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4. Echocardiographic determinants of the clinical condition in patients with a systemic right ventricle

Author

Winter, M.M., Bouma, B.J., Hardziyenka, M., Bruin-Bon, R.H. de, Tan, H.L., Konings, T.C., Dijk, A.P.J. van, Mulder, B.J., Cardiology, and ICaR - Heartfailure and pulmonary arterial hypertension

Subjects
Cardiovascular diseases [NCEBP 14]
Abstract

Item does not contain fulltext BACKGROUND: Ventricular systolic and diastolic function, as measured by echocardiography, are diminished in patients with a systemic right ventricle (RV). As the clinical implications of these finding remained unknown, we aimed to identify echocardiographic parameters of systolic and diastolic ventricular function that are independent determinants of the clinical condition in these patients. METHODS: Forty-six adult patients (61% male; mean age 33 [range 18-69] years) with a systemic RV underwent echocardiography to assess qualitative and quantitative systolic and diastolic function of the systemic RV and the subpulmonary left ventricle (LV). Uni- and multivariate linear regression analyses were performed to identify independent echocardiographic determinants for NYHA class, maximal exercise capacity (V'O(2peak)) and NT-proBNP levels. RESULTS: We found qualitative assessment of RV and LV function to be significantly associated with NYHA class (RV: beta= 0.26; P = 0.05 and LV: beta= 0.82; P < 0.01), V'O(2peak) (RV: beta=-10.4; P < 0.05 and LV: beta=-18.4; P < 0.05) and NT-proBNP levels (RV: beta= 0.58; P < 0.01 and LV: beta= 1.40; P < 0.001). Tricuspid annulus plane systolic excursion (TAPSE) was significantly associated with NYHA class (beta=-0.92; P = 0.001), V'O(2peak) (beta= 18.5; P = 0.05), and serum NT-proBNP levels (beta=-1.00; P < 0.05). Associations between quantitative parameters of systolic subpulmonary LV function and clinical parameters were less distinct. We found no associations between RV and LV diastolic function and clinical parameters. CONCLUSIONS: Qualitative function of the systemic RV and the subpulmonary LV, and TAPSE, are determinants of clinical condition in patients with a systemic RV. These patients' clinical condition could not be determined by echocardiographically measured diastolic RV function, and systolic and diastolic LV function. 01 november 2010

Published
2010
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5. Duration of right ventricular contraction predicts the efficacy of bosentan treatment in patients with pulmonary hypertension.

Author

Duffels, M.G., Hardziyenka, M., Surie, S., Bruin-Bon, R.H. de, Hoendermis, E.S., Dijk, A.P.J. van, Bouma, B.J., Tan, H.L., Berger, R.M., Bresser, P., Mulder, B.J., Duffels, M.G., Hardziyenka, M., Surie, S., Bruin-Bon, R.H. de, Hoendermis, E.S., Dijk, A.P.J. van, Bouma, B.J., Tan, H.L., Berger, R.M., Bresser, P., and Mulder, B.J.

Abstract

Contains fulltext : 80922.pdf (publisher's version ) (Closed access), AIMS: In patients with pulmonary hypertension (PH), elevated endothelin-1 levels are associated with prolonged duration of right ventricular (RV) contraction, which induces leftward ventricular septal bowing with impaired left diastolic filling. We hypothesized that baseline RV contraction duration predicts efficacy of endothelin receptor antagonist, bosentan. METHODS AND RESULTS: Eighteen PH patients (age 57, range 35-79 years, 33% male) received bosentan. Six minute walk distance (6-MWD) and echocardiography were performed at baseline and after 1 year follow-up. After 1 year of treatment, 6-MWD increased (mean 60 +/- 41 m) in 67% of patients (responders). Baseline RV contraction duration was longer in responders, compared with non-responders (612 +/- 66 vs. 514 +/- 23 ms; P < 0.01). A baseline RV contraction duration >550 ms was associated with improved 6-MWD (sensitivity 83%, specificity 83%; P < 0.01). CONCLUSION: An improvement of 6-MWD during bosentan treatment was associated with a decrease in RV contraction duration and could be predicted by a baseline RV contraction duration >550 ms.

Published
2009

7. Poster session 3

Author

Nanka, O., primary, Krejci, E., additional, Pesevski, Z., additional, Sedmera, D., additional, Smart, N., additional, Rossdeutsch, A., additional, Dube, K. N., additional, Riegler, J., additional, Price, A. N., additional, Taylor, A., additional, Muthurangu, V., additional, Turner, M., additional, Lythgoe, M. F., additional, Riley, P. R., additional, Kryvorot, S., additional, Vladimirskaya, T., additional, Shved, I., additional, Schwarzl, M., additional, Seiler, S., additional, Huber, S., additional, Steendijk, P., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Caprio, C., additional, Baldini, A., additional, Chiavacci, E., additional, Dolfi, L., additional, Verduci, L., additional, Meghini, F., additional, Cremisi, F., additional, Pitto, L., additional, Kuan, T.-C., additional, Chen, M.-C., additional, Yang, T.-H., additional, Wu, W.-T., additional, Lin, C. S., additional, Rai, H., additional, Kumar, S., additional, Sharma, A. K., additional, Mastana, S., additional, Kapoor, A., additional, Pandey, C. M., additional, Agrawal, S., additional, Sinha, N., additional, Orlowska-Baranowska, E. H., additional, Placha, G., additional, Gora, J., additional, Baranowski, R., additional, Abramczuk, E., additional, Hryniewiecki, T., additional, Gaciong, Z., additional, Verschuren, J. J. W., additional, Wessels, J. A. M., additional, Trompet, S., additional, Stott, D. J., additional, Sattar, N., additional, Buckley, B., additional, Guchelaar, H. J., additional, Jukema, J. W., additional, Gharanei, M., additional, Hussain, A., additional, Mee, C. J., additional, Maddock, H. L., additional, Wijnen, W. J., additional, Van Den Oever, S., additional, Van Der Made, I., additional, Hiller, M., additional, Tijsen, A. J., additional, Pinto, Y. M., additional, Creemers, E. E., additional, Nikulina, S. U. Y., additional, Chernova, A., additional, Petry, A., additional, Rzymski, T., additional, Kracun, D., additional, Riess, F., additional, Pike, L., additional, Harris, A. L., additional, Gorlach, A., additional, Katare, R., additional, Oikawa, A., additional, Riu, F., additional, Beltrami, A. P., additional, Cesseli, D., additional, Emanueli, C., additional, Madeddu, P., additional, Zaglia, T., additional, Milan, G., additional, Franzoso, M., additional, Pesce, P., additional, Sarais, C., additional, Sandri, M., additional, Mongillo, M., additional, Butler, T. J., additional, Seymour, A.-M. L., additional, Ashford, D., additional, Jaffre, F., additional, Bussen, M., additional, Flohrschutz, I., additional, Martin, G. R., additional, Engelhardt, S., additional, Kararigas, G., additional, Nguyen, B. T., additional, Jarry, H., additional, Regitz-Zagrosek, V., additional, Van Bilsen, M., additional, Daniels, A., additional, Munts, C., additional, Janssen, B. J. A., additional, Van Der Vusse, G. J., additional, Van Nieuwenhoven, F. A., additional, Montalvo, C., additional, Villar, A. V., additional, Merino, D., additional, Garcia, R., additional, Llano, M., additional, Ares, M., additional, Hurle, M. A., additional, Nistal, J. F., additional, Dembinska-Kiec, A., additional, Beata Kiec-Wilk, B. K. W., additional, Anna Polus, A. P., additional, Urszula Czech, U. C., additional, Tatiana Konovaleva, T. K., additional, Gerd Schmitz, G. S., additional, Bertrand, L., additional, Balteau, M., additional, Timmermans, A., additional, Viollet, B., additional, Sakamoto, K., additional, Feron, O., additional, Horman, S., additional, Vanoverschelde, J. L., additional, Beauloye, C., additional, De Meester, C., additional, Martinez, E., additional, Martin, R., additional, Miana, M., additional, Jurado, R., additional, Gomez-Hurtado, N., additional, Bartolome, M. V., additional, San Roman, J. A., additional, Lahera, V., additional, Nieto, M. 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L., additional, Azibani, F., additional, Tournoux, F., additional, Schlossarek, S., additional, Polidano, E., additional, Fazal, L., additional, Merval, R., additional, Carrier, L., additional, Chatziantoniou, C., additional, Buyandelger, B., additional, Linke, W., additional, Zou, P., additional, Kostin, S., additional, Ku, C., additional, Felkin, L., additional, Birks, E., additional, Barton, P., additional, Sattler, M., additional, Knoell, R., additional, Schroder, K., additional, Benkhoff, S., additional, Shimokawa, H., additional, Grisk, O., additional, Brandes, R. P., additional, Parepa, I. R., additional, Mazilu, L., additional, Suceveanu, A. I., additional, Suceveanu, A., additional, Rusali, L., additional, Cojocaru, L., additional, Matei, L., additional, Toringhibel, M., additional, Craiu, E., additional, Pires, A. 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J., additional, Simova, I., additional, Mateev, H., additional, Katova, T., additional, Haralanov, L., additional, Dimitrov, N., additional, Mironov, N., additional, Golitsyn, S. P., additional, Sokolov, S. F., additional, Yuricheva, Y. U. A., additional, Maikov, E. B., additional, Shlevkov, N. B., additional, Rosenstraukh, L. V., additional, Chazov, E. I., additional, Radosinska, J., additional, Knezl, V., additional, Benova, T., additional, Slezak, J., additional, Urban, L., additional, Tribulova, N., additional, Virag, L., additional, Kristof, A., additional, Kohajda, Z. S., additional, Szel, T., additional, Husti, Z., additional, Baczko, I., additional, Jost, N., additional, Varro, A., additional, Sarusi, A., additional, Farkas, A. S., additional, Orosz, S. Z., additional, Forster, T., additional, Farkas, A., additional, Zakhrabova-Zwiauer, O. M., additional, Hardziyenka, M., additional, Nieuwland, R., additional, Tan, H. L., additional, Raaijmakers, A. J. A., additional, Bourgonje, V. J. A., additional, Kok, G. J. M., additional, Van Veen, A. A. B., additional, Anderson, M. E., additional, Vos, M. A., additional, Bierhuizen, M. F. A., additional, Benes, J., additional, Sebestova, B., additional, Ghouri, I. A., additional, Kemi, O. J., additional, Kelly, A., additional, Burton, F. L., additional, Smith, G. L., additional, Ozdemir, S., additional, Acsai, K., additional, Doisne, N., additional, Van Der Nagel, R., additional, Beekman, H. D. M., additional, Van Veen, T. A. B., additional, Sipido, K. R., additional, Antoons, G., additional, Harmer, S. C., additional, Mohal, J. S., additional, Kemp, D., additional, Tinker, A., additional, Beech, D., additional, Burley, D. S., additional, Cox, C. D., additional, Wann, K. T., additional, Baxter, G. F., additional, Wilders, R., additional, Verkerk, A., additional, Fragkiadaki, P., additional, Germanakis, G., additional, Tsarouchas, K., additional, Tsitsimpikou, C., additional, Tsardi, M., additional, George, D., additional, Tsatsakis, A., additional, Rodrigues, P., additional, Barros, C., additional, Najmi, A. K., additional, Khan, V., additional, Akhtar, M., additional, Pillai, K. K., additional, Mujeeb, M., additional, Aqil, M., additional, Bayliss, C. R., additional, Messer, A. E., additional, Leung, M.-C., additional, Ward, D., additional, Van Der Velden, J., additional, Poggesi, C., additional, Redwood, C. S., additional, Marston, S., additional, Vite, A., additional, Gandjbakhch, E., additional, Gary, F., additional, Fressart, V., additional, Leprince, P., additional, Fontaine, G., additional, Komajda, M., additional, Charron, P., additional, Villard, E., additional, Falcao-Pires, I., additional, Gavina, C., additional, Hamdani, N., additional, Stienen, G. J. 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B., additional, Stridsberg, M., additional, Sjaastad, I., additional, Oie, E., additional, Omland, T., additional, Christensen, G., additional, Rosjo, H., additional, Cartledge, J., additional, Clark, L. A., additional, Ibrahim, M., additional, Siedlecka, U., additional, Navaratnarajah, M., additional, Yacoub, M. H., additional, Camelliti, P., additional, Terracciano, C. M., additional, Chester, A., additional, Gonzalez-Tendero, A., additional, Torre, I., additional, Garcia-Garcia, F., additional, Dopazo, J., additional, Gratacos, E., additional, Taylor, D., additional, Bhandari, S., additional, Seymour, A.-M., additional, Fliegner, D., additional, Jost, J., additional, Bugger, H., additional, Ventura-Clapier, R., additional, Carpi, A., additional, Campesan, M., additional, Canton, M., additional, Menabo, R., additional, Pelicci, P. 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L., additional, Ferdinandy, P., additional, Klevstigova, M., additional, Silhavy, J., additional, Manakov, D., additional, Papousek, F., additional, Novotny, J., additional, Pravenec, M., additional, Kolar, F., additional, Novakova, O., additional, Novak, F., additional, Neckar, J., additional, Barallobre-Barreiro, J., additional, Didangelos, A., additional, Yin, X., additional, Fernandez-Caggiano, M., additional, Drozdov, I., additional, Willeit, P., additional, Domenech, N., additional, Mayr, M., additional, Lemoine, S., additional, Allouche, S., additional, Coulbault, L., additional, Galera, P., additional, Gerard, J. L., additional, Hanouz, J. L., additional, Suveren, E., additional, Whiteman, M., additional, Studneva, I. M., additional, Pisarenko, O., additional, Shulzhenko, V., additional, Serebryakova, L., additional, Tskitishvili, O., additional, Timoshin, A., additional, Fauconnier, J., additional, Meli, A. 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M., additional, Thomas, A., additional, Staub, C., additional, Zimmer, A., additional, Cravatt, B., additional, Pacher, P., additional, Steffens, S., additional, Blanco, R., additional, Sarmiento, R., additional, Parisi, C., additional, Fandino, S., additional, Blanco, F., additional, Gigena, G., additional, Szarfer, J., additional, Rodriguez, A., additional, Garcia Escudero, A., additional, Riccitelli, M. A., additional, Wantha, S., additional, Simsekyilmaz, S., additional, Megens, R. T., additional, Van Zandvoort, M. A., additional, Liehn, E., additional, Zernecke, A., additional, Klee, D., additional, Weber, C., additional, Soehnlein, O., additional, Lima, L. M., additional, Carvalho, M. G., additional, Gomes, K. B., additional, Santos, I. R., additional, Sousa, M. O., additional, Morais, C. A. S., additional, Oliveira, S. H. V., additional, Gomes, I. F., additional, Brandao, F. C., additional, Lamego, M. R. A., additional, Fornai, L., additional, Kiss, A., additional, Giskes, F., additional, Eijkel, G., additional, Fedrigo, M., additional, Valente, M. L., additional, Heeren, R. M. A., additional, Grdinic, A., additional, Vojvodic, D., additional, Djukanovic, N., additional, Grdinic, A. G., additional, Obradovic, S., additional, Majstorovic, I., additional, Rusovic, S., additional, Vucinic, Z., additional, Tavciovski, D., additional, Ostojic, M., additional, Lai, S.-C., additional, Chen, M.-Y., additional, Wu, H.-T., additional, Gouweleeuw, L., additional, Oberdorf-Maass, S. U., additional, De Boer, R. A., additional, Van Gilst, W. H., additional, Maass, A. H., additional, Van Gelder, I. C., additional, Benard, L., additional, Li, C., additional, Warren, D., additional, Shanahan, C. M., additional, Zhang, Q. P., additional, Bye, A., additional, Vettukattil, R., additional, Aspenes, S. T., additional, Giskeodegaard, G., additional, Gribbestad, I. S., additional, Wisloff, U., additional, Bathen, T. F., additional, Cubedo, J., additional, Alonso, R., additional, Mata, P., additional, Ivic, I., additional, Vamos, Z., additional, Cseplo, P., additional, Kosa, D., additional, Torok, O., additional, Hamar, J., additional, Koller, A., additional, Norita, K., additional, De Noronha, S. V., additional, Sheppard, M. N., additional, Amat-Roldan, I., additional, Iruretagoiena, I., additional, Psilodimitrakopoulos, S., additional, Crispi, F., additional, Artigas, D., additional, Loza-Alvarez, P., additional, Harrison, J. C., additional, Smart, S. D., additional, Besely, E. H., additional, Kelly, J. R., additional, Yao, Y., additional, Sammut, I. A., additional, Hoepfner, M., additional, Kuzyniak, W., additional, Sekhosana, E., additional, Hoffmann, B., additional, Litwinski, C., additional, Pries, A., additional, Ermilov, E., additional, Fontoura, D., additional, Lourenco, A. P., additional, Vasques-Novoa, F., additional, Pinto, J. P., additional, Roncon-Albuquerque, R., additional, Oyeyipo, I. P., additional, Olatunji, L. A., additional, Usman, T. O., additional, Olatunji, V. A., additional, Bacova, B., additional, Viczenczova, C., additional, Dosenko, V., additional, Goncalvesova, E., additional, Vanrooyen, J., additional, Maulik, S. K., additional, Seth, S., additional, Dinda, A. K., additional, Jaiswal, A., additional, Mearini, G., additional, Khajetoorians, D., additional, Kraemer, E., additional, Gedicke-Hornung, C., additional, Precigout, G., additional, Eschenhagen, T., additional, Voit, T., additional, Garcia, L., additional, Lorain, S., additional, Mendes-Ferreira, P., additional, Maia-Rocha, C., additional, Adao, R., additional, Cerqueira, R. J., additional, Mendes, M. J., additional, Castro-Chaves, P., additional, De Keulenaer, G. W., additional, Bras-Silva, C., additional, Ruiter, G., additional, Wong, Y. Y., additional, Lubberink, M., additional, Knaapen, P., additional, Raijmakers, P., additional, Lammertsma, A. A., additional, Marcus, J. T., additional, Westerhof, N., additional, Van Der Laarse, W. J., additional, Vonk-Noordegraaf, A., additional, Steinbronn, N., additional, Koch, E., additional, Steiner, G., additional, Berezin, A., additional, Lisovaya, O. A., additional, Soldatova, A. M., additional, Kuznetcov, V. A., additional, Yenina, T. N., additional, Rychkov, A. Y. U., additional, Shebeko, P. V., additional, Altara, R., additional, Hessel, M. H. M., additional, Hermans, J. J. R., additional, Blankesteijn, W. M., additional, Berezina, T. A., additional, Seden, V., additional, Bonanad, C., additional, Nunez, J., additional, Navarro, D., additional, Chilet, M. F., additional, Sanchis, F., additional, Bodi, V., additional, Minana, G., additional, Chaustre, F., additional, Forteza, M. J., additional, Llacer, A., additional, Galasso, G., additional, Ferrara, N., additional, Akhmedov, A., additional, Klingenberg, R., additional, Brokopp, C., additional, Hof, D., additional, Zoller, S., additional, Corti, R., additional, Gay, S., additional, Von Eckardstein, A., additional, Hoerstrup, S. P., additional, Luescher, T. F., additional, Heijman, J., additional, Zaza, A., additional, Johnson, D. M., additional, Rudy, Y., additional, Peeters, R. L. M., additional, Volders, P. G. A., additional, Westra, R. L., additional, Fujita, S., additional, Okamoto, R., additional, Taniguchi, M., additional, Konishi, K., additional, Goto, I., additional, Sugimoto, K., additional, Nakamura, M., additional, Shiraki, K., additional, Buechler, C., additional, and Ito, M., additional

Published
2012
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12. A novel echocardiographic predictor of in-hospital mortality and mid-term haemodynamic improvement after pulmonary endarterectomy for chronic thrombo-embolic pulmonary hypertension

Author

Hardziyenka, M., primary, Reesink, H. J., additional, Bouma, B. J., additional, de Bruin-Bon, H.A.C.M. R., additional, Campian, M. E., additional, Tanck, M. W.T., additional, van den Brink, R. B.A., additional, Kloek, J. J., additional, Tan, H. L., additional, and Bresser, P., additional

Published
2007
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15. Electrocardiographic evidence of ventricular repolarization remodelling during atrial fibrillation.

Author

Tan HL, Smits JP, Loef A, Tanck MW, Hardziyenka M, and Campian ME

Abstract

Aims: Some atrial fibrillation (AF) patients develop excessive QTc prolongation and torsade de pointes when they take QTc-prolonging antiarrhythmic drugs (class IA/III) immediately after termination of AF. We hypothesized that this is caused by changes in ventricular repolarization during AF. We aimed to establish whether such ‘ventricular repolarization remodelling’ occurs. [ABSTRACT FROM PUBLISHER]

Published
2008

16. Sequence of Echocardiographic Changes During Development of Right Ventricular Failure in Rat

Author

Hardziyenka, M., Campian, M.E., Rianne de Bruin-Bon, H.A.C.M., Michel, M.C., and Tan, H.L.

Abstract

Background: The temporal relations between the onset of echocardiographic changes and clinical diagnosis of right ventricular (RV) failure are unresolved. We have characterized such relations in a rat monocrotaline (MCT) model of RV failure. Methods: Eight-week-old male Wistar rats were injected with MCT (60 mg/kg) or vehicle and underwent serial echocardiography. RV free-wall thickness (RVWT), pulmonary artery acceleration time normalized to cycle length (PAAT/CL), RV end-diastolic diameter (RVEDD), and tricuspid annular plane systolic excursion (TAPSE) were measured. Results: Significant differences in echocardiographic parameters between MCT-treated and control rats were found as early as 14 days before RV failure for RVWT, 10 days for PAAT/CL, and 7 days for RVEDD and TAPSE. The time intervals between the onset of changes in RVWT, PAAT/CL, RVEDD, and TAPSE and diagnosis of RV failure were 11.3 +/- 0.8, 10.9 +/- 0.7, 6.5 +/- 0.5, and 5.4 +/- 0.7 days, respectively. The sequence of echocardiographic changes was consistent in all animals during development of RV failure. Conclusions: Pulmonary hypertension (assessed by PAAT/CL) and RV free-wall thickening (characterized by RVWT) precede RV dilation and RV systolic dysfunction (measured by RVEDD and TAPSE, respectively). Echocardiographic analysis permits accurate determination of the stage of disease development in MCT-induced RV failure.

Published
2006
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17. Poster session Friday 13 December - AM: 13/12/2013, 08:30-12:30 * Location: Poster area

Author

Gertsen, M, Nemes, A, Szolnoky, G, Altmayer, A, Gavaller, H, Kemeny, L, Forster, T, Park, J R, Jo, SY, Kim, KH, Kho, JS, Kwack, CH, Hwang, JY, Popovic, D, Ostojic, MC, Petrovic, M, Vujisic-Tesic, B, Arandjelovic, A, Banovic, M, Vukcevic, V, Petrovic, I, Popovic, B, Damjanovic, S, Placido, R, Marta, L, Ramalho, AR, Nobre Menezes, M, Cortez-Dias, N, Martins, S, Goncalves, S, Almeida, AG, Silva-Marques, J, Nunes-Diogo, A, Germanakis, I, Kakouri, P, Karachaliou, M, Vassilaki, M, Chatzi, L, Roumeliotaki, T, Kogevinas, M, Horst, J-P, Kelter-Kloepping, A, Koerperich, H, Barth, P, Haas, NA, Kececioglu, D, Laser, KT, Laser, KT, Horst, J-P, Kelter-Kloepping, A, Barth, P, Haas, NA, Kececioglu, D, Koerperich, H, Samiei, N, Nabati, M, Azari-Jafari, M, Vakili-Zarch, A, Parsaee, M, Haghjoo, M, Ahmed, A J, Val-Mejias, J E, Von Bulow, F M, Baltussen, E J M, Darban, AM, Claus, P, Voigt, JU, Rodriguez Munoz, DA, Moya Mur, JL, Gonzalez, A, Garcia Martin, A, Becker Filho, D, Fernandez Santos, S, Lazaro Rivera, C, Recio Vazquez, M, Fernandez Golfin, C, Zamorano Gomez, JL, Bandera, F, Pellegrino, M, Generati, G, Alfonzetti, E, Donghi, V, Castelvecchio, S, Garatti, A, Menicanti, L, Guazzi, M, Kowalik, E, Klisiewicz, A, Hoffman, P, Kim, EJ, Cho, I J, Oh, J, Chang, HJ, Park, J, Shin, S, Shim, CY, Hong, GR, Ha, JW, Chung, N, Park, JH, Lee, HS, Kim, HS, Ahn, KT, Kim, JH, Lee, JH, Choi, SW, Jeong, JO, Seong, IW, Holzendorf, V, Gelbrich, G, Wachter, R, Loeffler, M, Pieske, BM, Broda, A, Edelmann, F, Failure, German Competence Network for Heart, Kim, YH, Kim, DH, Kim, SH, Ahn, JC, Song, WH, Hashimoto, G, Suzuki, M, Yoshikawa, H, Otsuka, T, Kusunose, Y, Nakamura, M, Sugi, K, De Knegt, M C, Biering-Sorensen, T, Sogaard, P, Sivertsen, J, Jensen, JS, Mogelvang, R, Murbraech, K, Smeland, KH, Holte, H, Loge, JH, Kiserud, CE, Aakhus, S, Peteiro, J, Gargallo-Fernandez, P, Garcia-Guimaraes, M, Bouzas-Mosquera, A, Yanez-Wronenburger, JC, Martinez-Ruiz, D, Castro-Beiras, A, Trzcinski, PT, Jaskowski, MJ, Nowak, JN, Pawlus, MP, Figiel, LF, Kasprzak, JDK, Lipiec, PL, Zhong, L, Su, Y, Teo, SK, Le, TT, Tan, RS, Tesic, M, Djordjevic-Dikic, A, Giga, V, Jovanovic, I, Paunovic, I, Petrovic, MT, Trifunovic, D, Beleslin, B, Stepanovic, J, Vujisic-Tesic, B, Parato, V M, Partemi, M, Nardini, E, Pasanisi, E, Park, T-H, Lee, J-E, Lee, D-H, Park, J-S, Park, K, Kim, M-H, Kim, Y-D, Vegsundvag, J, Holte, E, Wiseth, R, Hegbom, K, Hole, T, Fusini, L, Tamborini, G, Ghulam Ali, S, Muratori, M, Gripari, P, Cefalu, C, Maffessanti, F, Celeste, F, Alamanni, F, Pepi, M, Negrea, SL, Alexandrescu, C, Rossi, P, Iacuzio, L, Dreyfus, G, Moatemri, F, Mahdhaoui, A, Bouraoui, H, Ernez, S, Jeridi, G, Yuan, L, Feng, JL, Jin, X Y, Seoane Garcia, T, Delgado Ortega, M, Mesa Rubio, D, Ruiz Ortiz, M, Martin Hidalgo, M, Carrasco Avalos, F, Casares Mediavilla, J, Alados, P, Lopez Granados, A, Suarez De Lezo Cruz Conde, J, Mutuberria Urdaniz, M, Rodriguez-Palomares, JF, Baneras-Rius, JF, Acosta-Velez, JG, Buera-Surribas, I, Gonzalez-Alujas, MT, Teixido, G, Evangelista, A, Tornos, P, Garcia-Dorado, D, Iliuta, L, Boerlage-Van Dijk, K, Van Riel, ACMJ, De Bruin-Bon, HACM, Wiegerinck, EMA, Koch, KT, Vis, MM, Meregalli, PG, Piek, JJ, Bouma, BJ, Baan, J, Enache, R, Muraru, D, Piazza, R, Popescu, BA, Coman, M, Calin, A, Rosca, M, Beladan, CC, Nicolosi, GL, Ginghina, C, Song, JM, Kim, JJ, Ha, TY, Jung, SH, Hwang, IS, Lee, IC, Sun, BJ, Kim, DH, Kang, DH, Song, JK, Sturmberger, T, Ebner, CE, Aichinger, J, Tkalec, W, Niel, J, Steringer-Mascherbauer, R, Kabicher, G, Winter, S, Nesser, HJ, Hofmann-Bowman, M, Lin Yan, LY, Puri, TP, Chin, C W L, Doris, M, Shah, A, Mills, N, Semple, S, Prasad, S, White, A, Dweck, M, Newby, D, Debonnaire, P, Al Amri, I, Leong, DP, Joyce, E, Katsanos, S, Kamperidis, V, Schalij, MJ, Bax, JJ, Ajmone Marsan, N, Delgado, V, Cerin, G, Popa, B A, Lanzillo, G, Benea, D, Karazanishvili, L, Diena, M, Dedobbeleer, C, Schnell, F, Jotrand, E, El Mourad, M, Thebault, C, Plein, D, Donal, E, Unger, P, Spampinato, RA, Tasca, M, Da Rocha E Silva, JG, Strotdrees, E, Schloma, V, Dmitrieva, Y, Mende, M, Borger, MA, Mohr, FW, Veronesi, F, Muraru, D, Addetia, K, Corsi, C, Lamberti, C, Lang, RM, Mor-Avi, V, Badano, LP, Zemanek, D, Tomasov, P, Belehrad, M, Kara, T, Veselka, J, Igual Munoz, B, Estornell Erill, JORDI, Maceira Gonzalez Alicia, AMG, Monmeneu Menadas, JVMM, Lopez Lereu Pilar, PLL, Molina Aguilar, PMA, Domingo-Valero, DDV, Osca Asensi, JOA, Zorio Grima, EZG, Salvador Sanz Antonio, ASS, Ibrahimi, P, Bajraktari, G, Poniku, A, Hysenaj, V, Ahmeti, A, Jashari, F, Haliti, E, Henein, MY, Maramao, F, Conde, Y, Maramao, L, Rulli, F, Roussin, I, Drakopoulou, M, Bhattacharyya, S, Simpkin, V, Sharma, R, Rosen, S, Prasad, S, Senior, R, Lyon, AR, Kimura, K, Tanimoto, T, Akasaka, T, Fijalkowski, M, Jaguszewski, M, Fijalkowska, M, Nowak, R, Galaska, R, Rojek, A, Narkiewicz, K, Rynkiewicz, A, Azevedo, O, Marques, N, Cruz, I, Picarra, B, Lima, R, Amado, J, Pereira, V, Almeida, AR, SUNSHINE, Zito, C, Crea, P, Cusma Piccione, M, Vriz, O, Bitto, A, Minisini, R, Madaffari, A, Acri, E, Oteri, A, Carerj, S, Leggio, S, Buccheri, S, Tamburino, C, Monte, I P, Mihalcea, D, Florescu, M, Enescu, OA, Magda, LS, Radu, E, Acasandrei, AM, Balanescu, P, Rimbas, RC, Jinga, D, Vinereanu, D, 112/2011, Research grant, Miyoshi, T, Tanaka, H, Kaneko, A, Matsumoto, K, Imanishi, J, Motoji, Y, Mochizuki, Y, Minami, H, Kawai, H, Hirata, K, Ryu, SK, Shin, DG, Son, JW, Choi, JH, Goh, CW, Choi, JW, Park, JY, Hong, GR, Le Page, P, Mitchell, ARJ, Maclachlan, HI, Hurry, RW, Villagraz Tecedor, L, Jimenez Lopez Guarch, C, Alonso Chaterina, S, Mayordomo Gomez, S, Blazquez Arrollo, L, Lombera Romero, F, Lopez Melgar, B, Escribano Subias, MP, Lichodziejewska, B, Kurnicka, K, Goliszek, S, Kostrubiec, M, Dzikowska Diduch, O, Krupa, M, Grudzka, K, Ciurzynski, M, Palczewski, P, Pruszczyk, P, Lovric, D, Carmona, C, Bergerot, C, Schnell, F, Thibault, H, Barthelet, M, Ninet, J, Revel, D, Croisille, P, Derumeaux, G, Jensen, MT, Rossing, P, Sogaard, P, Andersen, HU, Bech, J, Hansen, TF, Gustafsson, I, Galatius, S, Jensen, JS, Shang, Q, Zhang, Q, Sanderson, JE, Tam, LS, Lee, A PW, Fang, F, Li, E KM, Yu, CM, Bruin De- Bon, HACM, Tan, HL, Hardziyenka, M, Symersky, P, Bonta, PI, Brink Van Den, RBA, Bouma, BJ, Bader, RS, Punn, R, Silverman, N, Cruz, C, Pinho, T, Lebreiro, A, Dias, CC, Silva Cardoso, J, Julia Maciel, M, Melao, F, Ribeiro, V, Cruz, C, Maciel, MJ, Attenhofer Jost, C H, Schmidt, D, Pfyffer, M, Biaggi, P, Seifert, B, Weber, R, De Pasquale, G, Kretschmar, O, Seeliger, T, Greutmann, M, Johansson, M C, Mirzada, N, Ladenvall, P, Besiroglu, F, Samadov, F, Atas, H, Sari, I, Tufekcioglu, O, Birincioglu, CL, Acar, B, Duman, I, Colak, A, Zagatina, A, Krylova, L, Zhuravskaya, N, Vareldzhyan, Y, Tyurina, TV, Clitsenko, O, Castro, M, Dores, H, Carvalho, MS, Reis, C, Horta, E, Trabulo, MS, Andrade, MJ, Mendes, M, Gasior, Z, Plonska-Gosciniak, E, Wita, K, Mizia-Stec, K, Kulach, A, Szwed, H, Chrzanowski, L, Tomaszewski, A, Sinkiewicz, W, Wojciechowska, C, Aggeli, C, Felekos, I, Stergiou, P, Roussakis, G, Kakiouzi, V, Kastellanos, S, Koutagiar, I, Stefanadis, C, Bouzas Mosquera, A, Peteiro, J, Alvarez-Garcia, N, Broullon, FJ, Garcia-Guimaraes, MM, Martinez-Ruiz, D, Yanez-Wonenburger, JC, Bouzas-Zubeldia, B, Fabregas, R, Castro-Beiras, A, Brugger, N, Huerzeler, M, Wustmann, K, Wahl, A, Steck, H, Seiler, C, Sarwar, R, Malhotra, A, Wong, KC, Betts, TR, Bashir, Y, Rajappan, K, Newton, JD, Casanova Rodriguez, C, Cano Carrizal, R, Iglesias Del Valle, D, Martin Penato Molina, A, Garcia Garcia, A, Prieto Moriche, E, Alvarez Rubio, J, Paredes Gonzalez, B, De Juan Baguda, J, Plaza Perez, I, Van Den Oord, SCH, Akkus, Z, Roeters Van Lennep, JE, Bosch, JG, Van Der Steen, AFW, Sijbrands, EJG, Schinkel, AFL, Muraru, D, Calore, C, Badano, LP, Melacini, C, Mihaila, S, Peluso, D, Puma, L, Kocabay, G, Rizzon, G, Iliceto, S, Bochard Villanueva, B, Paya-Serrano, R, Garcia-Gonzalez, P, Fabregat-Andres, O, Perez-Bosca, JL, Cubillos-Arango, A, Ferrando-Beltran, M, Chacon-Hernandez, N, Albiach-Montanana, C, Ridocci-Soriano, F, Ancona, R, Comenale Pinto, S, Caso, P, Arenga, F, Coppola, MG, Calabro, R, Tarr, A, Stoebe, S, Pfeiffer, D, Hagendorff, A, Hollekim, SM, Bjorgaas, MR, Tjonna, AE, Wisloff, U, Ingul, CB, (CERG), Cardiac Exercise Research Group, Oreto, L, Zito, C, Cusma-Piccione, M, Calabro, MP, Todaro, MC, Vita, GL, Messina, S, Vita, G, Sframeli, M, Carerj, S, Remoli, R, Lamberti, F, Bellini, C, Mercurio, M, Dottori, S, Bellusci, F, Mazzuca, V, Gaspardone, A, Rimbas, RC, Enescu, OA, Mihaila, S, Ciobanu, A, Vinereanu, D, Henri, C, Magne, J, Dulgheru, R, Laaraibi, S, Voilliot, D, Kou, S, Pierard, L, Lancellotti, P, Wellnhofer, E, Kriatselis, C, Gerds-Li, H, Furundzija, VESNA, Thanabalasingam, U, Fleck, E, Graefe, M, Kouris, N, Keramida, K, Karidas, V, Kostopoulos, V, Kostakou, P, Mprempos, G, Olympios, CD, Duchateau, N, Giraldeau, G, Gabrielli, L, Penela, D, Evertz, R, Mont, L, Brugada, J, Berruezo, A, Bijnens, BH, Sitges, M, Bernard, A, Donal, E, Reynaud, A, Schnell, F, Daubert, JC, Leclercq, C, Hernandez, A, Keramida, K, Kouris, N, Kostopoulos, V, Karidas, V, Dagre, A, Ntarladimas, I, Damaskos, D, Stamatelatou, M, Olympios, CD, Panetta, G L, Peraldo Neja, C, Urbano Moral, JA, Evangelista, A, Azzolini, P, Gaudio, C, Pandian, NG, Barbier, P, Mirea, O, Savioli, G, Cefalu, C, Guglielmo, M, Fusini, L, Maltagliati, A, Hamdy, AM, Fereig, HM, Nabih, MA, Abdel-Aziz, A, Ali, AA, Buccheri, S, Mangiafico, S, Leggio, S, B, VE, Tropea, L, Tamburino, C, Monte, I P, Garcia-Gonzalez, P, Chacon-Hernandez, N, Cozar-Santiago, P, Fabregat-Andres, O, Sanchez-Jurado, R, Higueras-Ortega, L, Albiach-Motanana, C, Perez-Bosca, JL, Paya-Serrano, R, Ridocci-Soriano, F, Flori, M, Valette, F, Guijarro, D, Pallardy, A, Le Tourneau, T, Kraeber-Bodere, F, Piriou, N, Saxena, A, Ramakrishnan, S, Tulunay Kaya, C, Ongun, A, Kilickap, M, Candemir, B, Altin, AT, Gerede, M, Ozcan, OU, Erol, C, Yue, WS, Yang, F, Huang, D, Gu, P, Luo, Y, Lv, Z, Siu, CW, Tse, HF, Yiu, KH, Saura Espin, D, Lopez Cuenca, A, Espinosa Garcia, MD, Oliva Sandoval, MJ, Lopez Ruiz, M, Gonzalez Carrillo, J, Garcia Navarro, MJ, Valdes Chavarri, M, De La Morena Valenzuela, G, Gustafsson, U, Spuhler, JH, Hoffman, J, Brodin, LÅ, Kisko, A, Dernarova, L, Hudakova, A, Santova, T, Jakubikova, M, Mikulak, M, Horlenko, O, Kishko, N, Svystak, V, Shyp, A, Faden, G, Gaibazzi, N, Rigo, F, Mureddu, GF, Moreo, A, Bussadori, G, Facchetti, R, Cesana, F, Giannattasio, C, Faggiano, P, and group, APRES collaborative

Abstract

Pulmonary vascular dysfunction is claimed to be a contributor to the development of pulmonary hypertension (PH). Impaired systemic vascular reactivity is one of the essential factors in the pathogenesis of cardiovascular disease. The aim of the investigation was to study whether there is any association between systemic vascular function and pulmonary artery pressure (PAP) in patients who have associated causes for PH development, such as coronary heart disease (CHD) and chronic obstructive pulmonary disease (COPD). Methods: The brachial artery vasodilator responses were measured by the ultrasound technique in twenty patients with mild to moderate COPD (group I) and twenty age–matched and COPD stage-matched patients who had past history of myocardial infarction (NYHA II) (group II).Conventional echocardiographic variables were measured in the said patients too. Results: Both flow-mediated dilatation (FMD) and nitrate-mediated dilatation (NMD) were significantly lower, and PAP was significantly higher in the group II patients compared to the same parameters of group I patients. NMD was inversely correlated with PAP (r=-0.7, p=0.02) in group I patients. There was no interrelation between FMD and PAP in patients from group I. Neither FMD nor NMD were correlated with PAP in group II patients. A significant positive correlation between PAP and left ventricular mass index (r=0.8, p=0.003) was revealed in the said patients as well. Conclusions: Attenuated vasodilator response of brachial artery to nitroglycerine is associated with PAP elevation in COPD patients. PH is closely related to cardiac remodeling in COPD patients in whom CHD developed. These data suggest different "stages" of vascular and cardiac remodeling in patients with COPD alone and in coexistence with CHD. The obtained data can be useful in the selection of treatment as regards these patient categories.

Published
2013
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18. Right ventricular pacing improves haemodynamics in right ventricular failure from pressure overload: an open observational proof-of-principle study in patients with chronic thromboembolic pulmonary hypertension.

Author

Hardziyenka M, Surie S, de Groot JR, de Bruin-Bon HA, Knops RE, Remmelink M, Yong ZY, Baan J Jr, Bouma BJ, Bresser P, and Tan HL

Subjects
Adult, Aged, Aged, 80 and over, Cardiac Output physiology, Chronic Disease, Diastole physiology, Electrocardiography, Female, Humans, Male, Middle Aged, Stroke Volume physiology, Ventricular Dysfunction, Right etiology, Cardiac Pacing, Artificial methods, Heart Ventricles physiopathology, Hemodynamics physiology, Hypertension, Pulmonary complications, Thromboembolism complications, Ventricular Dysfunction, Right physiopathology, Ventricular Dysfunction, Right therapy
Abstract

Aims: Right ventricular (RV) failure in patients with chronic thromboembolic pulmonary hypertension (CTEPH), and other types of pulmonary arterial hypertension is associated with right-to-left ventricle (LV) delay in peak myocardial shortening and, consequently, the onset of diastolic relaxation. We aimed to establish whether RV pacing may resynchronize the onsets of RV and LV diastolic relaxation, and improve haemodynamics., Methods and Results: Fourteen CTEPH patients (mean age 63.7 ± 12.0 years, 10 women) with large (≥60 ms) RV-to-LV delay in the onset of diastolic relaxation (DIVD, diastolic interventricular delay) were studied. Temporary RV pacing was performed by atrioventricular (A-V) sequential pacing with incremental shortening of A-V delay to advance RV activation. Effects were assessed using tissue Doppler echocardiography and LV pressure-conductance catheter measurements in a subset of patients. Compared with right atrial pacing, RV pacing at optimal A-V delay (average 140 ± 22 ms, range 120-180 ms) resulted in significant DIVD reduction (59 ± 19 to 3 ± 22 ms, P < 0.001), and increase in LV stroke volume as measured by LV outflow tract velocity-time integral (14.9 ± 2.8 to 16.9 ± 3.0 cm, P < 0.001), along with enhanced global RV contractility and LV diastolic filling., Conclusion: Right-to-left ventricle resynchronization of the onset of diastolic relaxation results in stroke volume increase in CTEPH patients. Whether RV pacing may be a novel therapeutic target in RV failure following chronic pressure overload remains to be investigated.

Published
2011
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19. Time course of restoration of systolic and diastolic right ventricular function after pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension.

Author

Surie S, Bouma BJ, Bruin-Bon RA, Hardziyenka M, Kloek JJ, Van der Plas MN, Reesink HJ, and Bresser P

Subjects
Adult, Aged, Chronic Disease, Female, Hemodynamics, Humans, Hypertension, Pulmonary etiology, Male, Middle Aged, Pulmonary Embolism complications, Recovery of Function, Time Factors, Endarterectomy, Hypertension, Pulmonary physiopathology, Hypertension, Pulmonary surgery, Pulmonary Artery surgery, Ventricular Function, Right
Abstract

Background: In chronic thromboembolic pulmonary hypertension, right ventricular (RV) pressure overload causes RV remodeling and dysfunction. Successful pulmonary endarterectomy (PEA) initiates restoration of RV remodeling and global function. Little is known on the restoration of systolic and diastolic RV function. Using transthoracic echocardiography, we studied the time course and extent of postoperative restoration of systolic and diastolic RV function., Methods: In chronic thromboembolic pulmonary hypertension (n = 55, 36 women, age 52 ± 14 years), transthoracic echocardiography was performed before PEA (pre-PEA) and 2 weeks, 3 months, and 1 year postoperatively., Results: Two weeks postoperatively, RV afterload and dimension had decreased significantly, without further improvement during follow-up. Global RV function, expressed by the myocardial performance index, showed a gradual improvement (from pre-PEA 0.58 ± 0.29 to 0.45 ± 0.38, 0.39 ± 0.19, and 0.37 ± 0.18). In contrast, 2 weeks after PEA systolic RV function, as assessed by tricuspid annular plane systolic velocity excursion and peak tricuspid annular systolic velocity of the RV, had worsened, with a subsequent incomplete restoration during follow-up: tricuspid annular plane systolic velocity excursion from 19.3 ± 5.0 to 12.4 ± 2.5, 15.3 ± 3.0, and 16.8 ± 2.9 mm and systolic velocity of the right ventricle from 11.4 ± 3.0 to 9.6 ± 2.0, 10.0 ± 1.8, and 10.3 ± 1.7 cm/s. Postoperative diastolic RV function also showed a biphasic response: tricuspid inflow-to-annulus ratio from 6.1 ± 3.0 to 9.5 ± 3.5, 6.8 ± 2.4, and 6.3 ± 2.2 cm/s. Dynamics and ultimate level of restoration of systolic and diastolic RV function were similar in patients with and without residual pulmonary hypertension., Conclusions: Postoperative reduction in RV afterload caused an immediate improvement in RV dimension and global function. In contrast, systolic and diastolic RV function deteriorated after PEA with subsequently a gradual yet incomplete restoration during 1-year follow-up., (Copyright © 2011 Mosby, Inc. All rights reserved.)

Published
2011
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20. Assessment of inflammation in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia.

Author

Campian ME, Verberne HJ, Hardziyenka M, de Groot EA, van Moerkerken AF, van Eck-Smit BL, and Tan HL

Subjects
Adult, Biological Transport, Cytokines blood, Female, Gallium Radioisotopes metabolism, Humans, Inflammation blood, Inflammation diagnostic imaging, Male, Middle Aged, Myocardium metabolism, Radionuclide Imaging, Young Adult, Arrhythmogenic Right Ventricular Dysplasia complications, Inflammation complications, Inflammation diagnosis
Abstract

Purpose: Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a myocardial disease that predominantly affects the right ventricle (RV). Its hallmark feature is fibro-fatty replacement of RV myocardium. However, patchy inflammatory infiltrates in the RV are also consistently reported using autopsy and myocardial biopsy. Although the role of inflammation in ARVC/D is unresolved, the ability to assess inflammation non-invasively may aid in the diagnostic process. We aimed to establish whether cardiac inflammation can be assessed non-invasively in ARVC/D patients., Methods: In eight ARVC/D patients and nine controls (haematology/oncology patients), the level of inflammatory activation was assessed by measuring plasma levels of inflammatory cytokines. Regional myocardial inflammation was assessed with (67)Ga scintigraphy., Results: ARVC/D patients had higher plasma levels than controls of the pro-inflammatory cytokines interleukin (IL)-1β (1.22 ± 0.07 vs 0.08 ± 0.01 pg/ml, p < 0.0001), IL-6 (3.16 ± 0.44 vs 0.38 ± 0.04 pg/ml, p < 0.0001) and tumour necrosis factor (TNF)-α (9.16 ± 0.90 vs 0.40 ± 0.06 pg/ml, p < 0.0001), while levels of the anti-inflammatory cytokine IL-10 were not significantly different (1.36 ± 0.15 vs 1.20 ± 0.30 pg/ml, p = 0.74). (67)Ga uptake in the RV was higher in ARVC/D patients than in controls. In ARVC/D patients, (67)Ga uptake in the RV wall was higher than in the interventricular septum or left ventricular wall., Conclusion: Inflammation in the RV wall of ARVC/D patients can be detected non-invasively with the combined analysis of plasma levels of inflammatory cytokines and cardiac (67)Ga scintigraphy.

Published
2010
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21. Early inflammatory response during the development of right ventricular heart failure in a rat model.

Author

Campian ME, Hardziyenka M, de Bruin K, van Eck-Smit BL, de Bakker JM, Verberne HJ, and Tan HL

Subjects
Animals, Autoradiography, Disease Models, Animal, Disease Progression, Gallium Radioisotopes, Gene Expression Profiling, Heart Failure blood, Heart Failure chemically induced, Hypertrophy, Right Ventricular blood, Immunochemistry, Male, Monocrotaline adverse effects, Myocardium metabolism, Neutrophil Activation physiology, Peroxidase metabolism, Radionuclide Imaging, Rats, Rats, Wistar, Tumor Necrosis Factor-alpha analysis, Ventricular Dysfunction, Right blood, Ventricular Dysfunction, Right complications, Ventricular Dysfunction, Right diagnostic imaging, Heart Failure physiopathology, Inflammation etiology
Abstract

Aims: Inflammatory activation plays an important role in the pathogenesis and progression of left ventricular (LV) heart failure. In right ventricular (RV) heart failure, little is known about the role of inflammatory activation. We aimed to study the role of inflammatory activation in RV heart failure by serial monitoring during disease progression., Methods and Results: Right ventricular heart failure was induced in male Wistar rats by intraperitoneal injection of monocrotaline (MCT). Two groups were studied: MCT-treated rats (MCT-rats), and age-matched controls (CON-rats). Serial echocardiography and in vivo 67-Gallium ((67)Ga) scintigraphy were performed. Local inflammation in the RV was assessed by (i) ex vivo semi-quantitative (67)Ga autoradiography, (ii) immunohistochemistry of myeloperoxidase (MPO), a marker of neutrophil activity, and (iii) mRNA assays of tumour necrosis factor-alpha (TNF-alpha). In MCT-rats, (67)Ga scintigraphy showed increased myocardial uptake which started during the early stages of RV disease. (67)Ga autoradiography revealed that this increased (67)Ga uptake occurred in the RV and inter-ventricular septum, but not in the LV. The stage-dependent increases of in vivo (67)Ga RV myocardial uptake were paralleled by increases in mRNA gene expression for TNF-alpha in RV, and increased MPO staining in RV., Conclusion: Development and progression of RV heart failure is associated with an early increase in RV inflammation. (67)Ga scintigraphy may be used for the serial assessment of inflammation and monitoring of disease progression in RV heart failure.

Published
2010
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22. Right-to-left ventricular diastolic delay in chronic thromboembolic pulmonary hypertension is associated with activation delay and action potential prolongation in right ventricle.

Author

Hardziyenka M, Campian ME, Bouma BJ, Linnenbank AC, de Bruin-Bon HA, Kloek JJ, van der Wal AC, Baan J Jr, de Beaumont EM, Reesink HJ, de Bakker JM, Bresser P, and Tan HL

Subjects
Action Potentials physiology, Analysis of Variance, Body Surface Potential Mapping methods, Diastole physiology, Echocardiography, Doppler, Endarterectomy, Female, Heart Conduction System diagnostic imaging, Humans, Hypertension, Pulmonary diagnostic imaging, Hypertension, Pulmonary surgery, Linear Models, Male, Middle Aged, Prospective Studies, Statistics, Nonparametric, Stroke Volume, Ventricular Dysfunction, Left diagnostic imaging, Ventricular Dysfunction, Right diagnostic imaging, Heart Conduction System physiopathology, Hypertension, Pulmonary physiopathology, Ventricular Dysfunction, Left physiopathology, Ventricular Dysfunction, Right physiopathology
Abstract

Background: Delayed left ventricle (LV)-to-right ventricle (RV) peak shortening results in cardiac output reduction in patients with chronic thromboembolic hypertension (CTEPH) and other types of pulmonary arterial hypertension. Why the synchrony between LV and RV is lost is unknown. We hypothesized that RV electrophysiological remodeling, notably, conduction slowing and action potential prolongation, contribute to this loss in synchrony., Methods and Results: We conducted epicardial mapping during pulmonary endarterectomy in 26 patients with CTEPH and compared these findings with clinical, hemodynamic, and echocardiographic variables. We consecutively placed a multielectrode grid on the epicardium of the RV free wall and LV lateral wall. These regions corresponded to RV and LV areas where echocardiographic Doppler sample volumes were placed to measure RV-to-LV diastolic interventricular delay. RV and LV epicardial action potential duration was assessed by measuring activation-recovery interval. Onset of diastolic relaxation of RV free wall with respect to LV lateral wall (diastolic interventricular delay) was delayed by 38+/-31 ms in patients with CTEPH versus -12+/-13 ms in control subjects (P<0.001), because, in patients with CTEPH, RV completed electric activation later than LV (65+/-20 versus 44+/-7 ms, P<0.001) and epicardial action potential duration, as assessed by activation-recovery interval measurement, was longer in RV free wall than in LV lateral wall (253+/-29 versus 240+/-22 ms, P<0.001)., Conclusions: Additive effects of electrophysiological changes in RV, notably, conduction slowing and action potential prolongation, assessed by epicardial activation-recovery interval, contribute to diastolic interventricular delay in patients with CTEPH.

Published
2009
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23. Serial noninvasive assessment of apoptosis during right ventricular disease progression in rats.

Author

Campian ME, Verberne HJ, Hardziyenka M, de Bruin K, Selwaness M, van den Hoff MJ, Ruijter JM, van Eck-Smit BL, de Bakker JM, and Tan HL

Subjects
Animals, Apoptosis, Disease Progression, Male, Radionuclide Imaging, Radiopharmaceuticals, Rats, Rats, Wistar, Reproducibility of Results, Sensitivity and Specificity, Ventricular Dysfunction, Right pathology, Annexin A5, Organotechnetium Compounds, Ventricular Dysfunction, Right diagnostic imaging
Abstract

Unlabelled: Right ventricular (RV) function is the major determinant of survival in patients with pulmonary hypertension. Yet, the pathophysiologic basis of RV disease is unresolved. We aimed to study the role of apoptosis in RV disease by monitoring it serially during disease progression using in vivo (99m)Tc-annexin-V ((99m)Tc-annexin) scintigraphy and study whether the reduction in apoptosis resulting from chronic treatment with valsartan can be detected by (99m)Tc-annexin scintigraphy., Methods: RV disease after pulmonary hypertension was induced by monocrotaline injection in rats. The following 3 groups were studied: rats treated with monocrotaline (monocrotaline rats), rats treated with monocrotaline plus valsartan (valsartan rats), and age-matched controls (control rats). Serial echocardiography and in vivo (99m)Tc-annexin scintigraphy were performed. Apoptosis was confirmed by (99m)Tc-annexin autoradiography and terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling. Fibrosis was assessed by picrosirius red staining., Results: In monocrotaline rats, in vivo (99m)Tc-annexin uptake peaked early and declined thereafter but remained elevated, compared with baseline. These stage-dependent changes of in vivo (99m)Tc-annexin uptake were paralleled by changes in autoradiography and terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labeling. Valsartan rats had longer RV failure-free survival than did monocrotaline rats and had reduced apoptosis. These changes were accompanied by commensurate delays in RV hypertrophy and RV dilation. Valsartan rats also had less fibrosis than monocrotaline rats at all disease stages., Conclusion: RV disease progression is associated with an early increase in RV apoptosis, as monitored using serial in vivo (99m)Tc-annexin scintigraphy. Delay in RV disease progression by valsartan is accompanied by reduction in RV apoptosis. Apoptosis plays a role in RV disease progression and may be assessed by serial in vivo (99m)Tc-annexin scintigraphy.

Published
2009
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24. How valid are animal models to evaluate treatments for pulmonary hypertension?

Author

Campian ME, Hardziyenka M, Michel MC, and Tan HL

Subjects
Animals, Animals, Genetically Modified, Disease Models, Animal, Ductus Arteriosus physiology, Embolism complications, Embolism physiopathology, Humans, Hypertension, Pulmonary chemically induced, Hypertension, Pulmonary physiopathology, Hypoxia physiopathology, Monocrotaline, Poisons, Hypertension, Pulmonary drug therapy
Abstract

Various animal models of pulmonary hypertension (PH) exist, among which injection of monocrotaline (MCT) and exposure to hypoxia are used most frequently. These animal models have not only been used to characterize the pathophysiology of PH and its sequelae such as right ventricular hypertrophy and failure, but also to test novel therapeutic strategies. This manuscript summarizes the available treatment studies in animal models of PH, and compares the findings to those obtained in patients with PH. The analysis shows that all approaches which have proven successful in patients, most notably prostacyclin and its analogs and endothelin receptor antagonists, are also effective in various animal models. However, the opposite it not always true. Therefore, promising results in animals have to be interpreted carefully until confirmed in clinical studies.

Published
2006
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