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1. Mechanistic assessment and ablation of left ventricular assist device related ventricular tachycardia in patients with severe heart failure

Author

Hohendanner, Felix, primary, Bock, Matthias, additional, Keznickl-Pulst, Julian, additional, Furundzija, Vesna, additional, Scholz, Sebastian, additional, Schöppenthau, Doreen, additional, Hrytsyna, Yuriy, additional, Falk, Volkmar, additional, Pieske, Burkert, additional, Hindricks, Gerhard, additional, Potapov, Evgenij, additional, and Gerds-Li, Jin-Hong, additional

Published
2023
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5. Western Blot und realtime PCR- basierte Identifizierung möglicher Hypertonie assoziierter Gene an einem definiertem Hypotoniemodell an Wistar-Kyoto Ratten

Author

Furundzija, Vesna

Subjects
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
Abstract

Der essentielle Hypertonus ist eine multifaktoriell bedingte Störung der Blutdruckregulation. Zurückzuführen ist das auf verschiedene Umweltfaktoren und eine Vielzahl von blutdruckrelevanten Genen. Bisher konnten einige Kandidatengene identifiziert werden, wobei weitere wahrscheinlich sind. Ziel der vorliegenden Arbeit ist einerseits die Verifizierung aber auch die Entdeckung neuer differentiell exprimierter blutdruckregulierender Gene. Über die Analyse der zugehörigen Genprodukte sollen neue blutdruckregulierende Systeme identifiziert werden können. Durch das Herbeiführen einer akuten Hypotension (Blutdruckreduktion um 31 ± 5%) bei normotensiven Ratten, wurde erwartet, dass das vasoregulatorische System der Hypotension entgegenwirken wird. Die durch diese Hypotension induzierte Aufregulation blutdruck- steigernder Gene in der Niere und thorakalen Aorta sollen anschließend in einer definierten Zeitreihe (Messpunkte nach induzierter Hypotonie) detektiert und mittels realtime-PCR und Western Blot verifiziert, quantifiziert und qualitativ erfasst werden. Die Hypothese, dass genau diese aufregulierten Gene einen Faktor in der Entstehung der Hypertonie darstellen könnten, durch z.B. unregulierte oder auch entkoppelte inadäquate Aufregulation der dazugehörigen Proteine, stellt die hier untersuchten Gene als eine der vielen möglichen genetischen Basismodelle der Blutdruckregulation dar. Zwei funktionell bekannte Gene (XDH und Cytochrom P450) waren bereits bei Voruntersuchungen mittels realtime- PCR und Microarray Analyse als signifikant aufreguliert (p < 0,1) gefunden worden, so dass in dieser Arbeit eine weitere Methode, der Western Blot, genutzt wurde, um dieses Ergebnis zu verifizieren. Des Weiteren wurden diese beiden Gene zu einem weiteren Messpunkt (12h) nach induzierter Hypotonie, im Gegensatz zur vorangegangenen Arbeit (letzter Messpunkt 6h), mittels realtime- PCR untersucht. Neben XDH und Cytochrom P450 wurden noch weitere Gene iNOS, eNOS, NOX1, NOX4 und HO-1 untersucht, die in ihrer Funktion ebenfalls einen hinreichenden Einfluss auf die Blutdruckregulation haben. Nach induzierter Hypotonie und anschließender Gewebeuntersuchung (Niere und Aorta) bei 0h, 3h, 6h und 12 h wurde die relative Transkriptionshäufigkeit dieser Gene mit der realtime- PCR detektiert. Zusammenfassend sind vier von den hier sieben untersuchten Genen sowohl in der Niere als auch in der Aorta aufreguliert (XDH, Cytochrom P450, iNOS und HO-1). NOX 1 und NOX 4 waren beide im aortalen Gewebe abreguliert und in der Niere aufreguliert. Die eNOS war in beiden Proben abreguliert Die untersuchten Gene besitzen einige charakteristische Funktionen in unserem Herz-Kreislauf-System. Außer der HO-1, die in ihrer Funktion schützend auf oxidativen Stress wirkt, kommen den restlichen Genen und ihren dazugehörenden Proteinen eine entscheidende Rolle im Metabolismus reaktiver Sauerstoffradikale (ROS) zu. XDH und Cytochrom P 450 sind über kopmlexe Reaktionen und ihren Zwischenprodukten in der Entstehung von Sauerstoffradikalen involviert. iNOS und eNOS sorgen über die Freisetzung von physiologischem aber auch toxischem NO zu vaskulären Tonusänderungen aber auch zu vielerlei Schäden auf Zellstrukturebene. Die erhöhte Expression von iNOS ist von einer deutlich höheren Bildung von Sauerstoffradikalen und Peroxynitrit vergesellschaftet und mündet somit wieder im Metabolismus reaktiver Sauerstoffradikale (ROS). Auch NOX 1 und NOX 4, eine analoge Untereinheiten zur gp 91 phox, sind Bestandteile der NADPH- Oxidase glatter Muskelzellen, die ein führendes Enzymsystem darstellen in der ROS- Bildung. Durch die Bildung von Sauerstoffradikalen und der damit einhergehenden Beteiligung am Metabolismus der ROS entsteht oxidativer Stress und somit eine Änderung des Gefäßtonus, was letztlich in eine endotheliale Dysfunktion mündet. Die Detektion neuer Kandidatengene des essentiellen Hypertonus ließe zum einen die Erstellung individueller Risikoprofile zu, die für die Diagnostik, Prävention und einen frühzeitigen Therapiebeginn, sowie eine individualspezifische antihypertensive Therapie von großer Bedeutung wären., Essential hypertension is a disturbance of blood pressure regulation and can be conditioned by a number of factors. The causes can be traced back to a variety of environmental factors and a range of genes relevant to blood pressure. A number of genes have been identified as possible candidates, although it is probable that others exist. The goal of the present work lies both in verification but also in the discovery of new differentially expressed genes that regulate blood pressure. The aim is to identify new blood regulating systems by analysing the corresponding gene products. The expectation was that, by causing an acute hypotension (blood pressure reduction by 31 ± 5%) in normotensive rats, their vasoregulatory system would respond to compensate the hypotension. The upregulation of blood pressure raising-genes in the kidney and thoracic aorta which this hypotension induces was then to be detected according to a defined time series (test points after the induced hypotension) and verified, quantified and qualitatively analysed using real-time PCR and western blot. The hypothesis that precisely these upregulated genes might constitute one contributing factor that can cause hypertension – for instance if the upregulation of the corresponding proteins is either unregulated or insufficiently regulated as a result of being unlinked – suggests that the genes examined here are one of the many possible basic genetic models for blood pressure regulation. In the course of preliminary investigations using real-time PCR and microarray analysis it was found that two genes whose function is already known (XDH and cytochrome P450) were upregulated significantly (p < 0.1), so that the present study employs a further method, western blot, to verify the findings. Furthermore these two genes were investigated using real-time PCR at a later time after induced hypotension (12 h) than that in the previous study (last test point 6 h). A number of other genes (iNOS, eNOS, NOX1, NOX4 and HO-1) which also have a significant effect on blood pressure regulation were examined besides XDH and cytochrome P450. Following induction of hypotension and subsequent examination of tissue (kidney and aorta) at 0h, 3h, 6h and 12h, real-time PCR was used to detect the relative transcription frequency of these genes. In summary: four of the seven genes investigated were upregulated both in the kidney and in the aorta (XDH, cytochrome P450, iNOS and HO-1). NOX 1 and NOX 4 were downregulated in the aortic tissue and upregulated in the renal tissue. eNOS was downregulated in both types of sample. The investigated genes have several characteristic functions in our cardiovascular system. Leaving aside HO-1, which appears to function as a protection against oxidative stress, the other genes all play a decisive role in the metabolism of reactive oxygen species (ROS). XDH and cytochrome P 450 are involved in the production of ROS via a number of complex reactions and intermediate products. However, by releasing both physiological and toxic NO, iNOS and eNOS do also affect vascular tonus as well as causing a considerable range of damage to cell structures. The heightened expression of iNOS is linked to a noticeably increased level of ROS and peroxynitrite production and thus again leads to the metabolism of reactive oxygen species (ROS). NOX 1 and NOX 4, subunits which are analogous to gp91-phox, are also components of the NADPH – oxidase in smooth muscle cells, which represents one of the main enzyme system in the production of ROS. The production of reactive oxygen species and the resulting involvement in the metabolism of ROS leads to oxidative stress and thus to changes in vascular tonus, and ultimately to endothelial dysfunction. The detection of new candidate genes responsible for essential hypertension would lead to the possibility of producing individual risk profiles which would be of great importance for diagnosis, prevention and an early commencement of therapy as well for individually tailored forms of antihypertensive therapy.

Published
2008
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10. 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, 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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, 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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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