrophy, Left Ventricular chemically induced, Hypertrophy, Left Ventricular diagnostic imaging, Lead Poisoning diagnosis, Male, Middle Aged, Occupational Diseases diagnosis, Occupational Exposure analysis, Poland epidemiology, Ultrasonography, Ventricular Dysfunction, Left chemically induced, Ventricular Dysfunction, Left diagnostic imaging, Ventricular Dysfunction, Left epidemiology, Hypertrophy, Left Ventricular epidemiology, Lead Poisoning epidemiology, Metallurgy, Occupational Diseases epidemiology, Occupational Exposure statistics & numerical data
- Abstract
Rhythm and conductivity disturbances in heart muscle, change in autonomic system function and raised arterial blood pressure have been described in workers exposed to lead. They may be accompanied by changes in echocardiography test and accordingly we undertook this investigation. The study population included employees of zinc and lead steelworks in the south of Poland that were divided into 2 groups: exposed to lead compounds (n=88) and the reference group - administration workers (n=55) with normal levels of lead concentration in blood (PbB) and zinc protoporphyrin in blood. Left ventricular enddiastolic dimension (LVDd), interventricular septal and posterior wall thickness, right ventricular diastolic, left atrium diameter, aortic diameter and left ventricular ejection fraction (EF) in echocardiograms were performed. Left ventricular mass LVM (g) and left ventricular mass index LVMI (g/m(2)) was calculated. In the group exposed to lead, EF decreased by 3 %, increased LVDd by 6 %, and raised LVM by 11 % and LVMI by 10 %. There was a positive relation between PbB and LVDd (R=0.18) and between PbB and LVM (R=0.14). Decreased EF, enlargement of the left ventricle and raised left ventricle mass in research undertaken, may be a result of raised arterial blood tension.
- Published
- 2005
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