19 results on '"Jermendy AL"'
Search Results
2. Poster session 5: Friday 5 December 2014, 14: 00–18: 00Location: Poster area
- Author
-
Jermendy, AL, Horcsik, DV, Horvath, T, Celeng, C, Nagy, E, Bartykowszki, A, Tarnoki, DL, Merkely, B, Maurovich-Horvat, P, and Jermendy, G
- Published
- 2014
3. Oral Abstract session: Multimodality imaging: Friday 5 December 2014, 11: 00–12: 30Location: Agora
- Author
-
Bartykowszki, A, Drobni, ZD, Panajotu, A, Celeng, C, Suhai, F, Jermendy, AL, Csobay-Novak, C, Merkely, B, and Maurovich-Horvat, P
- Published
- 2014
4. Moderated Posters session: complementary role of imaging techniquesP184Submillisievert computed tomography with model-based iterative reconstruction before pulmonary veins radiofrequency catheter ablation of atrial fibrillation: impact on radiation exposure and outcomeP185Calcium score and CT coronary angiography can be a low cost strategy for the investigation of patients with chest pain with low and intermediate predicted riskP186Impact of imaging modality on the heritability estimates of aortic root geometry: a classical twin studyP187Diagnosis of cardiac allograft vasculopathy with cardiac CT. Relation between clinical variables and mid-term prognosisP188Stress-only normal SPECT myocardial perfusion imaging: is it enough?P189Global longitudinal strain and its relation to cardiac autonomic denervation as assessed by 123-mIBG scintigraphy: insights from the BETTER-HF trialP190FDG-PET imaging in suspected inflammatory cardiomyopathies : comparison with the classical pattern of cardiac sarcoidosis and impact on diagnosisP191CT coronary angiography can be an effective alternative to imaging stress tests in patients with high pre-test probability of CADP192Outcomes at long term follow up of subclinical and mild coronary artery disease diagnosed with MDCT in Mediterranean EuropeP193Cardiac ct peri-device flow after percutaneous left atrial appendage closure using the amplatzer cardiac plug device
- Author
-
Pontone, G, primary, Demir, OM, primary, Celeng, C, primary, Llao-Ferrando, JI, primary, Kitsiou, A N, primary, Portugal, G, primary, Becoulet, L, primary, Marcos-Alberca Moreno, P, primary, Iriart, X, primary, Andreini, D, additional, Annoni, A, additional, Petulla, M, additional, Russo, E, additional, Innocenti, E, additional, Guglielmo, M, additional, Mushtaq, S, additional, Tondo, C, additional, Pepi, M, additional, Bashir, A, additional, Marshall, K, additional, Douglas, M, additional, Wasan, B, additional, Plein, S, additional, Alfakih, K, additional, Kolossvary, M, additional, Kovacs, A, additional, Szilveszter, B, additional, Molnar, A, additional, Horvath, T, additional, Jermendy, AL, additional, Tarnoki, AD, additional, Merkely, B, additional, Maurovich-Horvat, P, additional, Castro, JC, additional, Vilades-Medel, D, additional, Mirabet, S, additional, Pons-Llado, G, additional, Roig, E, additional, Leta, R, additional, Papanikolaou, S, additional, Griroriou, K, additional, Antonopoulos, M, additional, Mpouki, M, additional, Moustakas, G, additional, Giougi, A, additional, Giannakopoulos, V, additional, Gionakis, G, additional, Balomenos, A, additional, Abreu, A, additional, Rio, P, additional, Santos, V, additional, Martins Oliveira, M, additional, Silva Cunha, P, additional, Mota Carmo, M, additional, Branco, L M, additional, Morais, L, additional, Cruz Ferreira, R, additional, Guijarro, D, additional, Pallardy, A, additional, Mathieu, C, additional, Valette, F, additional, Gueffet, JP, additional, Serfaty, JM, additional, Kraeber-Bodere, F, additional, Trochu, JN, additional, Piriou, N, additional, Perez-Isla, L, additional, Palacios, J, additional, Gomez De Diego, JJ, additional, Islas, F, additional, De Agustin, JA, additional, Luaces, M, additional, Arrazola, J, additional, Garcia-Fernandez, MA, additional, Macaya, C, additional, Selmi, W, additional, Jalal, Z, additional, and Thambo, JB, additional
- Published
- 2015
- Full Text
- View/download PDF
5. Moderated Posters session: complementary role of imaging techniques
- Author
-
Pontone, G, Andreini, D, Annoni, A, Petulla, M, Russo, E, Innocenti, E, Guglielmo, M, Mushtaq, S, Tondo, C, Pepi, M, Demir, OM, Bashir, A, Marshall, K, Douglas, M, Wasan, B, Plein, S, Alfakih, K, Celeng, C, Kolossvary, M, Kovacs, A, Szilveszter, B, Molnar, A, Horvath, T, Jermendy, AL, Tarnoki, AD, Merkely, B, Maurovich-Horvat, P, Llao-Ferrando, JI, Castro, JC, Vilades-Medel, D, Mirabet, S, Pons-Llado, G, Roig, E, Leta, R, Kitsiou, A N, Papanikolaou, S, Griroriou, K, Antonopoulos, M, Mpouki, M, Moustakas, G, Giougi, A, Giannakopoulos, V, Gionakis, G, Balomenos, A, Portugal, G, Abreu, A, Rio, P, Santos, V, Martins Oliveira, M, Silva Cunha, P, Mota Carmo, M, Branco, L M, Morais, L, Cruz Ferreira, R, Becoulet, L, Guijarro, D, Pallardy, A, Mathieu, C, Valette, F, Gueffet, JP, Serfaty, JM, Kraeber-Bodere, F, Trochu, JN, Piriou, N, Demir, OM, Bashir, A, Marshall, K, Wasan, B, Plein, S, Alfakih, K, Marcos-Alberca Moreno, P, Perez-Isla, L, Palacios, J, Gomez De Diego, JJ, Islas, F, De Agustin, JA, Luaces, M, Arrazola, J, Garcia-Fernandez, MA, Macaya, C, Iriart, X, Selmi, W, Jalal, Z, and Thambo, JB
- Abstract
Background: The outcome of radiofrequency catheter ablation (RFCA) of atrial fibrillation (AF) has improved thanks to left atrium (LA) anatomy reconstruction by computed tomography with adaptive statistical iterative reconstruction algorithm (CT-ASIR) before the procedure. However, CT-ASIR strategy is associated to an increase of cumulative effective radiation dose (ED) in these patients. Recently, a model-based iterative reconstruction algorithm (MBIR, GE Healthcare, Waukesha,Wisconsin) has been developed (CT-MBIR) for image noise reduction reducing the ED close to chest X-ray exposure. The aim of this study is to compare the CT and RFCA characteristics, AF recurrence after procedure and radiation exposure between RFCA guided by image integration with CT-ASIR versus CT-MBIR Methods and Materials: One-hundred twenty consecutive patients with drug-refractory paroxysmal or persistent AF were addressed to CT-ASIR (Group 1; N: 60; mean age 60.3 ± 10.1 yo; male: 46) or CT-MBIR protocol (Group 2; N: 60; mean age 59.7 ± 11.3 yo; male:45) for evaluation of LA before RFCA. All patients were subsequently treated by image integration-supported RFCA. Image noise, signal to noise ratio (SNR), contrast to noise ratio (CNR), RFCA procedural characteristics, rate of AF recurrence and CT radiation exposure were measured and compared between the two groups. Results: The two groups were homogeneous in terms of demographic characteristics, cardiovascular risk factors, prevalence of persistent AF, medical therapy and echocardiographic characteristics. The mean follow-up was similar (578 ± 284 vs. 591 ± 278 days, respectively, p:ns). Group 2 showed a higher signal to noise ratio (25.9 ± 7.1 vs. 13.8 ± 5.1) and contrast to noise ratio (22.7 ± 6.5 vs. and 14.08 ± 4.1) of left atrium as compared to Group 1 (p<0.001). No differences were found in terms of RFCA parameter [procedural duration (130.9 ± 130.6. vs. 143.8 ± 80.4 min); fluoroscopy time (27.9 ± 14.1.0 vs. 32.0 ± 16.4 min); pulmonary veins isolated (3.8 ± 0.4 vs. 3.9 ± 0.4)] and the rate of AF recurrence (31% vs. 29%) between Group 2 vs Group 1. Group 2 showed a 94% reduction of ED as compared to Group 1 (0.4 ± 0.04 mSv vs 6.4 ± 1.8 mSv, p<0.01). Conclusions: CT-MBIR allows accurate non-invasive reconstruction of LA anatomy in AF patients undergoing to RFCA with a submillisievert effective radiation and comparable success rate of RFCA with CT-ASIR technique.
- Published
- 2015
- Full Text
- View/download PDF
6. Poster session 6: Saturday 6 December 2014, 08:30-12:30 * Location: Poster area
- Author
-
Goirigolzarri Artaza, J, Gallego Delgado, M, Jaimes Castellanos, CP, Cavero Gibanel, MA, Pastrana Ledesma, MA, Alonso Pulpon, LA, Gonzalez Mirelis, J, Al Ansi, R Z, Sokolovic, S, Cerin, G, Szychta, W, Popa, B A, Botezatu, D, Benea, D, Manganiello, S, Corlan, A, Jabour, A, Igual Munoz, B, Osaca Asensi, JOA, Andres La Huerta, AALH, Maceira Gonzalez, AMG, Estornell Erill, JEE, Cano Perez, OCP, Sancho-Tello, MJSTDC, Alonso Fernandez, PAF, Sepulveda Sanchez, PSS, Montero Argudo, AMA, Palombo, C, Morizzo, C, Baluci, M, Kozakova, M, Panajotu, A, Karady, J, Szeplaki, G, Horvath, T, Tarnoki, DL, Jermendy, AL, Geller, L, Merkely, B, Maurovich-Horvat, P, Group, MTA-SE "Lendület" Cardiovascular Imaging Research, Moustafa, S, Mookadam, F, Youssef, M, Zuhairy, H, Connelly, M, Prieur, T, Alvarez, N, Ashikhmin, Y, Drapkina, O, Boutsikou, M, Demerouti, E, Leontiadis, E, Petrou, E, Karatasakis, G, Kozakova, M, Morizzo, C, Bianchi, V, Marchi, B, Federico, G, Palombo, C, Chatzistamatiou, E, Moustakas, G, Memo, G, Konstantinidis, D, Mpampatzeva Vagena, I, Manakos, K, Traxanas, K, Vergi, N, Feretou, A, Kallikazaros, I, Goto, M, Uejima, T, Itatani, K, Pedrizzetti, G, Mada, RO, Daraban, AM, Duchenne, J, Voigt, JU, Chiu, D Y Y, Green, D, Johnstone, L, Sinha, S, Kalra, PA, Abidin, N, Group, Salford Vascular Research, Sikora-Frac, M, Zaborska, B, Maciejewski, P, Bednarz, B, Budaj, A, Nemes, A, Sasi, V, Gavaller, H, Kalapos, A, Domsik, P, Katona, A, Szucsborus, T, Ungi, T, Forster, T, Ungi, I, Pluchinotta, FR, Arcidiacono, C, Saracino, A, Carminati, M, Bussadori, C, Dahlslett, T, Karlsen, S, Grenne, B, Sjoli, B, Bendz, B, Skulstad, H, Smiseth, OA, Edvardsen, T, Brunvand, H, Vereckei, A, Szelenyi, ZS, Szenasi, G, Santoro, C, Galderisi, M, Niglio, T, Santoro, M, Stabile, E, Rapacciuolo, A, Spinelli, L, De Simone, G, Esposito, G, Trimarco, B, Hubert, S, Jacquier, A, Fromonot, J, Resseguier, C, Tessier, A, Guieu, R, Renard, S, Haentjiens, J, Lavoute, C, Habib, G, Menting, M E, Koopman, LP, Mcghie, JS, Rebel, B, Gnanam, D, Helbing, WA, Van Den Bosch, AE, Roos-Hesselink, JW, Shiino, K, Yamada, A, Sugimoto, K, Takada, K, Takakuwa, Y, Miyagi, M, Iwase, M, Ozaki, Y, Placido, R, Ramalho, A, Nobre E Menezes, M, Cortez-Dias, N, Goncalves, S, Guimaraes, T, Robalo Martins, S, Francisco, AR, Almeida, AG, Nunes Diogo, A, Hayashi, T, Itatani, K, Inuzuka, R, Shindo, T, Hirata, Y, Shimizu, N, Miyaji, K, Henri, C, Dulgheru, R, Magne, J, Kou, S, Davin, L, Nchimi, A, Oury, C, Pierard, L, Lancellotti, P, Kovalyova, O, Honchar, O, Tengku, WINDA, Ketaren, ANDRE, Mingo Santos, S, Monivas Palomero, V, Restrepo Cordoba, A, Rodriguez Gonzalez, E, Goirigolzarri Artaza, J, Sayago Silva, I, Garcia Lunar, I, Mitroi, C, Cavero Gibanel, M, Segovia Cubero, J, Ryu, SK, Park, JY, Kim, SH, Choi, JW, Goh, CW, Byun, YS, Choi, JH, Westholm, C, Johnson, J, Jernberg, T, Winter, R, Rio, P, Moura Branco, L, Galrinho, A, Pinto Teixeira, P, Viveiros Monteiro, A, Portugal, G, Pereira-Da-Silva, T, Afonso Nogueira, M, Abreu, J, Cruz Ferreira, R, Mazzone, A, Botto, N, Paradossi, U, Chabane, A, Francini, M, Cerone, E, Baroni, M, Maffei, S, Berti, S, Tatu-Chitoiu, G P, Deleanu, D, Macarie, C, Chioncel, O, Dorobantu, M, Udroiu, C, Calmac, L, Diaconeasa, A, Vintila, V, Vinereanu, D, investigators, RO-STEMI, Ghattas, A, Shantsila, E, Griffiths, H, Lip, GY, Galli, E, Guirette, Y, Daudin, M, Auffret, V, Mabo, P, Donal, E, Fabiani, I, Conte, L, Scatena, C, Barletta, V, Pratali, S, De Martino, A, Bortolotti, U, Naccarato, AG, Di Bello, V, Falanga, G, Alati, E, Di Giannuario, G, Zito, C, Cusma' Piccione, M, Carerj, S, Oreto, G, Dattilo, G, Alfieri, O, La Canna, G, Generati, G, Bandera, F, Pellegrino, M, Alfonzetti, E, Labate, V, Guazzi, M, Cho, EJ, Park, S-J, Lim, HJ, Yoon, HR, Chang, S-A, Lee, S-C, Park, SW, Cengiz, B, Sahin, S T, Yurdakul, S, Kahraman, S, Bozkurt, A, Aytekin, S, Borges, I P, Peixoto, ECS, Peixoto, RTS, Peixoto, RTS, Marcolla, VF, Venkateshvaran, A, Sola, S, Dash, P K, Thapa, P, Manouras, A, Winter, R, Brodin, LA, Govind, S C, Mizariene, V, Verseckaite, R, Bieseviciene, M, Karaliute, R, Jonkaitiene, R, Vaskelyte, J, Arzanauskiene, R, Janenaite, J, Jurkevicius, R, Rosner, S, Orban, M, Nadjiri, J, Lesevic, H, Hadamitzky, M, Sonne, C, Manganaro, R, Carerj, S, Cusma-Piccione, MC, Caprino, A, Boretti, I, Todaro, MC, Falanga, G, Oreto, L, D'angelo, MC, Zito, C, Le Tourneau, T, Cueff, C, Richardson, M, Hossein-Foucher, C, Fayad, G, Roussel, JC, Trochu, JN, Vincentelli, A, Obase, K, Weinert, L, Lang, R, Cavalli, G, Muraru, D, Miglioranza, MH, Addetia, K, Veronesi, F, Cucchini, U, Mihaila, S, Tadic, M, Lang, RM, Badano, L, Polizzi, V, Pino, PG, Luzi, G, Bellavia, D, Fiorilli, R, Chialastri, C, Madeo, A, Malouf, J, Buffa, V, Musumeci, F, Gripari, P, Tamborini, G, Bottari, V, Maffessanti, F, Carminati, C, Muratori, M, Vignati, C, Bartorelli, A, Alamanni, F, Pepi, M, Polymeros, S, Dimopoulos, A, Spargias, K, Karatasakis, G, Athanasopoulos, G, Pavlides, G, Dagres, N, Vavouranakis, E, Stefanadis, C, Cokkinos, DV, Pradel, S, Mohty, D, Magne, J, Darodes, N, Lavergne, D, Damy, T, Beaufort, C, Aboyans, V, Jaccard, A, Mzoughi, K, Zairi, I, Jabeur, M, Ben Moussa, F, Ben Chaabene, A, Kamoun, S, Mrabet, K, Fennira, S, Zargouni, A, Kraiem, S, Jovanova, S, Arnaudova-Dezjulovic, F, Correia, C E, Cruz, I, Marques, N, Fernandes, M, Bento, D, Moreira, D, Lopes, L, Azevedo, O, GROUP, SUNSHINE, Keramida, K, Kouris, N, Kostopoulos, V, Psarrou, G, Giannaris, V, Olympios, CD, Marketou, M, Parthenakis, F, Kalyva, N, Pontikoglou, CH, Maragkoudakis, S, Zacharis, E, Patrianakos, A, Roufas, K, Papadaki, H, Vardas, P, Dominguez Rodriguez, F, Monivas Palomero, V, Mingo Santos, S, Arribas Rivero, B, Cuenca Parra, S, Zegri Reiriz, I, Vazquez Lopez-Ibor, J, Garcia-Pavia, P, Szulik, M, Streb, W, Wozniak, A, Lenarczyk, R, Sliwinska, A, Kalarus, Z, Kukulski, T, Nemes, A, Domsik, P, Kalapos, A, Forster, T, Serra, W, Lumetti, FL, Mozzani, FM, Del Sante, GDS, Ariani, AA, Corros, C, Colunga, S, Garcia-Campos, A, Diaz, E, Martin, M, Rodriguez-Suarez, ML, Leon, V, Fidalgo, A, Moris, C, De La Hera, JM, Kylmala, M M, Rosengard-Barlund, M, Groop, P H, Lommi, J, Bruin De- Bon, HACM, Bilt Van Der, IA, Wilde, AA, Brink Van Den, RBA, Teske, AJ, Rinkel, GJ, Bouma, BJ, Teixeira, R, Monteiro, R, Garcia, J, Silva, A, Graca, M, Baptista, R, Ribeiro, M, Cardim, N, Goncalves, L, Duszanska, A, Skoczylas, I, Kukulski, T, Polonski, L, Kalarus, Z, Choi, J-H, Park, JS, Ahn, JH, Lee, JW, Ryu, SK, Ahn, J, Kim, DH, Lee, HO, Przewlocka-Kosmala, M, Mlynarczyk, J, Rojek, A, Mysiak, A, Kosmala, W, Pellissier, A, Larochelle, E, Krsticevic, L, Baron, E, Le, V, Roy, A, Deragon, A, Cote, M, Garcia, D, Tournoux, F, Yiangou, K, Azina, C, Yiangou, A, Zitti, M, Ioannides, M, Ricci, F, Dipace, G, Aquilani, R, Radico, F, Cicchitti, V, Bianco, F, Miniero, E, Petrini, F, De Caterina, R, Gallina, S, Jardim Prista Monteiro, R, Teixeira, R, Garcia, J, Baptista, R, Ribeiro, M, Cardim, N, Goncalves, L, Chung, H, Kim, JY, Joung, B, Uhm, JS, Pak, HN, Lee, MH, Lee, KY, Ragab, AM, Abdelwahab, AMIR, Yazeed, YASER, El Naggar, WAEL, Spahiu, K, Spahiu, E, Doko, A, Liesting, C, Brugts, JJ, Kofflard, MJM, Kitzen, JJEM, Boersma, E, Levin, M-D, Coppola, C, Piscopo, G, Rea, D, Maurea, C, Caronna, A, Capasso, I, Maurea, N, Azevedo, O, Tadeu, I, Lourenco, M, Portugues, J, Pereira, V, Lourenco, A, Nesukay, E, Kovalenko, V, Cherniuk, S, Danylenko, O, Muhammedov, MB, Ahmedova, DM, Hojakuliyev, BG, Atayeva, D, Nemes, A, Domsik, P, Kalapos, A, Lengyel, C, Varkonyi, TT, Orosz, A, Forster, T, Castro, M, Abecasis, J, Dores, H, Madeira, S, Horta, E, Ribeiras, R, Canada, M, Andrade, MJ, Mendes, M, Morosin, M, Piazza, R, Leonelli, V, Leiballi, E, Pecoraro, R, Cinello, M, Dell' Angela, L, Cassin, M, Sinagra, G, Nicolosi, GL, Wierzbowska-Drabik, K, Hamala, P, Kasprzak, JD, O'driscoll, J, Rossato, C, Gargallo-Fernandez, P, Araco, M, Sharma, S, Sharma, R, Jakus, N, Baricevic, Z, Ljubas Macek, J, Skoric, B, Skorak, I, Velagic, V, Separovic Hanzevacki, J, Milicic, D, Cikes, M, Deljanin Ilic, M, Ilic, S, Kocic, G, Pavlovic, R, Stoickov, V, Ilic, V, Nikolic, LJ, Generati, G, Bandera, F, Pellegrino, M, Alfonzetti, E, Labate, V, Guazzi, M, Labate, V, Bandera, F, Generati, G, Pellegrino, M, Donghi, V, Alfonzetti, E, Guazzi, M, Zakarkaite, D, Kramena, R, Aidietiene, S, Janusauskas, V, Rucinskas, K, Samalavicius, R, Norkiene, I, Speciali, G, Aidietis, A, Kemaloglu Oz, T, Ozpamuk Karadeniz, F, Akyuz, S, Unal Dayi, S, Esen Zencirci, A, Atasoy, I, Osken, A, Eren, M, Fazendas, P R, Caldeira, D, Stuart, B, Cruz, I, Rocha Lopes, L, Almeida, A R, Sousa, P, Joao, I, Cotrim, C, Pereira, H, Fazendas, P R, Caldeira, D, Stuart, B, Cruz, I, Rocha Lopes, L, Almeida, A R, Joao, I, Cotrim, C, Pereira, H, Sinem Cakal, SC, Elif Eroglu, EE, Baydar, O, Beytullah Cakal, BC, Mehmet Vefik Yazicioglu, MVY, Mustafa Bulut, MB, Cihan Dundar, CD, Kursat Tigen, KT, Birol Ozkan, BO, Ali Metin Esen, A, Yagasaki, H, Kawasaki, M, Tanaka, R, Minatoguchi, S, Houle, H, Warita, S, Ono, K, Noda, T, Watanabe, S, Minatoguchi, S, Cho, E J, Park, S J, Lim, H J, Chang, S A, Lee, S C, Park, S W, Cho, E J, Park, S J, Lim, H J, Chang, S A, Lee, S C, Park, S W, Mornos, C, Cozma, D, Ionac, A, Mornos, A, Popescu, I, Ionescu, G, Pescariu, S, Melzer, L, Faeh-Gunz, A, Seifert, B, Attenhofer Jost, C H, Storve, S, Haugen, BO, Dalen, H, Grue, JF, Samstad, S, Torp, H, Ferrarotti, L, Maggi, E, Piccinino, C, Sola, D, Pastore, F, Marino, PN, Ranjbar, S, Karvandi, M, Hassantash, SA, Karvandi, M, Ranjbar, S, Tierens, S, Remory, I, Bala, G, Gillis, K, Hernot, S, Droogmans, S, Cosyns, B, Lahoutte, T, Tran, N, Poelaert, J, Al-Mallah, M, Alsaileek, A, Nour, K, Celeng, CS, Horvath, T, Kolossvary, M, Karolyi, M, Panajotu, A, Kitslaar, P, Merkely, B, Maurovich Horvat, P, Group, MTA-SE "Lendület" Cardiovascular Imaging Research, Aguiar Rosa, S, Ramos, R, Marques, H, Portugal, G, Pereira Da Silva, T, Rio, P, Afonso Nogueira, M, Viveiros Monteiro, A, Figueiredo, L, and Cruz Ferreira, R
- Abstract
Introduction: The increase of left auricular volume (LAV) is a robust cardiovascular event predictor. Despite that echochardiography is more often used, cardiac MRI is considered more accurate. Our objetives are to validate "fast" LAV measures by MRI vs the considered gold standard (GS) and to compare Echo and MRI in a wide spectrum of patients. Methods: In a non-selected popullation with MRI study previously realized, we measured LAV by biplane method (BPMR) and by area-length in 4 chamber view (ALMR) and compared them with biplane (BPe) and discs method (MDDe) in 4 chamber view in echo. To validate MRI measurements, we measured LAV in short axis slices (Simpson Method, SM) in a group of patients and considered it the GS. Results: 186 patients were included (mean age 51 ± 17 age; 123 male; 14 in AF) with clinical indication of cardiac MRI (Philips 1,5 T). In 24 patients SM was calculated. 29% of cardiac MRI were considered normal. Mean underlying pathologies were myocardiopathy (27%), Ischemic myocardiopathy (17%), myopericarditis (10%), prior to AF ablation (4%), valvular disease (6%) and miscellaneous (7%). Excellent correlation was obtained between "fast" MRI measurements and SM in MRI (SM vs BPMR interclass correlation coefficient ICC=0.965 and SM vs ALMR, ICC=0.958; P<0.05) with low interobserver variability (ICC=0.983 for SM; ICC=0.949 for BPMR; ICC=0.931 for ALMR). "Fast" measurements by MRI showed stadistical correlation between them (CCI=0.910) (Figure). Correlation between Echo and MRI measures was only moderate. (BPRM vs BPe CCI=0,469 mean difference -30 ml; ALMR vs MDDe ICC=0,456 mean difference -24 mL). Conclusions: ‘fast’ LAV measures by MRI are comparable with the MRI GS and also between them. Echo values seem to underestimate compared to MRI, so its use may not be suitable.
- Published
- 2014
- Full Text
- View/download PDF
7. Poster session 5: Friday 5 December 2014, 14:00-18:00 * Location: Poster area
- Author
-
Turco, A, Duchenne, J, Nuyts, J, Gheysens, O, Voigt, J-U, Claus, P, Vunckx, K, Muhtarov, K, Ozer, N, Turk, G, Sunman, H, Karakulak, U, Sahiner, L, Kaya, B, Yorgun, H, Hazirolan, T, Aytemir, K, Warita, S, Kawasaki, M, Tanaka, R, Houle, H, Yagasaki, H, Nagaya, M, Ono, K, Noda, T, Watanabe, S, Minatoguchi, S, Kyle, AS, Dauphin, C, Lusson, J R, Dragoi Galrinho, R, Rimbas, RC, Ciobanu, AO, Marinescu, B, Cinteza, M, Vinereanu, D, 28343/04.11.2013, number, Medicine, Funding Authority: University of, Davila, Pharmacy Carol, "Young Researchers" Projects – 2013, Buchar, Dragoi Galrinho, R, Ciobanu, AO, Rimbas, RC, Marinescu, B, Cinteza, M, Vinereanu, D, 159/1.5/S/138907, Grant POSDRU, Aparina, O, Stukalova, O, Butorova, E, Makeev, M, Bolotova, M, Parkhomenko, D, Golitsyn, SP, Zengin, E, Hoffmann, B A, Ramuschkat, M, Ojeda, F, Weiss, C, Willems, S, Blankenberg, S, Schnabel, R B, Sinning, C R, Schubert, U, Suhai, F I, Toth, A, Kecskes, K, Czimbalmos, CS, Csecs, I, Maurovich-Horvat, P, Simor, T, Merkely, B, Vago, H, Slawek, D, Chrzanowski, L, Krecki, R, Binkowska, A, Kasprzak, J D, Palombo, C, Morizzo, C, Kozakova, M, Biering-Sorensen, T, Mogelvang, R, Jensen, JS, Charisopoulou, DC, Koulaouzidis, GK, Rydberg, AR, Henein, MH, Kovacs, A, Olah, A, Lux, A, Matyas, C, Nemeth, BT, Kellermayer, D, Ruppert, M, Birtalan, E, Merkely, B, Radovits, T, Sengelov, M, Biering-Sorensen, T, Jorgensen, PG, Bruun, NE, Fritz-Hansen, T, Bech, J, Olsen, FJ, Sivertsen, J, Jensen, JS, Henri, C, Dulgheru, R, Magne, J, Kou, S, Davin, L, Nchimi, A, Oury, C, Pierard, L, Lancellotti, P, Sahin, S T, Cengiz, B, Yurdakul, S, Altuntas, E, Aytekin, V, Aytekin, S, Bajraktari, G, Ibrahimi, P, Bytyci, I, Ahmeti, A, Batalli, A, Elezi, S, Henein, MY, Pavlyukova, EN, Tereshenkova, EK, Karpov, RS, Barbier, P, Mirea, O, Guglielmo, M, Savioli, G, Cefalu, C, Maltagliati, MC, Tumasyan, LR, Adamyan, KG, Chilingaryan, AL, Tunyan, LG, Kowalik, E, Klisiewicz, A, Biernacka, EK, Hoffman, P, Park, CS, Yi, JEY, Cho, JSC, Ihm, SHI, Kim, HYK, Cho, EJC, Jeon, HKJ, Jung, HOJ, Youn, HJY, Mcghie, JS, Menting, ME, Vletter, WB, Roos-Hesselink, JW, Geleijnse, ML, Van Der Zwaan, H, Van Den Bosch, A, Spethmann, S, Baldenhofer, G, Stangl, V, Baumann, G, Stangl, K, Laule, M, Dreger, H, Knebel, F, Erdei, T, Edwards, J, Braim, D, Yousef, Z, Fraser, AG, Cardiff, Investigators, MEDIA, Keramida, K, Kouris, N, Kostopoulos, V, Kostakou, P, Petrogiannos, CH, Olympios, CD, Bajraktari, G, Berisha, G, Bytyci, I, Ibrahimi, P, Rexhepaj, N, Henein, MY, Wdowiak-Okrojek, K, Shim, A, Wejner-Mik, P, Szymczyk, E, Michalski, B, Kasprzak, JD, Lipiec, P, Tarr, A, Stoebe, S, Pfeiffer, D, Hagendorff, A, Haykal, M, Ryu, SK, Park, JY, Kim, SH, Choi, JW, Goh, CW, Byun, YS, Choi, JH, Sonoko, M, Onishi, T, Fujimoto, W, Yamada, S, Taniguchi, Y, Yasaka, Y, Kawai, H, Okura, H, Sakamoto, Y, Murata, E, Kanai, M, Kataoka, T, Kimura, T, Watanabe, N, Kuriyama, N, Nakama, T, Furugen, M, Sagara, S, Koiwaya, H, Ashikaga, K, Matsuyama, A, Shibata, Y, Meimoun, P, Abouth, S, Martis, S, Boulanger, J, Elmkies, F, Zemir, H, Tzvetkov, B, Luycx-Bore, A, Clerc, J, Galli, E, Oger, E, Guirette, Y, Daudin, M, Fournet, M, Donal, E, Galli, E, Guirette, Y, Mabo, P, Donal, E, Keramida, K, Kouris, N, Kostopoulos, V, Psarrou, G, Petrogiannos, CH, Hatzigiannis, P, Olympios, CD, Igual Munoz, B, Erdociain Perales, MEP, Maceira Gonzalez Alicia, AMG, Vazquez Sanchez, ALEJAN, Miro Palau, VMP, Alonso Fernandez, PAF, Donate Bertolin, LDB, Estornell Erill, JEE, Cervera, AC, Montero Argudo Anastasio, AMA, Okura, H, Koyama, T, Maehama, T, Imai, K, Yamada, R, Kume, T, Neishi, Y, Caballero Jimenez, L, Garcia-Navarro, M, Saura, D, Oliva, MJ, Gonzalez-Carrillo, J, Espinosa, MD, Valdes, M, De La Morena, G, Venkateshvaran, A, Sola, S, Dash, P K, Annappa, C, Manouras, A, Winter, R, Brodin, LA, Govind, S C, Laufer-Perl, LM, Topilsky, Y, Stugaard, M, Koriyama, H, Katsuki, K, Masuda, K, Asanuma, T, Takeda, Y, Sakata, Y, Nakatani, S, Marta, L, Abecasis, J, Reis, C, Dores, H, Cafe, H, Ribeiras, R, Andrade, MJ, Mendes, M, Goebel, B, Hamadanchi, A, Schmidt-Winter, C, Otto, S, Jung, C, Figulla, HR, Poerner, TC, Kim, D-H, Sun, BJ, Jang, JY, Choi, HN, Song, J-M, Kang, D-H, Song, J-K, Zakhama, L, Slama, I, Boussabah, E, Antit, S, Herbegue, B, Annabi, MS, Jalled, A, Ben Ameur, W, Thameur, M, Ben Youssef, S, O' Grady, H, Gilmore, M, Delassus, P, Sturmberger, T, Ebner, C, Aichinger, J, Tkalec, W, Eder, V, Nesser, HJ, Caggegi, A M, Scandura, S, Capranzano, P, Grasso, C, Mangiafico, S, Ronsivalle, G, Dipasqua, F, Arcidiacono, A, Cannata, S, Tamburino, C, Chapman, M, Henthorn, RENEE, Surikow, S, Zoontjens, J, Stocker, B, Mclean, T, Zeitz, C J, Fabregat Andres, O, Estornell-Erill, J, Ridocci-Soriano, F, De La Espriella, R, Albiach-Montanana, C, Trejo-Velasco, B, Perdomo-Londono, D, Facila, L, Morell, S, Cortijo-Gimeno, J, Kouris, N, Keramida, K, Kostopoulos, V, Psarrou, G, Kostakou, P, Olympios, CD, Kuperstein, R, Blechman, I, Freimatk, D, Arad, M, Ochoa, J P, Fernandez, A, Vaisbuj, F, Salmo, F, Fava, AM, Casabe, H, Guevara, EG, Fernandes, A, Cateano, F, Almeida, I, Silva, J, Trigo, J, Botelho, A, Sanches, C, Venancio, M, Goncalves, L, Schnell, F, Daudin, M, Oger, E, Bouillet, P, Mabo, P, Carre, F, Donal, E, Petrella, L, Fabiani, D, Paparoni, S, De Remigis, F, Tomassoni, G, Prosperi, F, Napoletano, C, Marchel, M, Serafin, A, Kochanowski, J, Steckiewicz, R, Madej-Pilarczyk, A, Filipiak, KJ, Opolski, G, Abid, L, Ben Kahla, S, Charfeddine, S, Kammoun, S, Monivas Palomero, V, Mingo Santos, S, Goirigoizarri Artaza, J, Rodriguez Gonzalez, E, Restrepo Cordoba, A, Rivero Arribas, B, Garcia Lunar, I, Gomez Bueno, M, Sayago Silva, I, Segovia Cubero, J, Zengin, E, Radunski, U K, Klusmeier, M, Ojeda, F, Rybczynski, M, Barten, M, Muellerleile, K, Reichenspurner, H, Blankenberg, S, Sinning, C R, Romano, G, Licata, P, Tuzzolino, F, Clemenza, F, Di Gesaro, G, Hernandez Baravoglia, C, Scardulla, C, Pilato, M, Hashimoto, G, Suzuki, M, Yoshikawa, H, Otsuka, T, Isekame, Y, Iijima, R, Hara, H, Nakamura, M, Sugi, K, Melnikova, MA, Krestjyaninov, MV, Ruzov, VI, Magnino, C, Omede', P, Avenatti, E, Presutti, D, Moretti, C, Ravera, A, Sabia, L, Gaita, F, Veglio, F, Milan, A, Magda, SL, Mincu, RI, Soare, A, Mihai, CM, Florescu, M, Mihalcea, D, Cinteza, M, Vinereanu, D, POSDRU/159/1.5/S/141531, Grant, 112/2011, grant CNCSIS, Chatzistamatiou, E, Mpampatseva Vagena, I, Manakos, K, Moustakas, G, Konstantinidis, D, Memo, G, Mitsakis, O, Kasakogias, A, Syros, P, Kallikazaros, I, Petroni, R, Acitelli, A, Cicconetti, M, Di Mauro, M, Altorio, SF, Romano, S, Petroni, A, Penco, M, Apostolovic, S, Stanojevic, D, Jankovic-Tomasevic, R, Salinger-Martinovic, S, Pavlovic, M, Djordjevic-Radojkovic, D, Tahirovic, E, Dungen, HD, ELD, CIBIS, Jung, I H, Byun, Y S, Goh, C W, Kim, B O, Rhee, K J, Lee, D S, Kim, M J, Seo, H S, Kim, H Y, Tsverava, M, Tsverava, D, Zaletova, T, Shamsheva, D, Parkhomenko, O, Bogdanov, A, Derbeneva, S, Leotescu, A, Tudor, I, Gurghean, A, Bruckner, I, Plaskota, KJ, Trojnarska, O, Bartczak, A, Grajek, S, Sharma, P, Sharma, D, Garg, S, Vazquez Lopez-Ibor, J, Monivas Palomero, V, Solano-Lopez, JM, Zegri Reiriz, I, Dominguez Rodriguez, F, Gonzalez Mirelis, J, Mingo Santos, S, Sayago, I, Garcia Pavia, P, Segovia Cubero, J, Konecny, T, Noseworthy, P, Kapa, S, Cooper, LT, Mulpuru, SK, Asirvatham, S, Florescu, M, Mihalcea, D, Magda, S, Radu, E, Chirca, A, Acasandrei, AM, Jinga, D, Mincu, R, Enescu, OA, Vinereanu, D, 112/2011, no., PN-II-ID-PCE-2011-3-0791, Saura Espin, D, Caballero Jimenez, L, Oliva Sandoval, MJ, Gonzalez Carrillo, J, Garcia Navarro, M, Espinosa Garcia, MD, Valdes Chavarri, M, De La Morena Valenzuela, G, Abul Fadl, AAM, Mourad, MM, team, Primary care Echocardiography, Campanale, C M, Di Maria, S, Mega, S, Nusca, A, Marullo, F, Di Sciascio, G, Pardo Gonzalez, L, Delgado, M, Ruiz, M, Rodriguez, S, Hidalgo, F, Ortega, R, Mesa, D, Suarez De Lezo Cruz Conde, J, Bengrid, T M, Zhao, Y, Henein, MY, Kenjaev, S, Alavi, AL, Kenjaev, ML, Mendes, LM, Lima, S, Dantas, C, Melo, I, Madeira, V, Balao, S, Alves, H, Baptista, E, Mendes, P, Santos, JF, Scali, MC, Mandoli, GE, Simioniuc, A, Massaro, F, Di Bello, V, Marzilli, M, Dini, FL, Cifra, B, Dragulescu, A, Friedberg, MK, Mertens, L, Scali, MC, Bayramoglu, A, Tasolar, H, Otlu, YO, Hidayet, S, Kurt, F, Dogan, A, Pekdemir, H, Stefani, L, Galanti, GG, De Luca, ADL, Toncelli, LT, Pedrizzetti, GP, Gopal, A S, Saha, SK, Toole, RS, Kiotsekoglou, A, Cao, JJ, Reichek, N, Ho, S-J, Hung, S-C, Chang, F-Y, Liao, J-N, Niu, D-M, Yu, W-C, Nemes, A, Kalapos, A, Domsik, P, Forster, T, Siarkos, M, Sammut, E, Lee, L, Jackson, T, Carr-White, G, Rajani, R, Kapetanakis, S, Jarvinen, VM, Sipola, P, Madeo, A, Piras, P, Evangelista, A, Giura, G, Dominici, T, Nardinocchi, P, Varano, V, Chialastri, C, Puddu, PE, Torromeo, C, Sanchis Ruiz, L, Montserrat, S, Obach, V, Cervera, A, Bijnens, B, Sitges, M, Charisopoulou, D, Banner, N R, Rahman-Haley, S, Kim, BJ, Kang, JG, Lee, SH, Sung, KC, Kim, BS, Kang, JH, Lee, ES, Imperadore, F, Del Greco, M, Jermendy, AL, Horcsik, DV, Horvath, T, Celeng, C, Nagy, E, Bartykowszki, A, Tarnoki, DL, Merkely, B, Maurovich-Horvat, P, Jermendy, G, Whitaker, J, Demir, OM, Walton, J, Wragg, A, Alfakih, K, Karolyi, M, Szilveszter, B, Raaijmakers, R, Giepmans, W, Horvath, T, Merkely, B, Maurovich-Horvat, P, Koulaouzidis, GK, Charisopoulou, DC, Mcarthur, TM, Jenkins, PJJ, Henein, MH, Silva, T, Ramos, R, Oliveira, M, Marques, H, Cunha, P, Silva, MN, Barbosa, C, Sofia, A, Pimenta, R, Ferreira, RC, Al-Mallah, M, and Alsaileek, A
- Abstract
Clinical PET acquisitions of the heart suffer from artefacts and drops in image quality due to the poor spatial resolution of the PET system. Moreover, cardiac PET images are further degraded by the blur caused by the breathing and beating motions, thus hampering diagnosis and evaluation of myocardial pathologies. Anatomy-enhanced PET reconstruction, using a high-resolution CT, has proven useful in brain imaging. In cardiac datasets however, due to the motion artefacts, the application of any restoring technique on datasets affected by motion blur needs to be preceded by the validation of the proposed method on realistic static datasets. In this work, the validation is performed using static cardiac ex vivo datasets obtained from a number of sacrificed sheep, scanned on a clinical PET/CT scanner. The aim of this work is to assess the effectiveness of reconstructions of the acquired datasets with different CT-based anatomical priors, in comparison to reconstructions currently applied in clinical practise. The gold standard to which all reconstructions are compared consists of images of the same hearts scanned on a small-animal PET scanner, whose high spatial resolution allows for almost artefact-free images. Encouraging results were obtained so far, with improvements in volume delineation and uniformity of activity values when anatomical information was used. Fig 1 shows the gold standard image (left) compared to a regular clinical reconstruction (middle) and to a reconstruction using the high-resolution CT as anatomical information (right).
Figure - Published
- 2014
- Full Text
- View/download PDF
8. Oral Abstract session: Multimodality imaging: Friday 5 December 2014, 11:00-12:30 * Location: Agora
- Author
-
Szilveszter, B, Major, GP, Horvath, T, Kovacs, A, Pataki, S, Vago, H, Apor, A, Szidonya, L, Merkely, B, Maurovich-Horvat, P, Group, MTA-SE "Lendület" Cardiovascular Imaging Research, Mahmood, N, Almallah, M, Al-Mallah, M, Qureshi, W, Chattahi, J, Demir, OM, Dobson, P, Khan, J, Shaw, A, Papamichael, ND, Alfakih, K, Bartykowszki, A, Drobni, ZD, Panajotu, A, Celeng, C, Suhai, F, Jermendy, AL, Csobay-Novak, C, Merkely, B, Maurovich-Horvat, P, Group, MTA-SE "Lendület" Cardiovascular Imaging Research, Gargiulo, P, Spinelli, L, D'amore, C, Pellegrino, T, Pellegrino, A, Formisano, T, Mariniello, A, Trimarco, B, Perrone-Filardi, P, Bertella, E, Loguercio, M, Baggiano, A, Mushtaq, S, Aquaro, GD, Salerni, S, Rossi, C, Andreini, D, Masci, P, Pontone, G, Angelov, A, and Yotov, Y
- Abstract
Purpose: Transesophageal echocardiography (TEE) is the clinical gold standard technique to exclude left atrial thrombus prior to electrical- of pharmacological cardioversion of atrial fibrillation. We aimed to evaluate the diagnostic performance of cardiac computed tomography angiography (CTA) regarding the detection of left atrial thrombus compared to the gold standard TEE. Methods: In total 444 patients were referred to left atrial angiography before atrial fibrillation ablation procedure (149 women, 295 men, mean age 56y) between February 2011 and January 2014. We have investigated the patients who subsequently underwent TEE (n=201). Results: CTA excluded left atrial thrombi in 178 cases. In all negative CTA cases were confirmed by TEE (true negatives). In 23 cases CTA showed incomplete contrast filling in the left appendage: 19 false positives and 4 true positives. According to our results sensitivity of cardiac CT is 100% [95% CI: 40.2%-100%], specificity was 90.4% [95% CI: 85.4%-94.1%], negative predictive value was 100% [95% CI: 97.9%-100%] and positive predictive value was 17.4% [95% CI: 5.1%-38.8%]. Conclusion: Cardiac CT was very sensitive to diagnose left atrial thrombus, the negative predictive value proved to be 100%. In patients where cardiac CTA excludes left appendage thrombus subsequent TEE examination may be unnecessary.
- Published
- 2014
- Full Text
- View/download PDF
9. Heritability of Coronary Artery Disease: Insights From a Classical Twin Study.
- Author
-
Drobni ZD, Kolossvary M, Karady J, Jermendy AL, Tarnoki AD, Tarnoki DL, Simon J, Szilveszter B, Littvay L, Voros S, Jermendy G, Merkely B, and Maurovich-Horvat P
- Subjects
- Adult, Aged, Computed Tomography Angiography methods, Coronary Angiography methods, Coronary Vessels diagnostic imaging, Coronary Vessels pathology, Female, Humans, Male, Middle Aged, Prospective Studies, Risk Factors, Atherosclerosis pathology, Coronary Artery Disease diagnostic imaging, Coronary Artery Disease epidemiology, Coronary Artery Disease genetics, Plaque, Atherosclerotic genetics
- Abstract
Background: Genetics have a strong influence on calcified atherosclerotic plaques; however, data regarding the heritability of noncalcified plaque volume are scarce. We aimed to evaluate genetic versus environmental influences on calcium (coronary artery calcification) score, noncalcified and calcified plaque volumes by coronary computed tomography angiography in adult twin pairs without known coronary artery disease., Methods: In the prospective BUDAPEST-GLOBAL (Burden of Atherosclerotic Plaques Study in Twins-Genetic Loci and the Burden of Atherosclerotic Lesions) classical twin study, we analyzed twin pairs without known coronary artery disease. All twins underwent coronary computed tomography angiography to assess coronary atherosclerotic plaque volumes. Structural equation models were used to quantify the contribution of additive genetic, common environmental, and unique environmental components to plaque volumes adjusted for age, gender, or atherosclerotic cardiovascular disease risk estimate and statin use., Results: We included 196 twins (mean age±SD, 56±9 years, 63.3% females), 120 monozygotic and 76 same-gender dizygotic pairs. Using structural equation models, noncalcified plaque volume was predominantly determined by environmental factors (common environment, 63% [95% CI, 56%-67%], unique environment, 37% [95% CI, 33%-44%]), while coronary artery calcification score and calcified plaque volumes had a relatively strong genetic heritability (additive genetic, 58% [95% CI, 50%-66%]; unique environmental, 42% [95% CI, 34%-50%] and additive genetic, 78% [95% CI, 73%-80%]; unique environmental, 22% [95% CI, 20%-27%]), respectively., Conclusions: Noncalcified plaque volume is mainly influenced by shared environmental factors, whereas coronary artery calcification score and calcified plaque volume are more determined by genetics. These findings emphasize the importance of early lifestyle interventions in preventing coronary plaque formation., Registration: URL: https://www., Clinicaltrials: gov; Unique identifier: NCT01738828.
- Published
- 2022
- Full Text
- View/download PDF
10. Overlapping Genetic Background of Coronary Artery and Carotid/Femoral Atherosclerotic Calcification.
- Author
-
Hernyes A, Piroska M, Fejer B, Szalontai L, Szabo H, Forgo B, Jermendy AL, Molnar AA, Maurovich-Horvat P, Jermendy G, Merkely B, Tarnoki DL, and Tarnoki AD
- Subjects
- Coronary Vessels, Femoral Artery diagnostic imaging, Genetic Background, Humans, Risk Factors, Atherosclerosis diagnostic imaging, Atherosclerosis genetics, Carotid Artery Diseases, Coronary Artery Disease diagnostic imaging, Coronary Artery Disease genetics
- Abstract
Background and Objectives: Multivessel atherosclerosis and its genetic background are under-investigated, although atherosclerosis is seldom local and still causes high mortality. Alternative methods to assess coronary calcification (CAC) might incorporate genetic links between different arteries' atherosclerotic involvement, however, co-occurrences of coronary calcification have not been investigated in twins yet., Materials and Methods: We assessed the heritability of radio morphologically distinct atherosclerotic plaque types in coronary (non-enhanced CT, Agatston score), carotid, and femoral arteries (B-mode ultrasound) in 190 twin subjects (60 monozygotic, 35 dizygotic pairs). Four-segment scores were derived in order to assess the dissemination of the distinct plaque types in the carotid and femoral arteries taking bilaterality into account. We calculated the genetic correlation between phenotypically correlating plaque types in these arteries., Results: CAC and dissemination of calcified plaques in the carotid and femoral arteries (4S_hyper) were moderately heritable (0.67 [95% CI: 0.37-1] and 0.69 [95% CI: 0.38-1], respectively) when adjusted for age and sex. Hypoechoic plaques in the carotid and femoral arteries showed no heritability, while mixed plaques showed intermediate heritability (0.50 [95% CI: 0-0.76]). Age and sex-adjusted phenotypic correlation between CAC and 4segm_hyper was 0.48 [95% CI: 0.30-0.63] and the underlying genetic correlation was 0.86 [95% CI: 0.42-1]., Conclusions: Calcification of atherosclerotic plaques is moderately heritable in all investigated arteries and significant overlapping genetic factors can be attributed to the phenotypical resemblance of coronary and carotid or femoral atherosclerotic calcification. Our findings support the idea of screening extracoronary arteries in asymptomatic individuals. We also propose a hypothesis about primarily carotid-coronary and femoral-coronary atherosclerosis as two distinct genetic predispositions to co-localization.
- Published
- 2021
- Full Text
- View/download PDF
11. Genetic and environmental factors on heart rate, mean arterial pressure and carotid intima-media thickness: A longitudinal twin study.
- Author
-
Tarnoki AD, Szalontai L, Fagnani C, Tarnoki DL, Lucatelli P, Maurovich-Horvat P, Jermendy AL, Kovacs A, Molnar AA, Godor E, Fejer B, Hernyes A, Cirelli C, Fanelli F, Farina F, Baracchini C, Meneghetti G, Gyarmathy AV, Jermendy G, Merkely B, Pucci G, Schillaci G, Stazi MA, and Medda E
- Subjects
- Heart Rate, Humans, Risk Factors, Twins, Arterial Pressure, Carotid Intima-Media Thickness
- Abstract
Background: Heart rate (HR), mean arterial pressure (MAP) and carotid intima-media thickness (cIMT) are moderately heritable cardiovascular traits, but the environmental effects on the longitudinal change of their heritability have never been investigated., Methods: 368 Italian and Hungarian twins (107 monozygotic, 77 dizygotic) underwent oscillometric measurement and B-mode sonography of bilateral carotid arteries in 2009/2010 and 2014. Within- -individual/cross-study wave, cross-twin/within-study wave and cross-twin/cross-study wave correlations were estimated, and bivariate Cholesky models were fitted to decompose the total variance at each wave and covariance between study waves into additive genetic, shared and unique environmental components., Results: For each trait, a moderate longitudinal stability was observed, with within-individual/crosswave correlations of 0.42 (95% CI: 0.33-0.51) for HR, 0.34 (95% CI: 0.24-0.43) for MAP, and 0.23 (95% CI: 0.12-0.33) for cIMT. Cross-twin/cross-wave correlations in monozygotic pairs were all significant and substantially higher than the corresponding dizygotic correlations. Genetic continuity was the main source of longitudinal stability, with across-time genetic correlations of 0.52 (95% CI: 0.29-0.71) for HR, 0.56 (95% CI: 0.31-0.81) for MAP, and 0.36 (95% CI: 0.07-0.64) for cIMT. Overlapping genetic factors explained respectively 57%, 77%, and 68% of the longitudinal covariance of the HR, MAP and cIMT traits., Conclusions: Genetic factors have a substantial role in the longitudinal change of HR, MAP and cIMT; however, the influence of unique environmental factors remains relevant. Further studies should better elucidate whether epigenetic mechanisms have a role in influencing the stability of the investigated traits over time.
- Published
- 2021
- Full Text
- View/download PDF
12. Comprehensive coronary plaque assessment in patients with obstructive sleep apnea.
- Author
-
Bikov A, Kolossváry M, Jermendy AL, Drobni ZD, Tarnoki AD, Tarnoki DL, Forgó B, Kovacs DT, Losonczy G, Kunos L, Voros S, Merkely B, and Maurovich-Horvat P
- Subjects
- Female, Humans, Male, Middle Aged, Plaque, Atherosclerotic etiology, Plaque, Atherosclerotic pathology, Sleep Apnea, Obstructive diagnosis, Plaque, Atherosclerotic diagnosis, Polysomnography methods, Sleep Apnea, Obstructive complications
- Abstract
Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular disease. Previous studies have assessed the relationship between OSA and coronary artery disease (CAD) using coronary artery calcium score (CAC) measurements. However, limited data are available regarding the association of OSA with non-calcified plaque burden. We therefore aimed to assess the relationship between CAD severity as assessed by coronary computed tomography angiography (CTA) and OSA. Forty-one adult subjects (59 ± 9 years, 15 men) underwent a 256-slice coronary CTA, which was followed by a diagnostic attended cardiorespiratory polygraphy (n = 13) or polysomnography (n = 28). Segment involvement score (SIS), segment stenosis score (SSS) and CAC were used to quantify total CAD burden. Correlation analysis was used to assess potential associations between CAD and OSA. Twenty-two patients were diagnosed with OSA. SIS and SSS were elevated in OSA (2.90 ± 2.78 versus 1.79 ± 2.39 and 4.91 ± 5.94 versus 1.79 ± 4.54, OSA versus controls, SIS and SSS respectively, both p < 0.01) and correlated with OSA severity as measured by the apnea-hypopnea index (AHI, r = 0.41 and 0.43, p < 0.01) and oxygen desaturation index (ODI, r = 0.45 and 0.46, p < 0.01). However, no significant correlation was observed between CAC and OSA. Compared to CAC, SIS and SSS provide additional information on coronary plaque burden in OSA, which shows a significant association with OSA., (© 2019 European Sleep Research Society.)
- Published
- 2019
- Full Text
- View/download PDF
13. Genetic and environmental determinants of longitudinal stability of arterial stiffness and wave reflection: a twin study.
- Author
-
Pucci G, Tarnoki AD, Medda E, Tarnoki DL, Littvay L, Maurovich-Horvat P, Jermendy AL, Godor E, Fejer B, Hernyes A, Lucatelli P, Fanelli F, Farina F, Baracchini C, Meneghetti G, Jermendy G, Merkely B, Schillaci G, Fagnani C, and Stazi MA
- Subjects
- Adult, Aged, Aorta, Epigenesis, Genetic, Female, Gene-Environment Interaction, Humans, Male, Middle Aged, Pulse Wave Analysis, Twins, Dizygotic, Twins, Monozygotic, Vascular Stiffness genetics
- Abstract
Background: We aimed at evaluating the impact of genetic and environmental factors on longitudinal changes in aortic pulse wave velocity (aPWV) and aortic augmentation index (aAIx)., Method: Three hundred and sixty-eight Italian and Hungarian adult twins (214 monozygotic, 154 dizygotic) underwent repeated evaluations of aPWV and aAIx (TensioMed Arteriograph). Within-individual/cross-wave, cross-twin/within-wave and cross-twin/cross-wave correlations were calculated; bivariate Cholesky models were fitted to calculate additive genetic (A), shared environmental (C) and unique environmental (E) components., Results: For both aPWV and aAIx, cross-twin correlations in monozygotic pairs (r between 0.35 and 0.56) were all significant and always higher than in dizygotic pairs, both at wave 1 and at wave 2. Heritability and unshared environmental proportion of variance at each wave were substantially time-invariant for aPWV (heritability 0.51, 95% CI 0.36-0.63 at wave 1; 0.49, 95% CI 0.34-0.62 at wave 2), whereas for aAIx, we observed a diminished genetic effect (heritability 0.57, 95% CI 0.45-0.67 at wave 1; 0.37, 95% CI 0.21-0.51 at wave 2). Overlapping genetic factors explained a high proportion (0.88, 95% CI 0.61-1.00) of longitudinal covariance for aPWV, and had a relatively lower impact on aAIx (0.55, 95% CI 0.35-0.70). Genetic correlations of aPWV (r = 0.64, 95% CI 0.42-0.85) and aAIx (r = 0.70, 95% CI 0.52-0.87) between waves were lower than 1, suggesting a potential contribution of novel genetic variance on arterial stiffening., Conclusion: Changes in aPWV and aAIx over time are largely genetically determined. Our results might stimulate further studies on genetic and epigenetic factors influencing the process of vascular ageing.
- Published
- 2018
- Full Text
- View/download PDF
14. Genetic influence on femoral plaque and its relationship with carotid plaque: an international twin study.
- Author
-
Lucatelli P, Fagnani C, Tarnoki AD, Tarnoki DL, Sacconi B, Fejer B, Stazi MA, Salemi M, Cirelli C, d'Adamo A, Fanelli F, Catalano C, Maurovich-Horvat P, Jermendy AL, Jermendy G, Merkely B, Molnar AA, Pucci G, Schillaci G, Farina F, Meneghetti G, Baracchini C, and Medda E
- Subjects
- Adult, Aged, Carotid Arteries diagnostic imaging, Carotid Artery Diseases diagnostic imaging, Carotid Artery Diseases pathology, Carotid Intima-Media Thickness, Female, Femoral Artery diagnostic imaging, Humans, Hungary, Italy, Male, Middle Aged, Peripheral Arterial Disease diagnostic imaging, Peripheral Arterial Disease pathology, Risk Factors, Ultrasonography, Doppler, Color, Young Adult, Carotid Arteries pathology, Carotid Artery Diseases genetics, Femoral Artery pathology, Gene-Environment Interaction, Peripheral Arterial Disease genetics, Plaque, Atherosclerotic, Twins, Dizygotic genetics, Twins, Monozygotic genetics
- Abstract
To disentangle genetic and environmental influences on the development of femoral plaques using a population of adult twins. To evaluate the potential role of shared genetic and environmental factors in the co-occurrence of femoral and carotid plaques. The sample included 566 twins belonging to 164 monozygotic (MZ) and 119 dizygotic (DZ) twin pairs, who underwent peripheral arterial assessment by B-mode ultrasound in different centers. The variance in femoral plaques onset was due to genetic factors and the remaining 50% was explained by common (15%) and unique (35%) environmental factors. Findings on sidedness and number of femoral plaques indicated that also these traits were mainly under genetic control. No effect of common environment was found on plaques composition, and variability of this trait was explained by genetics (64%) and unique environment (36%). Covariation between the liabilities to carotid and femoral plaques was mainly attributed to shared genes (77%), with the remaining 23% explained by individual-specific environmental factors shared by the two districts. Inter-individual differences in plaque onset as well as in their number, sidedness and composition are mainly genetic in origin. The results on the cooccurrence of carotid and femoral plaque underline the genetic role in atherogenesis.
- Published
- 2018
- Full Text
- View/download PDF
15. Assessing genetic and environmental influences on epicardial and abdominal adipose tissue quantities: a classical twin study.
- Author
-
Jermendy AL, Kolossvary M, Drobni ZD, Tarnoki AD, Tarnoki DL, Karady J, Voros S, Lamb HJ, Merkely B, Jermendy G, and Maurovich-Horvat P
- Subjects
- Abdominal Fat diagnostic imaging, Adult, Cross-Sectional Studies, Female, Genetic Predisposition to Disease, Humans, Intra-Abdominal Fat diagnostic imaging, Male, Pericardium diagnostic imaging, Tomography, Spiral Computed, Abdominal Fat pathology, Cardiovascular Diseases genetics, Gene-Environment Interaction, Intra-Abdominal Fat pathology, Pericardium pathology, Twins, Dizygotic genetics, Twins, Monozygotic genetics
- Abstract
Background/objectives: Various adipose tissue compartments play an important role in the development of cardiometabolic diseases. The quantity of different fat compartments is influenced by genetic and environmental factors. The aim of our study was to evaluate the magnitude of genetic and environmental effects on epicardial, subcutaneous and visceral adipose tissue (EAT, SAT and VAT) quantities in a cohort of adult twin pairs., Subjects/methods: In this cross-sectional study we investigated adult twins (57 monozygotic (MZ) and 33 dizygotic (DZ) same-gender twin pairs; 180 twin subjects). We measured EAT volume using electrocardiogram-gated native computed tomography (CT) scan of the heart, and abdominal SAT and VAT areas were quantified between the third and fourth lumbar vertebra on native CT images. We calculated genetic and environmental impact on the size of various adipose tissue compartments by analyzing co-twin correlations in MZ and DZ pairs separately, and furthermore by using genetic structural equation models., Results: In co-twin analysis, MZ twins had stronger correlations than DZ twins for EAT (r
MZ =0.81, rDZ =0.32), similar to SAT and VAT quantities (rMZ =0.80, rDZ =0.68 and rMZ =0.79, rDZ =0.48, respectively). In multi-trait model fitting analysis, the overall contribution of genetic factors to EAT, SAT and VAT volumes were 80%, 78% and 70%, whereas environmental factors were 20%, 22% and 30%, respectively. Common pathway model analyses indicated that none of the EAT, SAT and VAT phenotypes was independent of the other two., Conclusions: Genetic factors have substantial influence, while environmental factors have only a modest impact on EAT volume, abdominal SAT and VAT quantities. There is a considerable amount of common genetic background influencing the quantities of all three adipose tissue compartments.- Published
- 2018
- Full Text
- View/download PDF
16. Clinical importance of epicardial adipose tissue.
- Author
-
Nagy E, Jermendy AL, Merkely B, and Maurovich-Horvat P
- Abstract
Different visceral fat compartments have several systemic effects and may play a role in the development of both insulin resistance and cardiovascular diseases. In the last couple of years special attention has been paid to the epicardial adipose tissue (EAT), which can be quantified by non-invasive cardiac imaging techniques. The epicardial fat is a unique fat compartment between the myocardium and the visceral pericardium sharing a common embryologic origin with the visceral fat depot. Epicardial adipose tissue has several specific roles, and its local effects on cardiac function are incorporated in the complex pathomechanism of coronary artery disease. Importantly, EAT may produce several adipocytokines and chemokines that may influence - through paracrine and vasocrine effects - the development and progression of coronary atherosclerosis. Epicardial adipose tissue volume has a relatively strong genetic dependence, similarly to other visceral fat depots. In this article, the anatomical and physiological as well as pathophysiological characteristics of the epicardial fat compartment are reviewed., Competing Interests: The authors declare no conflict of interest.
- Published
- 2017
- Full Text
- View/download PDF
17. Heritability of the femoral intima media thickness.
- Author
-
Fejer B, Tarnoki AD, Tarnoki DL, Lucatelli P, Littvay L, Maurovich-Horvat P, Jermendy AL, Kovacs A, Godor E, Fagnani C, Stazi MA, Molnar AA, Fanelli F, Cirelli C, Farina F, Baracchini C, Meneghetti G, Pucci G, Jermendy G, Merkely B, Schillaci G, and Medda E
- Subjects
- Adult, Aged, Biomarkers, Cross-Sectional Studies, Female, Gene-Environment Interaction, Genetic Predisposition to Disease, Humans, Hungary, Italy, Male, Mass Screening, Middle Aged, Regression Analysis, Risk Factors, Atherosclerosis diagnostic imaging, Atherosclerosis genetics, Carotid Artery, Common diagnostic imaging, Carotid Intima-Media Thickness, Femoral Artery diagnostic imaging
- Abstract
Background: The measurement of femoral intima-media thickness (IMT) is underutilized in the clinical practice, although it is a surrogate marker of cardiovascular disease., Materials and Methods: 388 Hungarian and Italian twins (121 monozygotic, 73 dizygotic pairs) underwent bilateral B-mode sonography of femoral arteries. IMT was measured by semiautomated software, where available, or by calipers., Results: Within-pair correlation in monozygotic twins was higher than in dizygotics for each parameter. Age-, sex- and country-adjusted genetic effect accounted for 43.9% (95% confidence interval, CI 21.3%-65.2%) and 47.2% (95% CI, 31.4%-62.6%) of the variance of common and superficial femoral artery IMT, respectively, and unshared environmental effect for 56.1% (95% CI 34.6%-78.5%) and 52.8% (95% CI, 37.2%-68.5%). These results did not change significantly after correcting for body mass index or central systolic blood pressure., Conclusions: Genetic factors have a moderate role in the determination of common and superficial femoral IMT; however, the influence of environmental (lifestyle) factors remains still relevant. Environmental factors may have a role in influencing the genetic predisposition for femoral vascular hypertrophy., (Copyright © 2017 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.)
- Published
- 2017
- Full Text
- View/download PDF
18. Genetic impact dominates over environmental effects in development of carotid artery stiffness: a twin study.
- Author
-
Horváth T, Osztovits J, Pintér A, Littvay L, Cseh D, Tárnoki AD, Tárnoki DL, Jermendy AL, Steinbach R, Métneki J, Schillaci G, Kollai M, and Jermendy G
- Subjects
- Adolescent, Adult, Aged, Aged, 80 and over, Anthropometry, Blood Pressure physiology, Carotid Arteries diagnostic imaging, Carotid Arteries physiology, Female, Hemodynamics physiology, Humans, Life Style, Male, Middle Aged, Pulse Wave Analysis, Risk Factors, Twins, Dizygotic, Twins, Monozygotic, Ultrasonography, Young Adult, Environment, Vascular Stiffness genetics, Vascular Stiffness physiology
- Abstract
Arterial stiffness is an independent predictor of cardiovascular, cerebrovascular and all-cause mortality. Quantifying the genetic influence on the stiff arterial phenotype allows us to better predict the development of arterial stiffness. In this study, we aimed to determine the heritability of carotid artery stiffness in healthy twins. We studied 98 twin pairs of both sexes. We determined carotid artery stiffness locally using echo tracking and applanation tonometry. We estimated the heritability of stiffness parameters using structural equation modeling. The carotid distensibility coefficient showed the highest heritability (64%, 95% confidence interval 45-77%). The incremental elastic modulus, compliance and stiffness index β also showed substantial heritability (62%, 61% and 58%, respectively). The remaining 36-42% phenotypic variance was attributed to unshared environmental effects. Genetic influence appears to dominate over environmental factors in the development of carotid artery stiffness. Environmental factors may have an important role in favorably influencing the genetic predisposition for accelerated arterial stiffening.
- Published
- 2014
- Full Text
- View/download PDF
19. Effect of genetic and environmental influences on cardiometabolic risk factors: a twin study.
- Author
-
Jermendy G, Horváth T, Littvay L, Steinbach R, Jermendy AL, Tárnoki AD, Tárnoki DL, Métneki J, and Osztovits J
- Subjects
- Adolescent, Adult, Aged, Aged, 80 and over, Blood Glucose genetics, Blood Glucose metabolism, Blood Pressure genetics, C-Reactive Protein genetics, C-Reactive Protein metabolism, Cholesterol, HDL blood, Cholesterol, HDL genetics, Cohort Studies, Cross-Sectional Studies, Female, Humans, Male, Middle Aged, Risk Factors, Waist Circumference genetics, Young Adult, Body Weight genetics, Cardiovascular Diseases genetics, Cardiovascular Diseases metabolism, Environment
- Abstract
Background: Both genetic and environmental factors play a role in the pathogenesis of type 2 diabetes and cardiovascular diseases. The magnitude of genetic and environmental influences may vary in different populations and can be investigated by twin studies., Methods: In this cross-sectional study, 101 (63 monozygotic and 38 dizygotic) adult twin pairs (n = 202; mean age: 44.3 ± 15.8 years) were investigated. Past medical history was recorded and physical examination was performed. Fasting venous blood samples were taken for measuring laboratory parameters. For assessing heritability of 14 cardiovascular risk factors, the structural equation (A-C-E) model was used., Results: The following risk factors were highly (> 70.0%) or moderately (50.0 - 69.0%) heritable: weight (88.1%), waist circumference (71.0%), systolic blood pressure (57.1%), diastolic blood pressure (57.7%), serum creatinine (64.1%), fibrinogen (59.9%), and serum C-reactive protein (51.9%). On the other hand, shared and unique environmental influences had the highest proportion of total phenotypic variance in serum total cholesterol (46.8% and 53.2%), serum HDL-cholesterol (58.1% and 14.9%), triglycerides (0.0% and 55.9%), fasting blood glucose (57.1% and 42.9%), fasting insulin (45.4% and 54.5%), serum uric acid (46.0% and 31.3%), and serum homocysteine (71.8% and 28.2%, respectively)., Conclusion: Some cardiometabolic risk factors have strong heritability while others are substantially influenced by environmental factors. Understanding the special heritability characteristics of a particular risk factor can substantiate further investigations, especially in molecular genetics. Moreover, identifying genetic and environmental contribution to certain cardiometabolic risk factors can help in designing prevention and treatment strategies in the population investigated.
- Published
- 2011
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.