47 results on '"Hasselberg, NE"'
Search Results
2. Disease progression rate is a strong predictor of ventricular arrhythmias in patients with cardiac laminopathy in a prospective cohort study
- Author
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Rootwelt-Norberg, C, primary, Skjolsvik, ET, additional, Chivulescu, M, additional, Bogsrud, MP, additional, Ribe, MP, additional, Beitnes, JO, additional, Brekke, PH, additional, Haland, TSF, additional, Hasselberg, NE, additional, Lie, OH, additional, and Haugaa, KH, additional
- Published
- 2022
- Full Text
- View/download PDF
3. Oral Abstract session: New insights in ventricular function: Friday 5 December 2014, 14: 00–15: 30Location: Agora
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Hasselberg, NE, Haugaa, KH, Bernard-Brunet, A, Kongsgaard, E, Donal, E, and Edvardsen, T
- Published
- 2014
4. Poster session 2: Thursday 4 December 2014, 08: 30–12: 30Location: Poster area
- Author
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Saberniak, J, Hasselberg, NE, Leren, IS, Haland, T, Borgquist, R, Platonov, PG, Edvardsen, T, and Haugaa, KH
- Published
- 2014
5. Oral Abstract session: Advanced echo techniques – New eyes on congenital heart disease: Thursday 4 December 2014, 08: 30–10: 00Location: Agora
- Author
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Leren, I S, Hasselberg, NE, Saberniak, J, Haland, TF, Kongsgard, E, Smiseth, OA, Edvardsen, T, and Haugaa, KH
- Published
- 2014
6. Poster Session Saturday 14 December - AM: 14/12/2013, 08: 30–12: 30Location: Poster area
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Saberniak, J, Hasselberg, NE, Borgquist, R, Platonov, PG, Holst, AG, Edvardsen, T, and Haugaa, KH
- Published
- 2013
7. Oral Abstract sessionNew insights in heart muscle diseases: 13/12/2013, 16: 30–18: 00Location: Bursa
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Hasselberg, NE, Saberniak, J, Berge, KE, Edvardsen, T, and Haugaa, KH
- Published
- 2013
8. Poster session Thursday 12 December - AM: 12/12/2013, 08: 30–12: 30Location: Poster area
- Author
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Leren, IS, Hasselberg, NE, Saberniak, J, Leren, TP, Edvardsen, T, and Haugaa, KH
- Published
- 2013
9. Moderated Posters sessionThe prognostic value of myocardial deformation imaging in cardiomyopathy: 12/12/2013, 08: 30–12: 30Location: Moderated Poster area
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Hasselberg, NE, Haugaa, KH, Brunet, A, Kongsgaard, E, Donal, E, and Edvardsen, T
- Published
- 2013
10. Poster session Wednesday 11 December all day display: 11/12/2013, 09: 30–16: 00Location: Poster area
- Author
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Hasselberg, NE, Haugaa, KH, Brunet, A, Kongsgaard, E, Donal, E, and Edvardsen, T
- Published
- 2013
11. Poster Session: Right ventricular systolic function
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Hasselberg, NE, Haugaa, KH, Petri, H, Berge, KE, Leren, TP, Bundgaard, H, and Edvardsen, T
- Published
- 2012
12. Moderated Posters session: advanced echo techniques in congenital heart diseaseP526Systolic function by strain echocardiography is related to cardiac fibrosis and arrhythmias in hypertrophic cardiomyopathyP527Natural history of bicuspid aortic valve valvulo-aortopathy in affected patients followed in a single centerP528Postsystolic thickening as a likely sign of altered deformation due to pressure overload in a Marfan murine model.P529Strain rate echocardiography in patients with hypertrophic cardiomyopathy undergoing surgical myectomy.P530Transthoracic echocardiography is a safe alternative for assessment and guidance of transcatheter closure of secundum atrial septal defect in childrenP531Aortic root dilatation and stiffness assessed by magnetic resonance imaging in adults with repaired tetralogy of FallotP532Assessment of biventricular and vascular function using three-dimensional speckle tracking echocardiography in adult patients with surgical repair of tetralogy of FallotP533A study of functional anatomy of aortic-mitral valve coupling using 3D echocardiography in patients with double orifice mitral valveP534Evaluation of bicuspid aortic valve and its repercussion in the left ventricle with cardiovascular magnetic resonanceP535Echocardiographic assessment of anomalous pulmonary venous connection.
- Author
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Haland, T, primary, Neglia, L, primary, Mas-Stachurska, A, primary, Malanin, D, primary, Baruteau, A-E, primary, Pontnau, F, primary, Capotosto, L, primary, Hristova, K, primary, Sevilla, T, primary, Wojtkowska, A, primary, Almaas, VM, additional, Hasselberg, NE, additional, Saberniak, J, additional, Leren, IS, additional, Hopp, E, additional, Edvardsen, T, additional, Haugaa, KH, additional, Piazza, R, additional, Doronzo, A, additional, Leonelli, V, additional, Morosin, M, additional, Leiballi, E, additional, Pecoraro, R, additional, Lutman, C, additional, Dragos, A, additional, Cassin, M, additional, Sitges, M, additional, Meirelles, T, additional, Hernandez, V, additional, Egea, G, additional, Bijnens, B, additional, Poggio, D, additional, Ferrazzi, P, additional, Spirito, P, additional, Specchia, G, additional, Grillo, M, additional, Amigoni, P, additional, Bersano, C, additional, Pisani, M, additional, Chioffi, M, additional, Hascoet, S, additional, Piot, D, additional, Lambert, V, additional, Petit, J, additional, Ladouceur, M, additional, Ferreira, A, additional, Iserin, L, additional, Mousseaux, E, additional, D'angeli, I, additional, Conde, Y, additional, Ashurov, R, additional, Miraldi, F, additional, Vitarelli, A, additional, Dasheva, A, additional, Marinov, R, additional, Lasarov, S, additional, Mitev, I, additional, Mitev, P, additional, Konstantinov, G, additional, Kaneva, A, additional, Katova, TZ, additional, Revilla-Orodea, A, additional, Uruena-Martinez, N, additional, Fuertes-Alija, JJ, additional, Rodriguez-Velasco, M, additional, Gomez-Salvador, I, additional, San Roman-Calvar, JA, additional, Tomaszewski, A, additional, Czekajska-Chehab, E, additional, Wysokinski, A, additional, Adamczyk, P, additional, Siek, E, additional, and Zakoscielna, M, additional
- Published
- 2015
- Full Text
- View/download PDF
13. Moderated Posters session: advanced echo techniques in congenital heart disease
- Author
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Haland, T, Almaas, VM, Hasselberg, NE, Saberniak, J, Leren, IS, Hopp, E, Edvardsen, T, Haugaa, KH, Neglia, L, Piazza, R, Doronzo, A, Leonelli, V, Morosin, M, Leiballi, E, Pecoraro, R, Lutman, C, Dragos, A, Cassin, M, Mas-Stachurska, A, Sitges, M, Meirelles, T, Hernandez, V, Egea, G, Bijnens, B, Malanin, D, Poggio, D, Ferrazzi, P, Spirito, P, Specchia, G, Grillo, M, Amigoni, P, Bersano, C, Pisani, M, Chioffi, M, Baruteau, A-E, Hascoet, S, Piot, D, Lambert, V, Petit, J, Pontnau, F, Ladouceur, M, Ferreira, A, Iserin, L, Mousseaux, E, Capotosto, L, D'angeli, I, Conde, Y, Ashurov, R, Miraldi, F, Vitarelli, A, Hristova, K, Dasheva, A, Marinov, R, Lasarov, S, Mitev, I, Mitev, P, Konstantinov, G, Kaneva, A, Katova, TZ, Sevilla, T, Revilla-Orodea, A, Uruena-Martinez, N, Fuertes-Alija, JJ, Rodriguez-Velasco, M, Gomez-Salvador, I, San Roman-Calvar, JA, Wojtkowska, A, Tomaszewski, A, Czekajska-Chehab, E, Wysokinski, A, Adamczyk, P, Siek, E, and Zakoscielna, M
- Abstract
Purpose: Myocardial fibrosis by cardiac magnetic resonance imaging (CMR) has been related to ventricular arrhythmias (VAs) in hypertrophic cardiomyopathy (HCM). We hypothesized that systolic function by strain echocardiography is related to VAs and to the extent of fibrosis by CMR. Methods: We studied 150 HCM patients (age 54 ± 14, 39% female). VAs were defined as ventricular tachycardia or aborted cardiac arrest. By speckle-tracking echocardiography we assessed global longitudinal strain (GLS) and mechanical dispersion defined as standard deviation of time from Q/R on ECG to peak negative longitudinal strain in 16 LV segments. Late gadolinium enhancement (LGE) was assessed by CMR and quantified as proportion of total LV myocardium (%LGE) Results: VAs were identified in 37 (25%) patients. Patients with VAs had worse GLS (-14.1 ± 3.6% vs. -16.3 ± 3.4%, p<0.01), more pronounced mechanical dispersion (79 ± 27 ms vs. 59 ± 16 ms, p<0.001), and higher %LGE (6.1 ± 7.8% vs. 0.5 ± 1.4%, p<0.001) than HCM patients without VAs (Figure). Mechanical dispersion was the only independent risk predictor of VAs (OR 1.6, 95%CI 1.1-2.3, p=0.02, per 10ms increase) in multivariate analysis. Mechanical dispersion correlated with %LGE (R= 0.52, p<0.001), and there was a weak, but significant correlation between GLS and % LGE (R=0.27, p=0.01), while neither EF (R=0.01, p=0.96) nor E/e’ (R=0.05, p=0.74) correlated with %LGE. Conclusion: Myocardial systolic function by strain echocardiography was related to VAs in HCM . Mechanical dispersion was a strong independent predictor of VAs and related to the extent of fibrosis on CMR and may improve risk stratification in HCM patients.
- Published
- 2015
- Full Text
- View/download PDF
14. Poster session 2: Thursday 4 December 2014, 08:30-12:30 * Location: Poster area
- Author
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Domingos, JS, Augustine, DX, Leeson, P, Noble, JA, Doan, H-L, Boubrit, L, Cheikh-Khalifa, R, Laveau, F, Djebbar, M, Pousset, F, Isnard, R, Hammoudi, N, Lisi, M, Cameli, M, Di Tommaso, C, Curci, V, Reccia, R, Maccherini, M, Henein, M Y, Mondillo, S, Leitman, M, Vered, Z, Rashid, H, Yalcin, M U, Gurses, K M, Kocyigit, D, Evranos, B, Yorgun, H, Sahiner, L, Kaya, B, Aytemir, K, Ozer, N, Bertella, E, Petulla', M, Baggiano, A, Mushtaq, S, Russo, E, Gripari, P, Innocenti, E, Andreini, D, Tondo, C, Pontone, G, Necas, J, Kovalova, S, Hristova, K, Shiue, I, Bogdanva, V, Teixido Tura, G, Sanchez, V, Rodriguez-Palomares, J, Gutierrez, L, Gonzalez-Alujas, T, Garcia-Dorado, D, Forteza, A, Evangelista, A, Timoteo, A T, Aguiar Rosa, S, Cruz Ferreira, R, Campbell, R, Carrick, D, Mccombe, C, Tzemos, N, Berry, C, Sonecki, P, Noda, M, Setoguchi, M, Ikenouchi, T, Nakamura, T, Yamamoto, Y, Murakami, T, Katou, Y, Usui, M, Ichikawa, K, Isobe, M, Kwon, BJ, Roh, JW, Kim, HY, Ihm, SH, Barron, A J, Francis, DP, Mayet, J, Wensel, R, Kosiuk, J, Dinov, B, Bollmann, A, Hindricks, G, Breithardt, OA, Rio, P, Moura Branco, L, Galrinho, A, Cacela, D, Pinto Teixeira, P, Afonso Nogueira, M, Pereira-Da-Silva, T, Abreu, J, Teresa Timoteo, A, Cruz Ferreira, R, Pavlyukova, EN, Tereshenkova, EK, Karpov, RS, Piatkowski, R, Kochanowski, J, Opolski, G, Barbier, P, Mirea, O, Guglielmo, M, Savioli, G, Cefalu, C, Pudil, R, Horakova, L, Rozloznik, M, Balestra, C, P37/03, PRVOUK, Rimbas, RC, Enescu, OA, Calin, S, Vinereanu, D, POSDRU/159/1.5/S/141531, Grant, Karsenty, C, Hascoet, S, Hadeed, K, Semet, F, Dulac, Y, Alacoque, X, Leobon, B, Acar, P, Dharma, S, Sukmawan, R, Soesanto, AM, Vebiona, KPP, Firdaus, I, Danny, SS, Driessen, M M P, Sieswerda, GTJ, Post, MC, Snijder, RJ, Van Dijk, APJ, Leiner, T, Meijboom, FJ, Chrysohoou, C, Tsitsinakis, G, Tsiachris, D, Aggelis, A, Herouvim, E, Vogiatzis, I, Pitsavos, C, Koulouris, G, Stefanadis, C, Erdei, T, Edwards, J, Braim, D, Yousef, Z, Fraser, AG, Cardiff, Investigators, MEDIA, Avenatti, E, Magnino, C, Omede', P, Presutti, D, Moretti, C, Iannaccone, A, Ravera, A, Gaita, F, Milan, A, Veglio, F, Barbier, P, Scali, MC, Simioniuc, A, Guglielmo, M, Savioli, G, Cefalu, C, Mirea, O, Fusini, L, Dini, F, Okura, H, Murata, E, Kataoka, T, Mikaelpoor, A, Ojaghi Haghighi, SH, Ojaghi Haghighi, SZ, Alizadeasl, A, Sharifi-Zarchi, A, Zaroui, A, Ben Halima, M, Mourali, MS, Mechmeche, R, Rodriguez Palomares, J F, Gutierrez, LG, Maldonado, GM, Garcia, GG, Otaegui, IO, Garcia Del Blanco, BGB, Teixido, GT, Gonzalez Alujas, MTGA, Evangelista, AE, Garcia Dorado, DGD, Godinho, A R, Correia, AS, Rangel, I, Rocha, A, Rodrigues, J, Araujo, V, Almeida, PB, Macedo, F, Maciel, MJ, Rekik, B, Mghaieth, F, Aloui, H, Boudiche, S, Jomaa, M, Ayari, J, Tabebi, N, Farhati, A, Mourali, S, Dekleva, M, Markovic-Nikolic, N, Zivkovic, M, Stankovic, A, Boljevic, D, Korac, N, Beleslin, B, Arandjelovic, A, Ostojic, M, Galli, E, Guirette, Y, Auffret, V, Daudin, M, Fournet, M, Mabo, P, Donal, E, Chin, C W L, Luo, E, Hwan, J, White, A, Newby, D, Dweck, M, Carstensen, H G, Larsen, L H, Hassager, C, Kofoed, K F, Jensen, J S, Mogelvang, R, Kowalczyk, M, Debska, M, Kolesnik, A, Dangel, J, Kawalec, W, Migliore, RA, Adaniya, ME, Barranco, MA, Miramont, G, Gonzalez, S, Tamagusuku, H, Davidsen, E S, Kuiper, K K J, Matre, K, Gerdts, E, Igual Munoz, B, Maceira Gonzalez, AMG, Erdociain Perales, MEP, Estornell Erill, JEE, Valera Martinez, FVM, Miro Palau, VMP, Piquer Gil, MPG, Sepulveda Sanchez, PSS, Cervera Zamora, ACZ, Montero Argudo, AMA, Placido, R, Silva Marques, J, Magalhaes, A, Guimaraes, T, Nobre E Menezes, M, Goncalves, S, Ramalho, A, Robalo Martins, S, Almeida, AG, Nunes Diogo, A, Abid, L, Ben Kahla, S, Charfeddine, S, Abid, D, Kammoun, S, Tounsi, A, Abid, LEILA, Abid, DORRA, Charfeddine, SALMA, Hammami, RANIA, Triki, FETEN, Akrout, MALEK, Mallek, SOUAD, Hentati, MOURAD, Kammoun, SAMIR, Sirbu, C F, Berrebi, A, Huber, A, Folliguet, T, Yang, L-T, Shih, JY, Liu, YW, Li, YH, Tsai, LM, Luo, CY, Tsai, WC, Babukov, R, Bartosh, F, Bazilev, V, Muraru, D, Cavalli, G, Addetia, K, Miglioranza, MH, Veronesi, F, Mihaila, S, Tadic, M, Cucchini, U, Badano, L, Lang, RM, Miyazaki, S, Slavich, M, Miyazaki, T, Figini, F, Lativ, A, Chieffo, A, Montrfano, M, Alfieri, O, Colombo, A, Agricola, E, Liu, D, Hu, K, Herrmann, S, Stoerk, S, Kramer, B, Ertl, G, Bijnens, B, Weidemann, F, Brand, M, Butz, T, Tzikas, S, Van Bracht, M, Roeing, J, Wennemann, R, Christ, M, Grett, M, Trappe, H-J, Scherzer, S, Geroldinger, AG, Krenn, L, Roth, C, Gangl, C, Maurer, G, Rosenhek, R, Neunteufl, T, Binder, T, Bergler-Klein, J, Martins, E, Pinho, T, Leite, S, Azevedo, O, Belo, A, Campelo, M, Amorim, S, Rocha-Goncalves, F, Goncalves, L, Silva-Cardoso, J, Ahn, HS, Kim, KT, Jeon, HK, Youn, HJ, Haland, T, Saberniak, J, Leren, IS, Edvardsen, T, Haugaa, KH, Ziolkowska, L, Boruc, A, Kowalczyk, M, Turska-Kmiec, A, Zubrzycka, M, Kawalec, W, Monivas Palomero, V, Mingo Santos, S, Goirigolzarri Artaza, J, Rodriguez Gonzalez, E, Rivero Arribas, B, Castro Urda, V, Dominguez Rodriguez, F, Mitroi, C, Gracia Lunar, I, Fernadez Lozano, I, Palecek, T, Masek, M, Kuchynka, P, Fikrle, M, Spicka, I, Rysava, R, Linhart, A, Saberniak, J, Hasselberg, NE, Leren, IS, Haland, T, Borgquist, R, Platonov, PG, Edvardsen, T, Haugaa, KH, Ancona, R, Comenale Pinto, S, Caso, P, Coopola, MG, Arenga, F, Rapisarda, O, D'onofrio, A, Sellitto, V, Calabro, R, Rosca, M, Popescu, BA, Calin, A, Mateescu, A, Beladan, CC, Jalba, M, Rusu, E, Zilisteanu, D, Ginghina, C, Pressman, G, Cepeda-Valery, B, Romero-Corral, A, Moldovan, R, Saenz, A, Orban, M, Samuel, SP, Fijalkowski, M, Fijalkowska, M, Gilis-Siek, N, Blaut, K, Galaska, R, Sworczak, K, Gruchala, M, Fijalkowski, M, Nowak, R, Gilis-Siek, N, Fijalkowska, M, Galaska, R, Gruchala, M, Ikonomidis, I, Triantafyllidi, H, Trivilou, P, Tzortzis, S, Papadopoulos, C, Pavlidis, G, Paraskevaidis, I, Lekakis, J, Padiyath, A, Li, L, Xiao, Y, Danford, DA, Kutty, S, Kaymaz, C, Aktemur, T, Poci, N, Ozturk, S, Akbal, O, Yilmaz, F, Tokgoz Demircan, HC, Kirca, N, Tanboga, IH, Ozdemir, N, Investigators, EUPHRATES, Greiner, S, Jud, A, Aurich, M, Hess, A, Hilbel, T, Hardt, S, Katus, HA, D'ascenzi, F, Cameli, M, Alvino, F, Lisi, M, Focardi, M, Solari, M, Bonifazi, M, Mondillo, S, Konopka, M, Krol, W, Klusiewicz, A, Burkhard, K, Chwalbinska, J, Pokrywka, A, Dluzniewski, M, Braksator, W, King, G J, Coen, K, Gannon, S, Fahy, N, Kindler, H, Clarke, J, Iliuta, L, Rac-Albu, M, Placido, R, Robalo Martins, S, Guimaraes, T, Nobre E Menezes, M, Cortez-Dias, N, Francisco, A, Silva, G, Goncalves, S, Almeida, AG, Nunes Diogo, A, Kyu, K, Kong, WKF, Songco, GG, Galupo, MJ, Castro, MD, Shin Hnin, W, Ronald Lee, CH, Poh, KK, Milazzo, V, Di Stefano, C, Tosello, F, Leone, D, Ravera, A, Sabia, L, Sobrero, G, Maule, S, Veglio, F, Milan, A, Jamiel, A M, Ahmed, A M, Farah, I, Al-Mallah, M H, Petroni, R, Magnano, R, Bencivenga, S, Di Mauro, M, Petroni, S, Altorio, SF, Romano, S, Penco, M, Kumor, M, Lipczynska, M, Klisiewicz, A, Wojcik, A, Konka, M, Kozuch, K, Szymanski, P, Hoffman, P, Rimbas, RC, Rimbas, M, Enescu, OA, Mihaila, S, Calin, S, Vinereanu, D, 112/2011, Grant CNCSIS, 159/1.5/S/141531, Grant POSDRU, Donal, E, Reynaud, A, Lund, LH, Persson, H, Hage, C, Oger, E, Linde, C, Daubert, JC, investigators, KaRen, Maria Oliveira Lima, M, Costa, H, Gomes Da Silva, M, Noman Alencar, MC, Carmo Pereira Nunes, M, Costa Rocha, MO, Abid, L, Charfeddine, S, Ben Kahla, S, Abid, D, Siala, A, Hentati, M, Kammoun, S, Kovalova, S, Necas, J, Ozawa, K, Funabashi, N, Takaoka, H, Kobayashi, Y, Matsumura, Y, Wada, M, Hirakawa, D, Yasuoka, Y, Morimoto, N, Takeuchi, H, Kitaoka, H, Sugiura, T, Lakkas, L, Naka, KK, Ntounousi, E, Gkirdis, I, Koutlas, V, Bechlioulis, A, Pappas, K, Katsouras, CS, Siamopoulos, K, Michalis, LK, Naka, KK, Evangelou, D, Kalaitzidis, R, Bechlioulis, A, Lakkas, L, Gkirdis, I, Tzeltzes, G, Nakas, G, Katsouras, CS, Michalis, LK, Generati, G, Bandera, F, Pellegrino, M, Labate, V, Alfonzetti, E, Guazzi, M, Zagatina, A, Zhuravskaya, N, Al-Mallah, M, Alsaileek, A, Qureshi, W, Karsenty, C, Hascoet, S, Peyre, M, Hadeed, K, Alacoque, X, Amadieu, R, Leobon, B, Dulac, Y, Acar, P, Yamanaka, Y, Sotomi, Y, Iwakura, K, Inoue, K, Toyoshima, Y, Tanaka, K, Oka, T, Tanaka, N, Orihara, Y, Fujii, K, Soulat-Dufour, L, Lang, S, Boyer-Chatenet, L, Van Der Vynckt, C, Ederhy, S, Adavane, S, Haddour, N, Boccara, F, Cohen, A, Huitema, MP, Boerman, S, Vorselaars, VMM, Grutters, JC, Post, MC, Gopal, A S, Saha, SK, Toole, RS, Kiotsekoglou, A, Cao, JJ, Reichek, N, Meyer, C G, Altiok, E, Al Ateah, G, Lehrke, M, Becker, M, Lotfi, S, Autschbach, R, Marx, N, Hoffmann, R, Frick, M, Nemes, A, Sepp, R, Kalapos, A, Domsik, P, Forster, T, Caro Codon, J, Blazquez Bermejo, Z, Lopez Fernandez, T, Valbuena Lopez, S C, Iniesta Manjavacas, A M, De Torres Alba, F, Dominguez Melcon, F, Pena Conde, L, Moreno Yanguela, M, Lopez-Sendon, J L, Nemes, A, Lengyel, C, Domsik, P, Kalapos, A, Orosz, A, Varkonyi, TT, Forster, T, Rendon, J, Saldarriaga, C I, Duarte, N, Nemes, A, Domsik, P, Kalapos, A, Forster, T, Nemes, A, Domsik, P, Kalapos, A, Sepp, R, Foldeak, D, Borbenyi, Z, Forster, T, Hamdy, AM, Fereig, HM, Nabih, MA, Abdel-Aziz, A, Ali, AA, Broyd, CJ, Wielandts, J-Y, De Buck, S, Michielsen, K, Louw, R, Garweg, C, Nuyts, J, Ector, J, Maes, F, Heidbuchel, H, Gillis, K, Bala, G, Tierens, S, Cosyns, B, Maurovich-Horvat, P, Horvath, T, Jermendy, A, Celeng, C, Panajotu, A, Bartykowszki, A, Karolyi, M, Tarnoki, AD, Jermendy, G, and Merkely, B
- Abstract
Purpose: 3D echocardiography (3DE) enables fast 3D acquisition but subsequent manual navigation to find 2D diagnostic planes can be time consuming. We have developed and validated an automated machine learning-based technique to find apical 2-, 3- and 4-chamber (A2C, A3C, A4C) views that enables fast volume navigation and analysis. Methods: 3DE volumes were acquired (Philips iE33: X3-1 and X5-1 probes) from 30 healthy volunteers and 36 clinical patients with suspected valve disease and coronary heart disease. 66 end diastolic volumes were used to assess the accuracy of apical standard view finding by our method against manual plane finding. To do this, dedicated software was developed with a machine learning approach and a 3-fold cross validation of results was performed. Results: Automatic A4C view detection was possible in 60/66 (91%) of volumes; detection failures were due to suboptimal myocardium wall integrity or lack of right ventricle in the scan. A2C and A3C views were extracted from the A4C view using the known geometrical relationships between apical standard views (A2C to A3C: 30°~40° and A2C to A4C: 90° of rotation over the left ventricle long axis, as shown in the Figure). In average, our method accurately found the heart apex and mitral valve centre with a 7.1 ± 5.7 mm and 7.2 ± 5.3 mm error, respectively. Conclusions: In order to automate clinical workflow, we have developed a new and fully automatic machine learning strategy for apical standard view finding which performed well (91% detection accuracy) on volunteer and clinical 3D echocardiograms.
Figure - Published
- 2014
- Full Text
- View/download PDF
15. Oral Abstract session: Advanced echo techniques - New eyes on congenital heart disease: Thursday 4 December 2014, 08:30-10:00 * Location: Agora
- Author
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Timoteo, A T, Moura Branco, L, Ramos, R, Aguiar Rosa, S, Agapito, A, Sousa, L, Oliveira, JA, Leal, A, Cruz Ferreira, R, Kutty, S, Li, L, Danford, D, Houle, H, Xiao, Y, Pedrizzetti, G, Porter, T, Leren, I S, Hasselberg, NE, Saberniak, J, Haland, TF, Kongsgard, E, Smiseth, OA, Edvardsen, T, Haugaa, KH, Ben Moussa, N, Cinteza, E, Giugno, L, Butera, G, Piazza, L, Micheletti, A, Saracino, A, Negura, D G, Carminati, M, Chessa, M, Kubik, M, Dabrowska-Kugacka, A, Lewicka, E, Danilowicz-Szymanowicz, L, Szalewska, D, Kutniewska-Kubik, M, Raczak, G, Enache, R, Mateescu, AD, Nastase, OA, Popescu, BA, Ginghina, C, Karsenty, C, Hadeed, K, Hascoet, S, Amadieu, R, Dulac, Y, Acar, P, Ammirati, A, Palmieri, R, Silvetti, MS, and Drago, F
- Abstract
Background: Adults with repaired tetralogy of Fallot (rTOF) are at increased risk for arrhythmic events. Objectives: To evaluate whether right ventricle (RV) and right atrial (RA) two-dimensional speckle tracking (2D strain) are associated with arrhythmic events in patients with rTOF. Methods: We studied 65 consecutive patients with rTOF (34 ± 10 years, 71% males) referred for routine echocardiographic evaluation. We obtained standard echocardiographic measurements that included right heart assessment: RV end-diastolic and systolic area (RVESA), RV fractional area change (RVFAC), tricuspide annular plane systolic excursion (TAPSE), Tei Index, tissue Doppler of the tricuspid ring, tricuspide and pulmonary valve evaluation, residual defects. RV and RA 2D strain was assessed in a 4-chamber view. Patients were divided into two groups: Group 1 (with previous documentation of arrhythmias) and Group 2 (without arrhythmias). Logistic regression analysis was used to assess the statistical association between the studied parameters and arrhythmic events. Results: There were 14 patients with arrhythmic events (8 supraventricular, 4 ventricular and 2 with both). Patients in Group 1 were older (44 ± 11 vs. 32 ± 9 years, p<0.001), had surgical repair at an older age (16 ± 13 vs. 9 ± 11 years, p=0.019) and had the echo examination later after repair (28 ± 11 vs. 23 ± 6 years, p=0.025). All the other measurements were similar between groups. RV strain correlated with all RV function parameters (RVFAC: r= - 0.35; RVESV: r=0.36; TAPSE: r= - 0.36; tricuspide S': r= - 0.30) and with RA strain (r= - 0.51). RA strain correlated also with tricuspide A' (r=0.31) and TAPSE (r=0.27). Patients in Group 1 had significantly reduced RV strain (-13.0 ± 6.3 vs. -16.9 ± 3.6%, p=0.043) and RA strain (33.0 ± 7.2 vs. 28.5 ± 9.2%, p=0.027). RV strain is an independent predictor for the presence of arrhythmic events (OR 1.26, 95% CI 1.04-1.52,p=0.018), adjusted for patient's age and time from repair. RA strain did not remain as an independent predictor after adjustment (OR 0.95, 95% CI 0.88-1.01, p=0.124). By ROC curve analysis, only RV strain predicted the presence of arrhythmias (AUC 0.765, 95% CI 0.594-0.936) with a cut-off value of < -11.2% (sensitivity 57% and specificity 94%). Conclusions: Compared with conventional echocardiographic parameters, 2D strain measurements of the right heart (particularly RV) are associated with the occurrence of arrhythmic events and RV 2D strain may be useful in risk stratification of patients with rTOF.
- Published
- 2014
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16. Oral Abstract session: New insights in ventricular function: Friday 5 December 2014, 14:00-15:30 * Location: Agora
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Guglielmo, M, Cefalu', C, Savioli, G, Mirea, O, Fusini, L, Scali, MC, Simioniuc, A, Dini, F, Barbier, P, Hasselberg, NE, Haugaa, KH, Bernard-Brunet, A, Kongsgaard, E, Donal, E, Edvardsen, T, Mada, RO, Lysyansky, P, Winter, S, Fehske, W, Stankovic, I, Voigt, JU, Domingos, JS, Boardman, H, Leeson, P, Noble, JA, Kou, S, Caballero, L, Henri, C, Dulgheru, R, Magne, J, Daimon, M, Watanabe, H, Ito, H, Yoshikawa, J, Lancellotti, P, Brunet Bernard, A, Donal, E, Leclercq, C, Schnell, F, Fournet, M, Reynaud, A, Thebault, C, Mabo, P, Daubert, JC, Hernandez, A, Park, J, Naksuk, N, Thongprayoon, C, Gaba, P, Sharma, S, Rosenbaum, A, Hu, T, Kapa, S, Bruce, C, Asirvatham, S, Kosmala, W, Rojek, A, Karolko, B, Mysiak, A, and Przewlocka-Kosmala, M
- Abstract
Purpose. We previously re-validated noninvasive estimation of pulmonary wedge pressure (PWP) measuring the CW pulmonary valve regurgitation end-diastolic pressure gradient (PWPecho). Using the latter as surrogate of PWP, we sought to test accuracy of left ventricular (LV) filling pressures estimation by the EAE guidelines algorithm (EAEalg) in a large non-selected population. Methods. We studied 1019 patients in sinus rhythm with GE Vivid7/9 systems (age: 10-93 y.; EF%: 13-83%, normal, n= 827 and reduced <50%, n= 192), in whom PWPecho could be measured (feasibility 75%), with normal pulmonary vascular resistances (WU< 2). The EAEalg combined E/e' (average), left atrial volume (LAV), E/A, Edec, pulmonary venous systolic fraction (SF), and echo-derived pulmonary systolic pressure (PSPe) to obtain 3 groups: normal, high PWP and not classifiable. These were compared to the PWPecho estimate. Results: Feasibility was high for all variables (E/E' 90%, LAV 93%, E/A 95%, Edec 90%, SF 91%, PSPe 92%), and for the EAEAlg (94%). Using the EAEAlg, 17% (n=137) of patients with normal in contrast to 10% (n=19) of patients with EF<50% were not classifiable, in the former secondary to the combination of a E/E'= 9-13 range, and LAV≥ 34ml/m2. In the remaining (classified, 84%) patients, utility of EAEalg even when limited to patients with EF<50% was still hampered by a low positive predictive value (PPV) (Table). Further, when only E/e' was tested in the same patients at ROC analysis (cutoff= 15; AUC=0.72, CI:0.6-0.8), accuracy was still impaired by a low PPV (53%), albeit a fair negative predictive value (NPV) (79%). Correlation between PWPecho and E/e' was modest even in patients with EF<50% (r=0.4, p<0.001), and at multiple regression analysis, E/e' was independently determined by age and mitral regurgitation in all patients, and by LV end-diastolic volume in EF<50% (r= 0.7, p<0.001) and by LV mass index in EF>50% (r= 0.64, p<.001). Conclusions. Noninvasive estimation of PWP by EAE guidelines is limited by a low PPV in both patients with and without reduced LV EF. In this setting, utility of the E/e' is limited, it being influenced by patient age, preload and LV mass.
1 Sensitivity Specificity PPV NPV EF≥50% 72% 78% 18% 98% EF<50% 71% 80% 65% 84% - Published
- 2014
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17. Poster session Thursday 12 December - AM: 12/12/2013, 08:30-12:30 * Location: Poster area
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Abdovic, E, Abdovic, S, Hristova, K, Hristova, K, Katova, TZ, Katova, TZ, Gocheva, N, Gocheva, N, Pavlova, M, Pavlova, M, Gurzun, M M, Ionescu, A, Canpolat, U, Yorgun, H, Sunman, H, Sahiner, L, Kaya, EB, Ozer, N, Tokgozoglu, L, Kabakci, G, Aytemir, K, Oto, A, Gonella, A, Dascenzo, F, Casasso, F, Conte, E, Margaria, F, Grosso Marra, W, Frea, S, Morello, M, Bobbio, M, Gaita, F, Seo, HY, Lee, SP, Lee, JM, Yoon, YE, Park, E, Kim, HK, Park, SJ, Lee, H, Kim, YJ, Sohn, DW, Nemes, A, Domsik, P, Kalapos, A, Orosz, A, Lengyel, C, Forster, T, Enache, R, Muraru, D, Popescu, BA, Calin, A, Nastase, O, Botezatu, D, Purcarea, F, Rosca, M, Beladan, CC, Ginghina, C, Canpolat, U, Aytemir, K, Ozer, N, Yorgun, H, Sahiner, L, Kaya, EB, Oto, A, Trial, Turkish Atrial Fibrosis, Muraru, D, Piasentini, E, Mihaila, S, Padayattil Jose, S, Peluso, D, Ucci, L, Naso, P, Puma, L, Iliceto, S, Badano, LP, Cikes, M, Jakus, N, Sutherland, GR, Haemers, P, Dhooge, J, Claus, P, Yurdakul, S, Oner, FATMA, Direskeneli, HANER, Sahin, TAYLAN, Cengiz, BETUL, Ercan, G, Bozkurt, AYSEN, Aytekin, SAIDE, Osa Saez, A M, Rodriguez-Serrano, M, Lopez-Vilella, R, Buendia-Fuentes, F, Domingo-Valero, D, Quesada-Carmona, A, Miro-Palau, VE, Arnau-Vives, MA, Palencia-Perez, M, Rueda-Soriano, J, Lipczynska, M, Piotr Szymanski, PS, Anna Klisiewicz, AK, Lukasz Mazurkiewicz, LM, Piotr Hoffman, PH, Kim, KH, Cho, SK, Ahn, Y, Jeong, MH, Cho, JG, Park, JC, Chinali, M, Franceschini, A, Matteucci, MC, Doyon, A, Esposito, C, Del Pasqua, A, Rinelli, G, Schaefer, F, group, the 4C study, Kowalik, E, Klisiewicz, A, Rybicka, J, Szymanski, P, Biernacka, EK, Hoffman, P, Lee, S, Kim, W, Yun, H, Jung, L, Kim, E, Ko, J, Ruddox, V, Norum, IB, Edvardsen, T, Baekkevar, M, Otterstad, JE, Erdei, T, Edwards, J, Braim, D, Yousef, Z, Fraser, AG, Cardiff, Investigators, MEDIA, Melcher, A, Reiner, B, Hansen, A, Strandberg, LE, Caidahl, K, Wellnhofer, E, Kriatselis, C, Gerd-Li, H, Furundzija, V, Thnabalasingam, U, Fleck, E, Graefe, M, Park, YJ, Moon, JG, Ahn, TH, Baydar, O, Kadriye Kilickesmez, KK, Ugur Coskun, UC, Polat Canbolat, PC, Veysel Oktay, VO, Umit Yasar Sinan, US, Okay Abaci, OA, Cuneyt Kocas, CK, Sinan Uner, SU, Serdar Kucukoglu, SK, Ferferieva, V, Claus, P, Rademakers, F, Dhooge, J, Le, T T, Wong, P, Tee, N, Huang, F, Tan, RS, Altman, M, Logeart, D, Bergerot, C, Gellen, B, Pare, C, Gerard, S, Sirol, M, Vicaut, E, Mercadier, JJ, Derumeaux, G A, investigators, PREGICA, Park, T-H, Park, J-I, Shin, S-W, Yun, S-H, Lee, J-E, Makavos, G, Kouris, N, Keramida, K, Dagre, A, Ntarladimas, I, Kostopoulos, V, Damaskos, D, Olympios, CD, Leong, DP, Piers, SRD, Hoogslag, GE, Hoke, U, Thijssen, J, Ajmone Marsan, N, Schalij, MJ, Bax, JJ, Zeppenfeld, K, Delgado, V, Rio, P, Branco, L, Galrinho, A, Cacela, D, Abreu, J, Timoteo, A, Teixeira, P, Pereira-Da-Silva, T, Selas, M, Cruz Ferreira, R, Popa, B A, Zamfir, L, Novelli, E, Lanzillo, G, Karazanishvili, L, Musica, G, Stelian, E, Benea, D, Diena, M, Cerin, G, Fusini, L, Mirea, O, Tamborini, G, Muratori, M, Gripari, P, Ghulam Ali, S, Cefalu, C, Maffessanti, F, Andreini, D, Pepi, M, Mamdoo, F, Goncalves, A, Peters, F, Matioda, H, Govender, S, Dos Santos, C, Essop, MR, Kuznetsov, V A, Yaroslavskaya, E I, Pushkarev, G S, Krinochkin, D V, Kolunin, G V, Bennadji, A, Hascoet, S, Dulac, Y, Hadeed, K, Peyre, M, Ricco, L, Clement, L, Acar, P, Ding, WH, Zhao, Y, Lindqvist, P, Nilson, J, Winter, R, Holmgren, A, Ruck, A, Henein, MY, Illatopa, V, Cordova, F, Espinoza, D, Ortega, J, Cavalcante, JL, Patel, MT, Katz, W, Schindler, J, Crock, F, Khanna, MK, Khandhar, S, Tsuruta, H, Kohsaka, S, Murata, M, Yasuda, R, Tokuda, H, Kawamura, A, Maekawa, Y, Hayashida, K, Fukuda, K, Le Tourneau, T, Kyndt, F, Lecointe, S, Duval, D, Rimbert, A, Merot, J, Trochu, JN, Probst, V, Le Marec, H, Schott, JJ, Veronesi, F, Addetia, K, Corsi, C, Lamberti, C, Lang, RM, Mor-Avi, V, Gjerdalen, G F, Hisdal, J, Solberg, EE, Andersen, TE, Radunovic, Z, Steine, K, Maffessanti, F, Gripari, P, Tamborini, G, Muratori, M, Fusini, L, Ferrari, C, Caiani, EG, Alamanni, F, Bartorelli, AL, Pepi, M, Dascenzi, F, Cameli, M, Iadanza, A, Lisi, M, Reccia, R, Curci, V, Sinicropi, G, Henein, M, Pierli, C, Mondillo, S, Rekhraj, S, Hoole, SP, Mcnab, DC, Densem, CG, Boyd, J, Parker, K, Shapiro, LM, Rana, BS, Kotrc, M, Vandendriessche, T, Bartunek, J, Claeys, MJ, Vanderheyden, M, Paelinck, B, De Bock, D, De Maeyer, C, Vrints, C, Penicka, M, Silveira, C, Albuquerque, ESA, Lamprea, DL, Larangeiras, VL, Moreira, CRPM, Victor Filho, MVF, Alencar, BMA, Silveira, AQMS, Castillo, JMDC, Zambon, E, Iorio, A, Carriere, C, Pantano, A, Barbati, G, Bobbo, M, Abate, E, Pinamonti, B, Di Lenarda, A, Sinagra, G, Salemi, V M C, Tavares, L, Ferreira Filho, JCA, Oliveira, AM, Pessoa, FG, Ramires, F, Fernandes, F, Mady, C, Cavarretta, E, Lotrionte, M, Abbate, A, Mezzaroma, E, De Marco, E, Peruzzi, M, Loperfido, F, Biondi-Zoccai, G, Frati, G, Palazzoni, G, Park, T-H, Lee, J-E, Lee, D-H, Park, J-S, Park, K, Kim, M-H, Kim, Y-D, Van T Sant, J, Gathier, WA, Leenders, GE, Meine, M, Doevendans, PA, Cramer, MJ, Poyhonen, P, Kivisto, S, Holmstrom, M, Hanninen, H, Schnell, F, Betancur, J, Daudin, M, Simon, A, Carre, F, Tavard, F, Hernandez, A, Garreau, M, Donal, E, Calore, C, Muraru, D, Badano, LP, Melacini, P, Mihaila, S, Denas, G, Naso, P, Casablanca, S, Santi, F, Iliceto, S, Aggeli, C, Venieri, E, Felekos, I, Anastasakis, A, Ritsatos, K, Kakiouzi, V, Kastellanos, S, Cutajar, I, Stefanadis, C, Palecek, T, Honzikova, J, Poupetova, H, Vlaskova, H, Kuchynka, P, Linhart, A, Elmasry, O, Mohamed, MH, Elguindy, WM, Bishara, PNI, Garcia-Gonzalez, P, Cozar-Santiago, P, Bochard-Villanueva, B, Fabregat-Andres, O, Cubillos-Arango, A, Valle-Munoz, A, Ferrer-Rebolleda, J, Paya-Serrano, R, Estornell-Erill, J, Ridocci-Soriano, F, Jensen, M, Havndrup, O, Christiansen, M, Andersen, PS, Axelsson, A, Kober, L, Bundgaard, H, Karapinar, H, Kaya, A, Uysal, EB, Guven, AS, Kucukdurmaz, Z, Oflaz, MB, Deveci, K, Sancakdar, E, Gul, I, Yilmaz, A, Tigen, M K, Karaahmet, T, Dundar, C, Yalcinsoy, M, Tasar, O, Bulut, M, Takir, M, Akkaya, E, Jedrzejewska, I, Braksator, W, Krol, W, Swiatowiec, A, Dluzniewski, M, Lipari, P, Bonapace, S, Zenari, L, Valbusa, F, Rossi, A, Lanzoni, L, Molon, G, Canali, G, Campopiano, E, Barbieri, E, Rueda Calle, E, Alfaro Rubio, F, Gomez Gonzalez, J, Gonzalez Santos, P, Cameli, M, Lisi, M, Focardi, M, Dascenzi, F, Solari, M, Galderisi, M, Mondillo, S, Pratali, L, Bruno, R M, Corciu, AI, Comassi, M, Passera, M, Gastaldelli, A, Mrakic-Sposta, S, Vezzoli, A, Picano, E, Perry, R, Penhall, A, De Pasquale, C, Selvanayagam, J, Joseph, M, Simova, I I, Katova, T M, Kostova, V, Hristova, K, Lalov, I, Dascenzi, F, Pelliccia, A, Natali, BM, Cameli, M, Alvino, F, Zorzi, A, Corrado, D, Bonifazi, M, Mondillo, S, Rees, E, Rakebrandt, F, Rees, DA, Halcox, JP, Fraser, AG, Odriscoll, J, Lau, N, Perez-Lopez, M, Sharma, R, Lichodziejewska, B, Goliszek, S, Kurnicka, K, Kostrubiec, M, Dzikowska Diduch, O, Krupa, M, Grudzka, K, Ciurzynski, M, Palczewski, P, Pruszczyk, P, Gheorghe, LL, Castillo Ortiz, J, Del Pozo Contreras, R, Calle Perez, G, Sancho Jaldon, M, Cabeza Lainez, P, Vazquez Garcia, R, Fernandez Garcia, P, Chueca Gonzalez, E, Arana Granados, R, Zhao, XX, Xu, XD, Bai, Y, Qin, YW, Leren, IS, Hasselberg, NE, Saberniak, J, Leren, TP, Edvardsen, T, Haugaa, KH, Daraban, A M, Sutherland, GR, Claus, P, Werner, B, Gewillig, M, Voigt, JU, Santoro, A, Ierano, P, De Stefano, F, Esposito, R, De Palma, D, Ippolito, R, Tufano, A, Galderisi, M, Costa, R, Fischer, C, Rodrigues, A, Monaco, C, Lira Filho, E, Vieira, M, Cordovil, A, Oliveira, E, Mohry, S, Gaudron, P, Niemann, M, Herrmann, S, Strotmann, J, Beer, M, Hu, K, Bijnens, B, Ertl, G, Weidemann, F, Baktir, AO, Sarli, B, Cicek, M, Karakas, MS, Saglam, H, Arinc, H, Akil, MA, Kaya, H, Ertas, F, Bilik, MZ, Yildiz, A, Oylumlu, M, Acet, H, Aydin, M, Yuksel, M, Alan, S, Odriscoll, J, Gravina, A, Di Fino, S, Thompson, M, Karthigelasingham, A, Ray, K, Sharma, R, De Chiara, B, Russo, CF, Alloni, M, Belli, O, Spano, F, Botta, L, Palmieri, B, Martinelli, L, Giannattasio, C, Moreo, A, Mateescu, AD, La Carrubba, S, Vriz, O, Di Bello, V, Carerj, S, Zito, C, Ginghina, C, Popescu, BA, Nicolosi, GL, Antonini-Canterin, F, Malev, E, Omelchenko, M, Vasina, L, Luneva, E, Zemtsovsky, E, Cikes, M, Velagic, V, Gasparovic, H, Kopjar, T, Colak, Z, Hlupic, LJ, Biocina, B, Milicic, D, Tomaszewski, A, Kutarski, A, Poterala, M, Tomaszewski, M, Brzozowski, W, Kijima, Y, Akagi, T, Nakagawa, K, Ikeda, M, Watanabe, N, Ueoka, A, Takaya, Y, Oe, H, Toh, N, Ito, H, Bochard Villanueva, B, Paya-Serrano, R, Fabregat-Andres, O, Garcia-Gonzalez, P, Perez-Bosca, JL, Cubillos-Arango, A, Chacon-Hernandez, N, Higueras-Ortega, L, De La Espriella-Juan, R, Ridocci-Soriano, F, Noack, T, Mukherjee, C, Ionasec, RI, Voigt, I, Kiefer, P, Hoebartner, M, Misfeld, M, Mohr, F-W, Seeburger, J, Daraban, A M, Baltussen, L, Amzulescu, MS, Bogaert, J, Jassens, S, Voigt, JU, Duchateau, N, Giraldeau, G, Gabrielli, L, Penela, D, Evertz, R, Mont, L, Brugada, J, Berruezo, A, Bijnens, BH, Sitges, M, Yoshikawa, H, Suzuki, M, Hashimoto, G, Kusunose, Y, Otsuka, T, Nakamura, M, Sugi, K, Ruiz Ortiz, M, Mesa, D, Romo, E, Delgado, M, Seoane, T, Martin, M, Carrasco, F, Lopez Granados, A, Arizon, JM, Suarez De Lezo, J, Magalhaes, A, Cortez-Dias, N, Silva, D, Menezes, M, Saraiva, M, Santos, L, Costa, A, Costa, L, Nunes Diogo, A, Fiuza, M, Ren, B, De Groot-De Laat, LE, Mcghie, J, Vletter, WB, Geleijnse, ML, Toda, H, Oe, H, Osawa, K, Miyoshi, T, Ugawa, S, Toh, N, Nakamura, K, Kohno, K, Morita, H, Ito, H, El Ghannudi, S, Germain, P, Samet, H, Jeung, M, Roy, C, Gangi, A, Orii, M, Hirata, K, Yamano, T, Tanimoto, T, Ino, Y, Yamaguchi, T, Kubo, T, Imanishi, T, Akasaka, T, Sunbul, M, Kivrak, T, Oguz, M, Ozguven, S, Gungor, S, Dede, F, Turoglu, HT, Yildizeli, B, Mutlu, B, Mihaila, S, Muraru, D, Piasentini, E, Peluso, D, Cucchini, U, Casablanca, S, Naso, P, Iliceto, S, Vinereanu, D, Badano, LP, Rodriguez Munoz, DA, Moya Mur, JL, Becker Filho, D, Gonzalez, A, Casas Rojo, E, Garcia Martin, A, Recio Vazquez, M, Rincon, LM, Fernandez Golfin, C, Zamorano Gomez, JL, Ledakowicz-Polak, A, Polak, L, Zielinska, M, Kamiyama, T, Nakade, T, Nakamura, Y, Ando, T, Kirimura, M, Inoue, Y, Sasaki, O, Nishioka, T, Farouk, H, Sakr, B, Elchilali, K, Said, K, Sorour, K, Salah, H, Mahmoud, G, Casanova Rodriguez, C, Cano Carrizal, R, Iglesias Del Valle, D, Martin Penato Molina, A, Garcia Garcia, A, Prieto Moriche, E, Alvarez Rubio, J, De Juan Bagua, J, Tejero Romero, C, Plaza Perez, I, Korlou, P, Stefanidis, A, Mpikakis, N, Ikonomidis, I, Anastasiadis, S, Komninos, K, Nikoloudi, P, Margos, P, and Pentzeridis, P
- Abstract
Purpose: Atrial fibrillation (AF) is the most prevalent sustained arrhythmia. It is a disease of the elderly and it is common in patients (pts) with structural heart disease. Hypertension (HA), hypertensive heart disease (HHD), diabetes mellitus (DM), coronary artery disease (CAD), heart failure (HF), and valvular heart disease (VHD) are recognized predisposing factors to AF. Objectives: To echocardiographicly disclose the most common predisposing morbidities to AF in our population sample. Methods: From June 2000 to February 2013, 3755 consecutive pts with AF were studied during echocardiographic check-up. According to transthoracic echo, pts were divided in groups based on dominative underlying heart diseases. Electrocardiographically documented AF was subdivided in two groups: transitory and chronic. Transitory AF fulfilled criteria for paroxysmal or persistent AF. Chronic AF were cases of long-standing persistent or permanent AF. Results: The median age was 72 years, age range between 16 and 96 years. There were 51.4% of females. Chronic AF was observed in 68.3% pts. Distribution of underlying heart diseases is shown in figure. Lone AF was diagnosed in only 25 pts, mostly in younger males (median age 48 years, range 29–59, men 80%). Chronic AF was predominant in groups with advanced cardiac remodeling such as dilatative cardiomyopaty (DCM) and VHD, mostly in elderly. HA and DM were found in 75.4% and 18.8%, respectively. Almost 1/2 of pts with AF had HF and 59.2% had diastolic HF. Conclusion: Up to now, echocardiographic categorization of the predisposing factors to AF was not reported. Echocardiographic evaluation of patients with AF could facilitate in identification and well-timed treatment of predisposing comorbidites.
Figure Etiological distribution of AF - Published
- 2013
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18. Moderated Posters session * The prognostic value of myocardial deformation imaging in cardiomyopathy: 12/12/2013, 08:30-12:30 * Location: Moderated Poster area
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Cakmak, H, Ural, E, Sahin, T, Al, N, Emre, E, Saracoglu, E, Akbulut, T, Ural, D, Rangel, I, Goncalves, A, Sousa, C, Rodrigues, J, Macedo, F, Silva-Cardoso, J, Maciel, MJ, Iliuta, L, Nagata, Y, Takeuchi, M, Kuwaki, H, Hasyashi, A, Otani, K, Yoshitani, H, Osuji, Y, Haberka, M, Liszka, J, Kozyra, A, Tabor, Z, Finik, M, Gasior, Z, Hasselberg, NE, Haugaa, KH, Brunet, A, Kongsgaard, E, Donal, E, Edvardsen, T, Sugano, A, Seo, Y, Sato, K, Atsumi, A, Yamamoto, M, Machino, T, Harimura, Y, Kawamura, R, Ishizu, T, Aonuma, K, Biering-Sorensen, T, Hoffmann, S, Mogelvang, R, Iversen, AZ, Fritz-Hansen, T, Bech, J, Jensen, JS, Flarup Dons, M, Biering-Soerensen, T, Skov Jensen, J, Fritz Hansen, T, Bech, J, Chantal De Knegt, M, Sivertsen, J, and Moegelvang, R
- Abstract
Aim: We aimed to investigate the prognostic value and reveal the role of a novel method speckle tracking echocardiography for predicting adverse cardiovascular events in STEMI patients undergoing successful primary percutaneous intervention (PCI). Methods: We included 117 patients who admitted to University Cardiology Clinic with STEMI and underwent successful PCI between June 2011 and January 2012. After PCI, in the first three days (baseline) and at the first month after discharge (control), echocardiographic evaluations of patients were carried out. The relationship between cardiac adverse events that occurred during the six-month follow-up and echocardiographic parameters were evaluated. Patients were divided into two groups according to development of adverse event (a composite of revascularization, reinfarction and hospitalization for heart failure) and comparisons between groups were made. Results: When we compare the baseline strain values of patients included in the study, the baseline average global longitudinal strain (GLS) of event group (n=20) was -12,10 ± 2,59; the baseline average GLS of event free group (n=97) was -14,46 ± 3,65. In the group with event, we determined statistically significant lower baseline GLS values. In terms of baseline circumferential strain (CS) and radial strain (RS) values, there was no statistically significant difference between the two groups. In the roc analysis, when we use the threshold values below -12,9 for the baseline GLS, we detected that baseline GLS predicted the development of adverse events with % 75 sensitivity and % 70 specificity. While there was no change in control GLS values from the baseline in the event group at first month echocardiography, in the event free group, statistically significant higher and improved strain values were observed. According to these results, increased strain values at the first month were associated with better prognosis. In terms of CS and RS values, there was no statistically significant difference between baseline and control in both groups. Conclusion: Our study revealed that strain analysis with speckle tracking echocardiography is a new echocardiographic method which can be used to determine the prognosis of patients with STEMI.
- Published
- 2013
- Full Text
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19. Poster Session Saturday 14 December - AM: 14/12/2013, 08:30-12:30 * Location: Poster area
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Muraru, D, Addetia, K, Veronesi, F, Corsi, C, Mor-Avi, V, Yamat, M, Weinert, L, Lang, RM, Badano, LP, Faita, F, Di Lascio, N, Bruno, RM, Bianchini, E, Ghiadoni, L, Sicari, R, Gemignani, V, Angelis, A, Ageli, K, Ioakimidis, N, Chrysohoou, C, Agelakas, A, Felekos, I, Vaina, S, Aznaourides, K, Vlachopoulos, C, Stefanadis, C, Nemes, A, Szolnoky, G, Gavaller, H, Gonczy, A, Kemeny, L, Forster, T, Ramalho, A, Placido, R, Marta, L, Menezes, M, Magalhaes, A, Cortez Dias, N, Martins, S, Almeida, A, Pinto, F, Nunes Diogo, A, Botezatu, C-D, Enache, R, Popescu, BA, Nastase, O, Coman, MC, Ghiorghiu, I, Calin, A, Rosca, M, Beladan, C, Ginghina, C, Grapsa, J, Cabrita, IZ, Durighel, G, Oregan, D, Dawson, D, Nihoyannopoulos, P, Pellicori, P, Kallvikbacka-Bennett, A, Zhang, J, Lukaschuk, E, Joseph, A, Bourantas, C, Loh, H, Bragadeesh, T, Clark, A, Cleland, JG, Kallvikbacka-Bennett, A, Pellicori, P, Lomax, S, Putzu, P, Diercx, R, Parsons, S, Dicken, B, Zhang, J, Clark, A, Cleland, JG, Vered, Z, Adirevitz, L, Dragu, R, Blatt, A, Karev, E, Malca, Y, Roytvarf, A, Marek, D, Sovova, E, Berkova, M, Cihalik, C, Taborsky, M, Lindqvist, P, Tossavainen, ERIK, Soderberg, S, Gonzales, M, Gustavsson, S, Henein, MY, Sonne, C, Bott-Fluegel, L, Hauck, S, Lesevic, H, Hadamitzky, M, Wolf, P, Kolb, C, Bandera, F, Pellegrino, M, Generati, G, Donghi, V, Alfonzetti, E, Castelvecchio, S, Menicanti, L, Guazzi, M, Buchyte, S, Rinkuniene, D, Jurkevicius, R, Smarz, K, Zaborska, B, Jaxa-Chamiec, T, Maciejewski, P, Budaj, A, Santoro, A, Federico Alvino, FA, Giovanni Antonelli, GA, Roberta Molle, RM, Matteo Bertini, MB, Stefano Lunghetti, SL, Sergio Mondillo, SM, Henri, C, Magne, J, Dulgheru, R, Laaraibi, S, Voilliot, D, Kou, S, Pierard, L, Lancellotti, P, Szulik, M, Stabryla-Deska, J, Kalinowski, M, Sliwinska, A, Szymala, M, Lenarczyk, R, Kalarus, Z, Kukulski, T, Investigators, TRUST CRT, Yiangou, K, Azina, C, Yiangou, A, Ioannides, M, Chimonides, S, Baysal, S, Pirat, B, Okyay, K, Bal, U, Muderrisoglu, H, Popovic, D, Ostojic, M, Petrovic, M, Vujisic-Tesic, B, Arandjelovic, A, Petrovic, I, Banovic, M, Popovic, B, Vukcevic, V, Damjanovic, S, Velasco Del Castillo, S, Onaindia Gandarias, JJ, Arana Achaga, X, Laraudogoitia Zaldumbide, E, Rodriguez Sanchez, I, Cacicedo De Bobadilla, A, Romero Pereiro, A, Aguirre Larracoechea, U, Salinas, T, Subinas, A, Elzbieciak, M, Wita, K, Grabka, M, Chmurawa, J, Doruchowska, A, Turski, M, Filipecki, A, Wybraniec, M, Mizia-Stec, K, Varho, VV, Karjalainen, PP, Lehtinen, T, Airaksinen, JKE, Ylitalo, A, Kiviniemi, TO, Gargiulo, P, Galderisi, M, D Amore, C, Lo Iudice, F, Savarese, G, Casaretti, L, Pellegrino, AM, Fabiani, I, La Mura, L, Perrone Filardi, P, Kim, J Y, Chung, WB, Yu, JS, Choi, YS, Park, CS, Youn, HJ, Lee, MY, Nagy, AI, Manouras, A, Gunyeli, E, Gustafsson, U, Shahgaldi, K, Winter, R, Johnsson, J, Zagatina, A, Krylova, L, Zhuravskaya, N, Vareldzyan, Y, Tyurina, TV, Clitsenko, O, Khalifa, E A, Ashour, Z, Elnagar, W, Jung, IH, Seo, HS, Lee, SJ, Lim, DS, Mizariene, V, Verseckaite, R, Janenaite, J, Jonkaitiene, R, Jurkevicius, R, Sanchez Espino, AD, Bonaque Gonzalez, JC, Merchan Ortega, G, Bolivar Herrera, N, Ikuta, I, Macancela Quinones, JJ, Gomez Recio, M, Silva Fazendas Adame, P R, Caldeira, D, Stuart, B, Almeida, S, Cruz, I, Ferreira, A, Freire, G, Lopes, L, Cotrim, C, Pereira, H, Mediratta, A, Addetia, K, Moss, JD, Nayak, HM, Yamat, M, Weinert, L, Mor-Avi, V, Lang, RM, Al Amri, I, Debonnaire, P, Van Der Kley, F, Schalij, MJ, Bax, JJ, Ajmone Marsan, N, Delgado, V, Schmidt, F P, Gniewosz, T, Jabs, A, Munzel, T, Jansen, T, Kaempfner, D, Hink, U, Von Bardeleben, RS, Jose, J, George, OK, Joseph, G, Jose, J, Adawi, S, Najjar, R, Ahronson, D, Shiran, A, Van Riel, ACMJ, Boerlage - Van Dijk, K, De Bruin - Bon, HACM, Araki, M, Meregalli, PG, Koch, KT, Vis, MM, Mulder, BJM, Baan, J, Bouma, BJ, Marciniak, A, Elton, D, Glover, K, Campbell, I, Sharma, R, Batalha, S, Lourenco, C, Oliveira Da Silva, C, Manouras, A, Shahgaldi, K, Caballero, L, Garcia-Lara, J, Gonzalez-Carrillo, J, Oliva, MJ, Saura, D, Garcia-Navarro, M, Espinosa, MD, Pinar, E, Valdes, M, De La Morena, G, Barreiro Perez, M, Lopez Perez, M, Roy, D, Brecker, S, Sharma, R, Venkateshvaran, A, Dash, P K, Sola, S, Barooah, B, Govind, S C, Winter, R, Shahgaldi, K, Brodin, L A, Manouras, A, Saura Espin, D, Caballero Jimenez, L, Gonzalez Carrillo, J, Oliva Sandoval, MJ, Lopez Ruiz, M, Garcia Navarro, M, Espinosa Garcia, MD, Valdes Chavarri, M, De La Morena Valenzuela, G, Gatti, G, Dellangela, L, Pinamonti, B, Benussi, B, Sinagra, G, Pappalardo, A, Group, Heart Muscle Disease Study, Hernandez, V, Saavedra, J, Gonzalez, A, Iglesias, P, Civantos, S, Guijarro, G, Monereo, S, Ikeda, M, Toh, N, Oe, H, Tanabe, Y, Watanabe, N, Ito, H, Ciampi, Q, Cortigiani, L, Pratali, L, Rigo, F, Villari, B, Picano, E, Sicari, R, Yoon, JH, Sohn, JW, Kim, YJ, Chang, HJ, Hong, GR, Kim, TH, Ha, JW, Choi, BW, Rim, SJ, Choi, EY, Tibazarwa, K, Sliwa, K, Wonkam, A, Mayosi, BM, Oryshchyn, N, Ivaniv, Y, Pavlyk, S, Lourenco, M R, Azevedo, O, Moutinho, J, Nogueira, I, Fernandes, M, Pereira, V, Quelhas, I, Lourenco, A, Sunbul, M, Tigen, K, Karaahmet, T, Dundar, C, Ozben, B, Guler, A, Cincin, A, Bulut, M, Sari, I, Basaran, Y, Baydar, O, Kadriye Kilickesmez, KK, Ugur Coskun, UC, Polat Canbolat, PC, Veysel Oktay, VO, Umit Yasar Sinan, US, Okay Abaci, OA, Cuneyt Kocas, CK, Sinan Uner, SU, Serdar Kucukoglu, SK, Zaroui, A, Mourali, MS, Ben Said, R, Asmi, M, Aloui, H, Kaabachi, N, Mechmeche, R, Saberniak, J, Hasselberg, NE, Borgquist, R, Platonov, PG, Holst, AG, Edvardsen, T, Haugaa, KH, Lourenco, M R, Azevedo, O, Nogueira, I, Moutinho, J, Fernandes, M, Pereira, V, Quelhas, I, Lourenco, A, Eran, A, Yueksel, D, Er, F, Gassanov, N, Rosenkranz, S, Baldus, S, Guedelhoefer, H, Faust, M, Caglayan, E, Matveeva, N, Nartsissova, G, Chernjavskij, A, Ippolito, R, De Palma, D, Muscariello, R, Santoro, C, Raia, R, Schiano-Lomoriello, V, Gargiulo, F, Galderisi, M, Lipari, P, Bonapace, S, Zenari, L, Valbusa, F, Rossi, A, Lanzoni, L, Canali, G, Molon, G, Campopiano, E, Barbieri, E, Ikonomidis, I, Varoudi, M, Papadavid, E, Theodoropoulos, K, Papadakis, I, Pavlidis, G, Triantafyllidi, H, Anastasiou - Nana, M, Rigopoulos, D, Lekakis, J, Sunbul, M, Tigen, K, Ozen, G, Durmus, E, Kivrak, T, Cincin, A, Ozben, B, Atas, H, Direskeneli, H, Basaran, Y, Stevanovic, A, Dekleva, M, Trajic, S, Paunovic, N, Simic, A, Khan, SG, Mushemi-Blake, S, Jouhra, F, Dennes, W, Monaghan, M, Melikian, N, Shah, AM, Division, Cardiovascular, Excellence, Kings BHF Centre of, Maceira Gonzalez, A M, Lopez-Lereu, MP, Monmeneu, JV, Igual, B, Estornell, J, Boraita, A, Kosmala, W, Rojek, A, Bialy, D, Mysiak, A, Przewlocka-Kosmala, M, Popescu, I, Mancas, S, Mornos, C, Serbescu, I, Ionescu, G, Ionac, A, Gaudron, P, Niemann, M, Herrmann, S, Hu, K, Liu, D, Wojciech, K, Frantz, S, Bijnens, B, Ertl, G, Weidemann, F, Maceira Gonzalez, A M, Cosin-Sales, J, Ruvira, J, Diago, JL, Aguilar, J, Igual, B, Lopez-Lereu, MP, Monmeneu, J, Estornell, J, Cruz, C, Pinho, T, Madureira, AJ, Lebreiro, A, Dias, CC, Ramos, I, Silva Cardoso, J, Julia Maciel, M, De Meester, P, Van De Bruaene, A, Herijgers, P, Voigt, J-U, Budts, W, Franzoso, F, Voser, EM, Wohlmut, C, Kellenberger, CJ, Valsangiacomo Buechel, E, Carrero, C, Benger, J, Parcerisa, MF, Falconi, M, Oberti, PF, Granja, M, Cagide, AM, Del Pasqua, A, Secinaro, A, Antonelli, G, Iacomino, M, Toscano, A, Chinali, M, Esposito, C, Carotti, A, Pongiglione, G, Rinelli, G, Youssef Moustafa, A, Al Murayeh, M, Al Masswary, A, Al Sheikh, K, Moselhy, M, Dardir, MD, Deising, J, Butz, T, Suermeci, G, Liebeton, J, Wennemann, R, Tzikas, S, Van Bracht, M, Prull, MW, Trappe, H-J, Martin Hidalgo, M, Delgado Ortega, M, Ruiz Ortiz, M, Mesa Rubio, D, Carrasco Avalos, F, Seoane Garcia, T, Pan Alvarez-Ossorio, M, Lopez Aguilera, J, Puentes Chiachio, M, Suarez De Lezo Cruz Conde, J, Petrovic, M T, Giga, V, Stepanovic, J, Tesic, M, Jovanovic, I, Djordjevic-Dikic, A, Generati, G, Pellegrino, M, Bandera, F, Donghi, V, Alfonzetti, E, Guazzi, M, Piatkowski, R, Kochanowski, J, Scislo, P, Opolski, G, Zagatina, A, Zhuravskaya, N, Krylova, L, Vareldzhyan, Y, Tyurina, TV, Clitsenko, O, Bombardini, T, Gherardi, S, Leone, O, Picano, E, Michelotto, E, Ciccarone, A, Tarantino, N, Ostuni, V, Rubino, M, Genco, W, Santoro, G, Carretta, D, Romito, R, Colonna, P, foundation, Cassa di Risparmio di Puglia, Cameli, M, Lunghetti, S, Lisi, M, Curci, V, Cameli, P, Focardi, M, Favilli, R, Galderisi, M, Mondillo, S, Hoffmann, R, Barletta, G, Von Bardeleben, S, Kasprzak, J, Greis, C, Vanoverschelde, J, Becher, H, Machida, T, Izumo, M, Suzuki, K, Kaimijima, R, Mizukoshi, K, Manabe-Uematsu, M, Takai, M, Harada, T, Akashi, YJ, Medicine., St. Marianna University School of, Cardiology, Division of, Martin Garcia, A, Arribas-Jimenez, A, Cruz-Gonzalez, I, Nieto, F, Iscar, A, Merchan, S, Martin-Luengo, C, Brecht, A, Theres, L, Spethmann, S, Dreger, H, Baumann, G, Knebel, F, Jasaityte, R, Heyde, B, Rademakers, F, Claus, P, Dhooge, J, Lervik Nilsen, L C, Lund, J, Brekke, B, Stoylen, A, Giraldeau, G, Duchateau, N, Gabrielli, L, Penela, D, Evertz, R, Mont, L, Brugada, J, Berruezo, A, Bijnens, BH, Sitges, M, Kordybach, M, Kowalski, M, Hoffman, P, Pilichowska, E, Zaborska, B, Baran, J, Kulakowski, P, Budaj, A, Wahi, S, Vollbon, W, Leano, R, Thomas, A, Bricknell, K, Holland, D, Napier, S, Stanton, T, Teferici, D, Qirko, S, Petrela, E, Dibra, A, Bajraktari, G, Bara, P, Sanchis Ruiz, L, Gabrielli, L, Andrea, R, Falces, C, Duchateau, N, Perez-Villa, F, Bijnens, B, Sitges, M, Sulemane, S, Panoulas, VF, Bratsas, AH, Tam, FW, Nihoyannopoulos, P, Abduch, MCD, Alencar, AM, Coracin, FL, Barban, A, Saboya, R, Dulley, FL, Mathias, W, Vieira, MLC, Buccheri, S, Mangiafico, S, Arcidiacono, A, Bottari, VE, Leggio, S, Tamburino, C, Monte, I P, Cruz, C, Lebreiro, A, Pinho, T, Dias, CC, Silva Cardoso, J, Julia Maciel, M, Spitzer, E, Beitzke, D, Kaneider, A, Pavo, N, Gottsauner-Wolf, M, Wolf, F, Loewe, C, Mushtaq, S, Andreini, D, Pontone, G, Bertella, E, Conte, E, Baggiano, A, Annoni, A, Cortinovis, S, Fiorentini, C, Pepi, M, Gustafsson, M, Alehagen, U, Dahlstrom, U, Johansson, P, Faden, G, Faggiano, P, Albertini, L, Reverberi, C, Gaibazzi, N, Taylor, R J, Moody, WE, Umar, F, Edwards, NC, Townend, JN, Steeds, RP, Leyva, F, Mihaila, S, Muraru, D, Piasentini, E, Peluso, D, Casablanca, S, Naso, P, Puma, L, Iliceto, S, Vinereanu, D, Badano, LP, Ciciarello, F L, Agati, L, Cimino, S, De Luca, L, Petronilli, V, Fedele, F, and Tsverava, M
- Abstract
Purpose: Transthoracic 3D echocardiography (3DE) allows an unparalleled opportunity for quantifying the dynamic changes of the tricuspid annulus (TA). Accordingly, our aims were: (I) to assess the determinants of TA size during cardiac cycle in healthy subjects; (II) to propose an approach and timing for TA sizing using 3DE. Methods: In 50 healthy volunteers (45±14 yrs, range 18-74, 27 males, with no risk factors, symptoms, signs or history of cardiovascular disease and on no medication), a full-volume dataset of the right ventricle (RV) containing the tricuspid valve (TV) was acquired (Vivid E9, GE Healthcare). TA diameters (septo-lateral, SL; antero-posterior, AP) and areas were measured on multiplanar images (Flexi-slice, EchoPac BT12, GE Healthcare) at 5 time points during the cardiac cycle: OS (onset of systole, at TV closure); MS (mid-systole); ES (end-systole); ED (onset of diastole); LD (late diastole, after the P wave). RV volumes and ejection fraction (EF) were analyzed with commercial software (4D RV analysis, TomTec, D). Results: Temporal resolution of the 3D datasets was 32±4 vps (range 24-53). TA areas were more closely correlated with RV volumes and body surface area (BSA) than with either SL or AP diameters. TA areas increased during systole from OS (3.9±0.6 cm2/m2) to ES (4.9±0.8 cm2/m2) and reached its largest area in LD (6.7±1.0 cm2/m2). All 5 TA areas were correlated with BSA (r range 0.57-0.62) and RV volumes (r ranges 0.53-0.60 for end-diastolic volume and 0.43-0.50 for end-systolic volume, p<0.0001 for all). Indexed TA areas were not related to either age or gender. With multivariable analysis, both RV end-diastolic volume and BSA determined TA areas during systole and early diastole, while TA area at LD and at OS were independently related with BSA only. Conclusions: In healthy subjects, the main determinants of TA size are RV volume and BSA. The largest TA area occurs at LD and is independently related with BSA only. Therefore, normative values should be based on TA areas measured at LD and indexed for BSA. However, the rapid change in TA areas occurring from LD to OS underscores the importance of adequate temporal resolution of 3DE data sets for reliable TA measurements.
- Published
- 2013
- Full Text
- View/download PDF
20. Poster session Wednesday 11 December all day display: 11/12/2013, 09:30-16:00 * Location: Poster area
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Bertrand, PB, Grieten, L, Smeets, C, Verbrugge, FH, Mullens, W, Vrolix, M, Rivero-Ayerza, M, Verhaert, D, Vandervoort, P, Tong, L, Ramalli, A, Tortoli, P, Dhoge, J, Bajraktari, G, Lindqvist, P, Henein, MY, Obremska, M, Boratynska, MB, Kurcz, JK, Zysko, DZ, Baran, TB, Klinger, MK, Darahim, K, Mueller, H, Carballo, D, Popova, N, Vallee, J-P, Floria, M, Chistol, R, Tinica, G, Grecu, M, Rodriguez Serrano, M, Osa-Saez, A, Rueda-Soriano, J, Buendia-Fuentes, F, Domingo-Valero, D, Igual-Munoz, B, Alonso-Fernandez, P, Quesada-Carmona, A, Miro-Palau, V, Palencia-Perez, M, Bech-Hanssen, O, Polte, CL, Lagerstrand, K, Janulewicz, M, Gao, S, Erdogan, E, Akkaya, M, Bacaksiz, A, Tasal, A, Sonmez, O, Turfan, M, Kul, S, Vatankulu, MA, Uyarel, H, Goktekin, O, Mincu, RI, Magda, LS, Mihaila, S, Florescu, M, Mihalcea, D, Enescu, OE, Chiru, A, Popescu, B, Tiu, C, Vinereanu, D, 112/2011, Research grant, Broch, K, Kunszt, G, Massey, R, De Marchi, SF, Aakhus, S, Gullestad, L, Urheim, S, Yuan, L, Feng, JL, Jin, XY, Bombardini, T, Casartelli, M, Simon, D, Gaspari, MG, Procaccio, F, Hasselberg, NE, Haugaa, KH, Brunet, A, Kongsgaard, E, Donal, E, Edvardsen, T, Sahin, TAYLAN, Yurdakul, S, Cengiz, BETUL, Bozkurt, AYSEN, Aytekin, SAIDE, Cesana, F, Spano, F, Santambrogio, G, Alloni, M, Vallerio, P, Salvetti, M, Carerj, S, Gaibazzi, N, Rigo, F, Moreo, A, Group, APRES Collaborative, Wdowiak-Okrojek, K, Michalski, B, Kasprzak, JD, Shim, A, Lipiec, P, Generati, G, Pellegrino, M, Bandera, F, Donghi, V, Alfonzetti, E, Guazzi, M, Marcun, R, Stankovic, I, Farkas, J, Vlahovic-Stipac, A, Putnikovic, B, Kadivec, S, Kosnik, M, Neskovic, AN, Lainscak, M, Iliuta, L, Szymanski, P, Lipczynska, M, Klisiewicz, A, Sobieszczanska-Malek, M, Zielinski, T, Hoffman, P, Gjerdalen, G F, Hisdal, J, Solberg, EE, Andersen, TE, Radunovic, Z, Steine, K, Svanadze, A, Poteshkina, N, Krylova, N, Mogutova, P, Shim, A, Kasprzak, JD, Szymczyk, E, Wdowiak-Okrojek, K, Michalski, B, Stefanczyk, L, Lipiec, P, Benedek, T, Matei, C, Jako, B, Suciu, ZS, Benedek, I, Yaroshchuk, N A, Kochmasheva, V V, Dityatev, V P, Kerbikov, O B, Przewlocka-Kosmala, M, Orda, A, Karolko, B, Mysiak, A, Kosmala, W, Rechcinski, T, Wierzbowska-Drabik, K, Lipiec, P, Chmiela, M, Kasprzak, JD, Aziz, A, Hooper, J, Rayasamudra, S, Uppal, H, Asghar, O, Potluri, R, Zaroui, A, Mourali, MS, Rezine, Z, Mbarki, S, Jemaa, M, Aloui, H, Mechmeche, R, Farhati, A, Gripari, P, Maffessanti, F, Tamborini, G, Muratori, M, Fusini, L, Vignati, C, Bartorelli, AL, Alamanni, F, Agostoni, PG, Pepi, M, Ruiz Ortiz, M, Mesa, D, Delgado, M, Seoane, T, Carrasco, F, Martin, M, Mazuelos, F, Suarez De Lezo Herreros De Tejada, J, Romero, M, Suarez De Lezo, J, Brili, S, Stamatopoulos, I, Misailidou, M, Chrisochoou, C, Christoforatou, E, Stefanadis, C, Ruiz Ortiz, M, Mesa, D, Delgado, M, Martin, M, Seoane, T, Carrasco, F, Ojeda, S, Segura, J, Pan, M, Suarez De Lezo, J, Cammalleri, V, Ussia, GP, Muscoli, S, Marchei, M, Sergi, D, Mazzotta, E, Romeo, F, Igual Munoz, B, Bel Minguez, ABM, Perez Guillen, MPG, Maceira Gonzalez, AMG, Monmeneu Menadas, JVMM, Hernandez Acuna, CHA, Estornell Erill, JEE, Lopez Lereu, PLL, Francisco Jose Valera Martinez, FJVM, Montero Argudo, AMA, Sunbul, M, Akhundova, A, Sari, I, Erdogan, O, Mutlu, B, Cacicedo, A, Velasco Del Castillo, S, Anton Ladislao, A, Aguirre Larracoechea, U, Rodriguez Sanchez, I, Subinas Elorriaga, A, Oria Gonzalez, G, Onaindia Gandarias, J, Laraudogoitia Zaldumbide, E, Lekuona Goya, I, Ding, W, Zhao, Y, Lindqvist, P, Nilson, J, Winter, R, Holmgren, A, Ruck, A, Henein, MY, Attenhofer Jost, C H, Soyka, R, Oxenius, A, Kretschmar, O, Valsangiacomo Buechel, ER, Greutmann, M, Weber, R, Keramida, K, Kouris, N, Kostopoulos, V, Karidas, V, Damaskos, D, Makavos, G, Paraskevopoulos, K, Olympios, CD, Eskesen, K, Olsen, NT, Fritz-Hansen, T, Sogaard, P, Cameli, M, Lisi, M, Righini, FM, Curci, V, Massoni, A, Natali, B, Maccherini, M, Chiavarelli, M, Massetti, M, Mondillo, S, Mabrouk Salem Omar, A, Ahmed Abdel-Rahman, M, Khorshid, H, Rifaie, O, Santoro, C, Santoro, A, Ippolito, R, De Palma, D, De Stefano, F, Muscariiello, R, Galderisi, M, Squeri, A, Censi, S, Baldelli, M, Grattoni, C, Cremonesi, A, Bosi, S, Saura Espin, D, Gonzalez Canovas, C, Gonzalez Carrillo, J, Oliva Sandoval, MJ, Caballero Jimenez, L, Espinosa Garcia, MD, Garcia Navarro, M, Valdes Chavarri, M, De La Morena Valenzuela, G, Ryu, SK, Shin, DG, Son, JW, Choi, JH, Goh, CW, Choi, JW, Park, JY, Hong, GR, Sklyanna, O, Yuan, L, Yuan, L, Planinc, I, Bagadur, G, Ljubas, J, Baricevic, Z, Skoric, B, Velagic, V, Bijnens, B, Milicic, D, Cikes, M, Gospodinova, M, Chamova, T, Guergueltcheva, V, Ivanova, R, Tournev, I, Denchev, S, Ancona, R, Comenale Pinto, S, Caso, P, Arenga, F, Coppola, MG, Calabro, R, Neametalla, H, Boitard, S, Hamdi, H, Planat-Benard, V, Casteilla, L, Li, Z, Hagege, AA, Mericskay, M, Menasche, P, Agbulut, O, Merlo, M, Stolfo, D, Anzini, M, Negri, F, Pinamonti, B, Barbati, G, Di Lenarda, A, Sinagra, G, Stolfo, D, Merlo, M, Pinamonti, B, Gigli, M, Poli, S, Porto, A, Di Nora, C, Barbati, G, Di Lenarda, A, Sinagra, G, Coppola, C, Piscopo, G, Cipresso, C, Rea, D, Maurea, C, Esposito, E, Arra, C, Maurea, N, Nemes, A, Kalapos, A, Domsik, P, Forster, T, Voilliot, D, Huttin, O, Vaugrenard, T, Schwartz, J, Sellal, J-M, Aliot, E, Juilliere, Y, Selton-Suty, C, Sanchez Millan, P J, Cabeza Lainez, P, Castillo Ortiz, J, Chueca Gonzalez, EM, Gheorghe, L, Fernandez Garcia, P, Herruzo Rojas, MS, Del Pozo Contreras, R, Fernandez Garcia, M, Vazquez Garcia, R, Rosca, M, Popescu, BA, Botezatu, D, Calin, A, Beladan, CC, Gurzun, M, Enache, R, Ginghina, C, Farouk, H, Al-Maimoony, T, Alhadad, A, El Serafi, M, Abdel Ghany, M, Poorzand, H, Mirfeizi, SZ, Javanbakht, A, center, Preventive Cardiovascular care research, center, Lupus Research, sciences, Mashhad university of medical, Tellatin, S, Famoso, G, Dassie, F, Martini, C, Osto, E, Maffei, P, Iliceto, S, Tona, F, Radunovic, Z, Steine, KS, Jedrzejewska, I, Braksator, W, Krol, W, Swiatowiec, A, Sawicki, J, Kostarska-Srokosz, E, Dluzniewski, M, Maceira Gonzalez, A M, Cosin-Sales, J, Diago, JL, Aguilar, J, Ruvira, J, Monmeneu, J, Igual, B, Lopez-Lereu, MP, Estornell, J, Olszanecka, A, Dragan, A, Kawecka-Jaszcz, K, Czarnecka, D, Scholz, F, Gaudron, PD, Hu, K, Liu, D, Florescu, C, Herrmann, S, Bijnens, B, Ertl, G, Stoerk, S, Weidemann, F, Krestjyaninov, M, Razin, VA, Gimaev, RH, Bogdanovic, Z, Burazor, I, Deljanin Ilic, M, Peluso, D, Muraru, D, Cucchini, U, Mihaila, S, Casablanca, S, Pigatto, E, Cozzi, F, Punzi, L, Badano, LP, Iliceto, S, Zhdanova, E, Rameev, VV, Safarova, AF, Moisseyev, SV, Kobalava, ZD, Magnino, C, Omede, P, Avenatti, E, Presutti, D, Losano, I, Moretti, C, Bucca, C, Gaita, F, Veglio, F, Milan, A, Bellsham-Revell, H, Bell, AJ, Miller, OI, Simpson, JM, Hwang, YM, Kim, GH, Jung, MH, Woo, GH, Medicine, Department of Internal, Hospital, St.Vincents, Korea, The Catholic University of, Suwon, Division of Cardiology, Repu, Driessen, MMP, Leiner, T, Schoof, PH, Breur, JMPJ, Sieswerda, GT, Meijboom, FJ, Bellsham-Revell, H, Hayes, N, Anderson, D, Austin, BC, Razavi, R, Greil, GF, Simpson, JM, Bell, AJ, Zhao, XX, Xu, XD, Qin, YW, Szmigielski, C A, Styczynski, G, Sobczynska, M, Placha, G, Kuch-Wocial, A, Ikonomidis, I, Voumbourakis, A, Triantafyllidi, H, Pavlidis, G, Varoudi, M, Papadakis, I, Trivilou, P, Paraskevaidis, I, Anastasiou-Nana, M, Lekakis, I, Kong, WILL, Yip, JAMES, Ling, LH, Milan, A, Tosello, F, Leone, D, Bruno, G, Losano, I, Avenatti, E, Sabia, L, Veglio, F, Zaborska, B, Baran, J, Pilichowska-Paszkiet, E, Sikora-Frac, M, Michalowska, I, Kulakowski, P, Budaj, A, Mega, S, Bono, MC, De Francesco, V, Castiglione, I, Ranocchi, F, Casacalenda, A, Goffredo, C, Patti, G, Di Sciascio, G, Musumeci, F, Kennedy, M, Waterhouse, DF, Sheahan, R, Foley, DF, Mcadam, BF, Ancona, R, Comenale Pinto, S, Caso, P, Arenga, F, Coppola, MG, Calabro, R, Remme, E W, Smedsrud, M K, Hasselberg, N E, Smiseth, O A, Edvardsen, T, Halmai, L, Nemes, A, Kardos, A, Neubauer, S, Degiovanni, A, Baduena, L, Dellera, G, Occhetta, E, Marino, P, Hotchi, J, Yamada, H, Nishio, S, Bando, M, Hayashi, S, Hirata, Y, Amano, R, Soeki, T, Wakatsuki, T, Sata, M, Lamia, B, Molano, LC, Viacroze, C, Cuvelier, A, Muir, JF, Lipczynska, M, Piotr Szymanski, PS, Anna Klisiewicz, AK, Lukasz Mazurkiewicz, LM, Piotr Hoffman, PH, Van T Sant, J, Wijers, SC, Ter Horst, IAH, Leenders, GE, Cramer, MJ, Doevendans, PA, Meine, M, Hatam, N, Goetzenich, A, Aljalloud, A, Mischke, K, Hoffmann, R, Autschbach, R, Sikora-Frac, M, Zaborska, B, Maciejewski, P, Bednarz, B, Budaj, A, Evangelista, A, Torromeo, C, Pandian, NG, Nardinocchi, P, Varano, V, Schiariti, M, Teresi, L, Puddu, PE, Storve, S, Dalen, H, Snare, SR, Haugen, BO, Torp, H, Fehri, W, Mahfoudhi, H, Mezni, F, Annabi, MS, Taamallah, K, Dahmani, R, Haggui, A, Hajlaoui, N, Lahidheb, D, Haouala, H, Colombo, A, Carminati, MC, Maffessanti, F, Gripari, P, Pepi, M, Lang, RM, Caiani, EG, Walker, JR, Abadi, S, Agmon, Y, Carasso, S, Aronson, D, Mutlak, D, Lessick, J, Saxena, A, Ramakrishnan, S, Juneja, R, Ljubas, J, Reskovic Luksic, V, Matasic, R, Pezo Nikolic, B, Lovric, D, Separovic Hanzevacki, J, Quattrone, A, Zito, C, Alongi, G, Vizzari, G, Bitto, A, De Caridi, G, Greco, M, Tripodi, R, Pizzino, G, Carerj, S, Ibrahimi, P, Jashari, F, Johansson, E, Gronlund, C, Bajraktari, G, Wester, P, Henein, MY, Kosmala, W, Marwick, TH, Souza, J R M, Zacharias, L G T, Geloneze, B, Pareja, J C, Chaim, A, Nadruz, W JR, Coelho, O R, Apostolovic, S, Stanojevic, D, Jankovic-Tomasevic, R, Salinger-Martinovic, S, Djordjevic-Radojkovic, D, Pavlovic, M, Tahirovic, E, Musial-Bright, L, Lainscak, M, Duengen, HD, group, CIBIS ELD study, Filipiak, D, Kasprzak, JD, and Lipiec, P
- Abstract
Purpose: With the advent of percutaneous transcatheter device closures in congenital heart defects and the emergence of percutaneous left atrial appendage closure, there is an increasingly important role for echocardiographic guidance and control of device position and function. Disc occluder devices frequently present as an unexplained ‘figure-of-8’ on echocardiography. The aim of this study was to clarify this ‘figure-of-8’ display and to relate its morphology to transducer position and device type. Methods: A mathematical model was developed to resemble disc occluder geometry and to allow a numerical simulation of the echocardiographic appearance. In addition, we developed an in vitro set-up for echocardiographic analysis of various disc occluders and various transducer positions. Results: In the mathematical model of an epitrochoid curve (closely resembling disc occluder geometry) a ‘figure-of-8’ display is obtained when emphasizing points with tangent vector perpendicular to the direction of ultrasound waves. Decreasing imaging depth results in a more asymmetric ‘figure-of-8’, with small upper part and wide lower part. Clinical and in vitro data are in close agreement with these results (Figure 1). Furthermore a ‘figure-of-8’ display is only obtained in a coronal imaging position, and is similar for different commercially available disc occluder types. Conclusions: The ‘figure-of-8’ display in the ultrasound image of a disc occluder is an imaging artifact due to the specific ‘epitrochoidal’ geometry of a deployed device and its interaction with ultrasound waves. The morphology of the ‘figure-of-8’ depends on transducer position, i.e. imaging depth, and is similar for different device types.
Figure 1 Impact of imaging depth - Published
- 2013
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21. Oral Abstract session * New insights in heart muscle diseases: 13/12/2013, 16:30-18:00 * Location: Bursa
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Tsang, W, Abduch, CM, Salgo, IS, Appareti, K, Ackerman, W, Cruz, V, Lima, M, Tsutsui, J, Mathias, W, Lang, RM, Teske, AJ, Mast, T P, Groeneweg, JA, Te Riele, AS, Van Der Heijden, JF, Velthuis, BK, Hauer, RN, Doevendans, PF, Cramer, MJM, Cautela, JC, Krastevich, MK, Michel, NM, Saby, LS, Copel, CC, Hubert, SH, Avierinos, JFA, Thuny, FT, Guieu, RG, Habib, G, Muraru, D, Calore, C, Badano, LP, Melacini, P, Mihaila, S, Naso, P, Casablanca, S, Ortile, A, Padayattil Jose, S, Iliceto, S, Hasselberg, NE, Saberniak, J, Berge, KE, Edvardsen, T, and Haugaa, KH
- Abstract
Background: Adverse left ventricular (LV) remodeling is associated with poorer outcomes in patients with cardiomyopathies. Using 3D echocardiography (3DE), adverse LV remodeling can be assessed by changes in global LV curvature parameters and global longitudinal strain (GLS). While GLS has been shown to be predictive of adverse outcomes, the value of LV curvature remains unclear. We examined the prognostic value of: 1) Global LV curvature alone and 2) LV curvature and GLS in predicting outcomes in patients with angiographically proven, non-ischemic dilated cardiomyopathies (NICM). Methods: Baseline demographics and 2D echocardiography-derived 4-chamber (4C) GLS (QLAB 9.0, Philips) were obtained in 71 NICM patients (51 males, 51 ± 12 yrs). Seven types of LV curvature (QLAB 9.0, Philips; custom software) were measured at end-systole and end-diastole from 3DE-derived LV endocardial shells. These curvatures included: minimum, maximum, mean, Gaussian, difference, longitudinal and circumferential. Clinical outcomes of ER visit, rehospitalization or death were obtained at a median follow-up of 3.1 years. Predictors of outcome were identified from univariable analyses. Hierarchical, multivariable Cox regression models were constructed. C-index was used to compare non-nested models. Results: Overall event rate was 45%. 4C-GLS, left atrial volume, and end-systolic Gaussian curvature were significant univariable predictors of outcomes. However, the combination of 4C-GLS and end-systolic Gaussian curvature provided a better predictive model than either variable alone (Figure). Conclusions: This study demonstrates that changes in LV shape provide additive value to GLS in predicting outcomes in NICM patients.
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- 2013
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22. Prediction of severe ventricular arrhythmias in patients with mitral valve prolapse by exercise ECG.
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Five CK, Hasselberg NE, Chivulescu M, Rootwelt-Norberg C, Ribe MP, Dejgaard LA, Castrini AI, Aabel EW, and Haugaa KH
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Competing Interests: Disclosures The authors have no conflict of interest to disclose.
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- 2024
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23. Stretch of the papillary insertion triggers reentrant arrhythmia: an in silico patient study.
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Myklebust L, Monopoli G, Balaban G, Aabel EW, Ribe M, Castrini AI, Hasselberg NE, Bugge C, Five C, Haugaa K, Maleckar MM, and Arevalo H
- Abstract
Background: The electrophysiological mechanism connecting mitral valve prolapse (MVP), premature ventricular complexes and life-threatening ventricular arrhythmia is unknown. A common hypothesis is that stretch activated channels (SACs) play a significant role. SACs can trigger depolarizations or shorten repolarization times in response to myocardial stretch. Through these mechanisms, pathological traction of the papillary muscle (PM), as has been observed in patients with MVP, may induce irregular electrical activity and result in reentrant arrhythmia., Methods: Based on a patient with MVP and mitral annulus disjunction, we modeled the effect of excessive PM traction in a detailed medical image-derived ventricular model by activating SACs in the PM insertion region. By systematically varying the onset of SAC activation following sinus pacing, we identified vulnerability windows for reentry with 1 ms resolution. We explored how reentry was affected by the SAC reversal potential ( E SAC ) and the size of the region with simulated stretch (SAC region). Finally, the effect of global or focal fibrosis, modeled as reduction in tissue conductivity or mesh splitting (fibrotic microstructure), was investigated., Results: In models with healthy tissue or fibrosis modeled solely as CV slowing, we observed two vulnerable periods of reentry: For E SAC of -10 and -30 mV, SAC activated during the T-wave could cause depolarization of the SAC region which lead to reentry. For E SAC of -40 and -70 mV, SAC activated during the QRS complex could result in early repolarization of the SAC region and subsequent reentry. In models with fibrotic microstructure in the SAC region, we observed micro-reentries and a larger variability in which times of SAC activation triggered reentry. In these models, 86% of reentries were triggered during the QRS complex or T-wave. We only observed reentry for sufficiently large SAC regions ( > = 8 mm radius in models with healthy tissue)., Conclusion: Stretch of the PM insertion region following sinus activation may initiate ventricular reentry in patients with MVP, with or without fibrosis. Depending on the SAC reversal potential and timing of stretch, reentry may be triggered by ectopy due to SAC-induced depolarizations or by early repolarization within the SAC region., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Myklebust, Monopoli, Balaban, Aabel, Ribe, Castrini, Hasselberg, Bugge, Five, Haugaa, Maleckar and Arevalo.)
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- 2024
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24. Progression of myocardial dysfunction and prediction of arrhythmic events in patients with exercise-induced arrhythmogenic cardiomyopathy.
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Aaserud LT, Rootwelt-Norberg C, Five CK, Aabel EW, Hasselberg NE, Lyseggen E, Haugaa KH, and Lie ØH
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Background: Several reports exist of an acquired exercise-induced arrhythmogenic cardiomyopathy. Little is known about myocardial disease progression and arrhythmia prediction in this population., Objective: The study sought to explore the evolution of myocardial function and structure and its relation to incident life-threatening ventricular arrhythmias (VA), to identify markers of impending events., Methods: We included athletes (individuals with exercise doses >24 metabolic equivalent of task hours per week, >6 consecutive years, participating in organized and competitive sports) who had VA, absence of family history and known genetic variants associated with cardiac disease, and no other identified etiology, in a tertiary referral single-center, longitudinal cohort study of patients with exercise-induced arrhythmogenic cardiomyopathy (EiAC). Evolution of myocardial function and structure was assessed by repeated echocardiographic examinations during long-term follow-up. Life-threatening VA were assessed at baseline and during long-term follow-up., Results: Forty-one EiAC patients (15% women, age 45 ± 13 years) were followed for 80 (interquartile range 48-115) months. There were no changes in myocardial function or structure in the overall population during follow-up. We observed high incidence rate and high recurrence rate of life-threatening VA in EiAC patients. Subtle deterioration of right ventricular function was strongly associated with subsequent first-time VA (odds ratio 1.12, 95% confidence interval 1.01-1.25, P = .031, per 1% deterioration of right ventricular free wall longitudinal strain)., Conclusion: There were no clear changes in myocardial function or structure during follow-up in the overall population, but there was a high incidence rate and high recurrence rate of life-threatening VA. Subtle right ventricular deterioration by free wall longitudinal strain was a strong predictor of impending first-time life-threatening VA during follow-up., (© 2024 Heart Rhythm Society. Published by Elsevier Inc.)
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- 2024
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25. Implantable cardioverter defibrillator use in arrhythmogenic right ventricular cardiomyopathy in North America and Europe.
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Carrick RT, De Marco C, Gasperetti A, Bosman LP, Gourraud JB, Trancuccio A, Mazzanti A, Murray B, Pendleton C, Tichnell C, Tandri H, Zeppenfeld K, Wilde AAM, Davies B, Seifer C, Roberts JD, Healey JS, MacIntyre C, Alqarawi W, Tadros R, Cutler MJ, Targetti M, Calò L, Vitali F, Bertini M, Compagnucci P, Casella M, Dello Russo A, Cappelletto C, De Luca A, Stolfo D, Duru F, Jensen HK, Svensson A, Dahlberg P, Hasselberg NE, Di Marco A, Jordà P, Arbelo E, Moreno Weidmann Z, Borowiec K, Delinière A, Biernacka EK, van Tintelen JP, Platonov PG, Olivotto I, Saguner AM, Haugaa KH, Cox M, Tondo C, Merlo M, Krahn AD, Te Riele ASJM, Wu KC, Calkins H, James CA, and Cadrin-Tourigny J
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- Humans, Retrospective Studies, Arrhythmias, Cardiac epidemiology, Arrhythmias, Cardiac therapy, Arrhythmias, Cardiac etiology, Death, Sudden, Cardiac epidemiology, Death, Sudden, Cardiac prevention & control, Death, Sudden, Cardiac etiology, Risk Factors, North America epidemiology, Europe epidemiology, Defibrillators, Implantable adverse effects, Arrhythmogenic Right Ventricular Dysplasia complications, Arrhythmogenic Right Ventricular Dysplasia epidemiology, Arrhythmogenic Right Ventricular Dysplasia therapy
- Abstract
Background and Aims: Implantable cardioverter-defibrillators (ICDs) are critical for preventing sudden cardiac death (SCD) in arrhythmogenic right ventricular cardiomyopathy (ARVC). This study aims to identify cross-continental differences in utilization of primary prevention ICDs and survival free from sustained ventricular arrhythmia (VA) in ARVC., Methods: This was a retrospective analysis of ARVC patients without prior VA enrolled in clinical registries from 11 countries throughout Europe and North America. Patients were classified according to whether they received treatment in North America or Europe and were further stratified by baseline predicted VA risk into low- (<10%/5 years), intermediate- (10%-25%/5 years), and high-risk (>25%/5 years) groups. Differences in ICD implantation and survival free from sustained VA events (including appropriate ICD therapy) were assessed., Results: One thousand ninety-eight patients were followed for a median of 5.1 years; 554 (50.5%) received a primary prevention ICD, and 286 (26.0%) experienced a first VA event. After adjusting for baseline risk factors, North Americans were more than three times as likely to receive ICDs {hazard ratio (HR) 3.1 [95% confidence interval (CI) 2.5, 3.8]} but had only mildly increased risk for incident sustained VA [HR 1.4 (95% CI 1.1, 1.8)]. North Americans without ICDs were at higher risk for incident sustained VA [HR 2.1 (95% CI 1.3, 3.4)] than Europeans., Conclusions: North American ARVC patients were substantially more likely than Europeans to receive primary prevention ICDs across all arrhythmic risk strata. A lower rate of ICD implantation in Europe was not associated with a higher rate of VA events in those without ICDs., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)
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- 2024
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26. The added value of abnormal regional myocardial function for risk prediction in arrhythmogenic right ventricular cardiomyopathy.
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Kirkels FP, Rootwelt-Norberg C, Bosman LP, Aabel EW, Muller SA, Castrini AI, Taha K, van Osta N, Lie ØH, Asselbergs FW, Lumens J, Te Riele ASJM, Hasselberg NE, Cramer MJ, Haugaa KH, and Teske AJ
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- Humans, Female, Male, Myocardium, Arrhythmias, Cardiac, Prognosis, Echocardiography, Ventricular Function, Right, Arrhythmogenic Right Ventricular Dysplasia diagnostic imaging
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Aims: A risk calculator for individualized prediction of first-time sustained ventricular arrhythmia (VA) in arrhythmogenic right ventricular cardiomyopathy (ARVC) patients has recently been developed and validated (www.ARVCrisk.com). This study aimed to investigate whether regional functional abnormalities, measured by echocardiographic deformation imaging, can provide additional prognostic value., Methods and Results: From two referral centres, 150 consecutive patients with a definite ARVC diagnosis, no prior sustained VA, and an echocardiogram suitable for deformation analysis were included (aged 41 ± 17 years, 50% female). During a median follow-up of 6.3 (interquartile range 3.1-9.8) years, 37 (25%) experienced a first-time sustained VA. All tested left and right ventricular (LV and RV) deformation parameters were univariate predictors for first-time VA. While LV function did not add predictive value in multivariate analysis, two RV deformation parameters did; RV free wall longitudinal strain and regional RV deformation patterns remained independent predictors after adjusting for the calculator-predicted risk [hazard ratio 1.07 (95% CI 1.02-1.11); P = 0.004 and 4.45 (95% CI 1.07-18.57); P = 0.040, respectively] and improved its discriminative value (from C-statistic 0.78 to 0.82 in both; Akaike information criterion change > 2). Importantly, all patients who experienced VA within 5 years from the echocardiographic assessment had abnormal regional RV deformation patterns at baseline., Conclusions: This study showed that regional functional abnormalities measured by echocardiographic deformation imaging can further refine personalized arrhythmic risk prediction when added to the ARVC risk calculator. The excellent negative predictive value of normal RV deformation could support clinicians considering the timing of implantable cardioverter defibrillator implantation in patients with intermediate arrhythmic risk., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.)
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- 2023
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27. Lifetime exercise dose and ventricular arrhythmias in patients with mitral valve prolapse.
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Five CK, Hasselberg NE, Aaserud LT, Castrini AI, Vlaisavljevic K, Lie Ø, Rootwelt-Norberg C, Aabel EW, and Haugaa KH
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- Humans, Female, Male, Retrospective Studies, Arrhythmias, Cardiac diagnosis, Arrhythmias, Cardiac etiology, Arrhythmias, Cardiac therapy, Mitral Valve Prolapse complications, Mitral Valve Prolapse diagnosis, Tachycardia, Ventricular diagnosis, Tachycardia, Ventricular etiology, Tachycardia, Ventricular prevention & control, Heart Arrest
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Aims: Patients with mitral valve prolapse (MVP) have high risk of life-threatening ventricular arrhythmias (VAs). Data on the impact of exercise on arrhythmic risk in these patients are lacking. We explored whether lifetime exercise dose was associated with severe VA and with established risk factors in patients with MVP. Furthermore, we explored the circumstances at the VA event., Methods and Results: In this retrospective cohort study, we included patients with MVP and assessed lifetime exercise dose as metabolic equivalents of task (MET) hours/week. Severe VA was defined as sustained ventricular tachycardia or fibrillation, aborted cardiac arrest, and appropriate shock by a primary preventive implantable cardioverter defibrillator. We included 136 MVP patients (48 years [interquartile range (IQR) 35-59], 61% female), and 17 (13%) had previous severe VA. The lifetime exercise dose did not differ in patients with and without severe VA (17 MET h/week [IQR 9-27] vs. 14 MET h/week [IQR 6-31], P = 0.34). Lifetime exercise dose > 9.6 MET h/week was a borderline significant marker for severe VA (OR 3.38, 95% CI 0.92-12.40, P = 0.07), while not when adjusted for age (OR 2.63, 95% CI 0.66-10.56, P = 0.17). Ventricular arrhythmia events occurred most frequently during wakeful rest (53%), followed by exercise (29%) and sleep (12%)., Conclusion: We found no clear association between moderate lifetime exercise dose and severe VA in patients with MVP. We cannot exclude an upper threshold for safe levels of exercise. Further studies are needed to explore exercise and risk of severe VA., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.)
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- 2023
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28. Flecainide in patients with arrhythmic mitral valve syndrome: A case series.
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Aabel EW, Dejgaard LA, Chivulescu M, Helle-Valle TM, Edvardsen T, Hasselberg NE, Hegbom F, Lie ØH, and Haugaa KH
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- Humans, Mitral Valve diagnostic imaging, Flecainide therapeutic use, Mitral Valve Prolapse, Mitral Valve Insufficiency complications, Mitral Valve Insufficiency diagnosis, Mitral Valve Insufficiency drug therapy
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- 2023
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29. Timing of cardioverter-defibrillator implantation in patients with cardiac laminopathies-External validation of the LMNA-risk ventricular tachyarrhythmia calculator.
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Rootwelt-Norberg C, Christensen AH, Skjølsvik ET, Chivulescu M, Vissing CR, Bundgaard H, Aabel EW, Bogsrud MP, Hasselberg NE, Lie ØH, and Haugaa KH
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- Male, Female, Humans, Stroke Volume, Ventricular Function, Left, Electrocardiography, Lamin Type A, Defibrillators, Implantable adverse effects, Tachycardia, Ventricular etiology, Laminopathies complications
- Abstract
Background: LMNA genotype-positive patients have high risk of experiencing life-threatening ventricular tachyarrhythmias (VTAs). The LMNA-risk VTA calculator published in 2019 has not been externally validated., Objective: The purpose of this study was to validate the LMNA-risk VTA calculator., Methods: We included LMNA genotype-positive patients without previous VTAs from 2 large Scandinavian centers. Patients underwent electrocardiography, 24-hour Holter monitoring, and echocardiographic examinations at baseline and repeatedly during follow-up. Validation of the LMNA-risk VTA calculator was performed using Harrell's C-statistic derived from multivariable Cox regression analysis., Results: We included 118 patients (age 37 years [IQR 27-49 years]; 39 [33%] probands; 65 [55%] women; 100 [85%] with non-missense LMNA variants). Twenty-three patients (19%) experienced VTA during 6.1 years (interquartile range 3.0-9.1 years) follow-up, resulting in 3.0% (95% confidence interval 2.0%-4.5%) yearly incidence rate. Atrioventricular block and reduced left ventricular ejection fraction were independent predictors of VTAs, while nonsustained ventricular tachycardia, male sex, and non-missense LMNA variants were not. The LMNA-risk VTA calculator showed 83% sensitivity and 26% specificity for identifying patients with VTAs during the coming 5 years, and a Harrell's C-statistic of 0.85, when applying ≥7% predicted 5-year VTA risk as threshold. The sensitivity increased to 100% when reevaluating risk at the time of last consultation before VTA. The calculator overestimated arrhythmic risk in patients with mild and moderate phenotype, particularly in men., Conclusion: Validation of the LMNA-risk VTA calculator showed high sensitivity for subsequent VTAs, but overestimated arrhythmic risk when using ≥7% predicted 5-year risk as threshold. Frequent reevaluation of risk was necessary to maintain the sensitivity of the model., (Copyright © 2022 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)
- Published
- 2023
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30. Disease progression rate is a strong predictor of ventricular arrhythmias in patients with cardiac laminopathies: a primary prevention cohort study.
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Rootwelt-Norberg C, Skjølsvik ET, Chivulescu M, Bogsrud MP, Ribe MP, Aabel EW, Beitnes JO, Brekke PH, Håland TF, Hasselberg NE, Lie ØH, and Haugaa KH
- Subjects
- Female, Male, Humans, Stroke Volume, Cohort Studies, Ventricular Function, Left, Risk Factors, Arrhythmias, Cardiac diagnosis, Arrhythmias, Cardiac genetics, Primary Prevention, Disease Progression, Defibrillators, Implantable adverse effects, Laminopathies complications
- Abstract
Aims: Cardiac disease progression prior to first ventricular arrhythmia (VA) in LMNA genotype-positive patients is not described., Methods and Results: We performed a primary prevention cohort study, including consecutive LMNA genotype-positive patients from our centre. Patients underwent repeated clinical, electrocardiographic, and echocardiographic examinations. Electrocardiographic and echocardiographic disease progression as a predictor of first-time VA was evaluated by generalized estimation equation analyses. Threshold values at transition to an arrhythmic phenotype were assessed by threshold regression analyses. We included 94 LMNA genotype-positive patients without previous VA (age 38 ± 15 years, 32% probands, 53% females). Nineteen (20%) patients experienced VA during 4.6 (interquartile range 2.1-7.3) years follow up, at mean age 50 ± 11 years. We analysed 536 echocardiographic and 261 electrocardiogram examinations. Individual patient disease progression was associated with VA [left ventricular ejection fraction (LVEF) odds ratio (OR) 1.4, 95% confidence interval (CI) 1.2-1.6 per 5% reduction, left ventricular end-diastolic volume index (LVEDVi) OR 1.2 (95% CI 1.1-1.3) per 5 mL/m2 increase, PR interval OR 1.2 (95% CI 1.1-1.4) per 10 ms increase]. Threshold values for transition to an arrhythmic phenotype were LVEF 44%, LVEDVi 77 mL/m2, and PR interval 280 ms., Conclusions: Incidence of first-time VA was 20% during 4.6 years follow up in LMNA genotype-positive patients. Individual patient disease progression by ECG and echocardiography were strong predictors of VA, indicating that disease progression rate may have additional value to absolute measurements when considering primary preventive ICD. Threshold values of LVEF <44%, LVEDVi >77 mL/m2, and PR interval >280 ms indicated transition to a more arrhythmogenic phenotype., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.)
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- 2023
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31. Highly malignant disease in childhood-onset arrhythmogenic right ventricular cardiomyopathy.
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Smedsrud MK, Chivulescu M, Forså MI, Castrini I, Aabel EW, Rootwelt-Norberg C, Bogsrud MP, Edvardsen T, Hasselberg NE, Früh A, and Haugaa KH
- Subjects
- Humans, Risk Factors, Arrhythmias, Cardiac epidemiology, Electrocardiography, Cohort Studies, Arrhythmogenic Right Ventricular Dysplasia diagnosis, Arrhythmogenic Right Ventricular Dysplasia epidemiology, Arrhythmogenic Right Ventricular Dysplasia genetics
- Abstract
Aims: This study aimed to explore the incidence of severe cardiac events in paediatric arrhythmogenic right ventricular cardiomyopathy (ARVC) patients and ARVC penetrance in paediatric relatives. Furthermore, the phenotype in childhood-onset ARVC was described., Methods: Consecutive ARVC paediatric patients and genotype positive relatives ≤18 years of age were followed with electrocardiographic, structural, and arrhythmic characteristics according to the 2010 revised Task Force Criteria. Penetrance of ARVC disease was defined as fulfilling definite ARVC criteria and severe cardiac events were defined as cardiac death, heart transplantation (HTx) or severe ventricular arrhythmias. Childhood-onset disease was defined as meeting definite ARVC criteria ≤12 years of age., Results: Among 62 individuals [age 9.8 (5.0-14.0) years, 11 probands], 20 (32%) fulfilled definite ARVC diagnosis, of which 8 (40%) had childhood-onset disease. The incidence of severe cardiac events was 23% (n = 14) by last follow-up and half of them occurred in patients ≤12 years of age. Among the eight patients with childhood-onset disease, five had biventricular involvement needing HTx and three had severe arrhythmic events. Among the 51 relatives, 6% (n = 3) met definite ARVC criteria at time of genetic diagnosis, increasing to 18% (n = 9) at end of follow-up., Conclusions: In a paediatric ARVC cohort, there was a high incidence of severe cardiac events and half of them occurred in children ≤12 years of age. The ARVC penetrance in genotype positive paediatric relatives was 18%. These findings of a high-malignant phenotype in childhood-onset ARVC indicate a need for ARVC family screening at younger age than currently recommended., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology.)
- Published
- 2022
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32. Level 1 of Entrustable Professional Activities in adult echocardiography: a position statement from the EACVI regarding the training and competence requirements for selecting and interpreting echocardiographic examinations.
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Stankovic I, Muraru D, Fox K, Di Salvo G, Hasselberg NE, Breithardt OA, Hansen TB, Neskovic AN, Gargani L, Cosyns B, and Edvardsen T
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- Adult, Cardiac Imaging Techniques, Clinical Competence, Humans, Cardiology education, Echocardiography
- Abstract
The goal of Level 1 training in echocardiography is to enable the trainee to select echocardiography appropriately for the evaluation of a specific clinical question, and then to interpret the report. It is not the goal of Level 1 training to teach how to perform the examination itself-that is the goal of higher levels of training. However, understanding the principles, indications, and findings of this crucial technique is valuable to many medical professionals including outside cardiology. This should be seen as part of a general understanding of cardiac imaging modalities. The purpose of this position statement is to define the scope and outline the general requirements for Level 1 training and competence in echocardiography. Moreover, the document aims to make a clear distinction between Level 1 competence in echocardiography and focus cardiac ultrasound (FoCUS)., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.)
- Published
- 2021
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33. The Prognostic Value of Right Atrial Strain Imaging in Patients with Precapillary Pulmonary Hypertension.
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Hasselberg NE, Kagiyama N, Soyama Y, Sugahara M, Goda A, Ryo-Koriyama K, Batel O, Chakinala M, Simon MA, and Gorcsan J 3rd
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- Adult, Aged, Echocardiography, Female, Heart Atria diagnostic imaging, Humans, Male, Middle Aged, Prognosis, Ventricular Function, Right, Hypertension, Pulmonary diagnostic imaging, Ventricular Dysfunction, Right diagnostic imaging
- Abstract
Background: Right ventricular (RV) failure in patients with pulmonary hypertension (PH) is associated with unfavorable clinical events and a poor prognosis. Elevation of right atrial (RA) pressure is established as a marker for RV failure. However, the additive prognostic value of RA mechanical function is unclear., Methods: The authors tested the hypothesis that RA function by strain echocardiography has prognostic usefulness by studying 165 consecutive patients with precapillary PH defined invasively: mean pulmonary artery pressure ≥ 25 mm Hg and pulmonary capillary wedge pressure < 15 mm Hg. Speckle-tracking strain analyses of the right atrium and right ventricle were performed, along with routine measures. Peak RA strain values from six segments using generic speckle-tracking software were averaged to RA peak longitudinal strain, representing RA global reservoir function. The primary end point was all-cause mortality during 5 years of follow-up. RA strain was similarly analyzed in a control group of 16 normal subjects for comparison., Results: There were 151 patients with PH (mean age, 55 ± 16 years; 73% women; mean World Health Organization functional class, 2.6 ± 0.6), after 14 exclusions (three with atrial septal defects and 11 with left ventricular ejection fractions < 50%). RA strain measurement was feasible in 93% of patients and RV strain measurement in 88%. RA peak longitudinal strain was significantly reduced in patients with PH compared with control subjects, as expected (P < .001). During 5-year follow-up, 73 patients (48%) died. Patients with RA peak strain in the lowest quartile (<25%) had a significant risk for death (P = .006), even after correcting for confounding variables. RA strain was independently associated with survival in multivariate analysis (P = .039) and had additive prognostic value to RV strain (log-rank P = .01) in subgroup analysis., Conclusions: RA peak longitudinal strain had additive prognostic usefulness to other clinical measures, including RV strain, RA area, and RA pressure, in patients with PH. RA mechanical function by strain imaging has potential for clinical applications in patients with PH., (Copyright © 2021 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.)
- Published
- 2021
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34. Exercise is Associated With Impaired Left Ventricular Systolic Function in Patients With Lamin A/C Genotype.
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Skjølsvik ET, Hasselberg NE, Dejgaard LA, Lie ØH, Andersen K, Holm T, Edvardsen T, and Haugaa KH
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- Adult, Age Factors, Cardiomyopathy, Dilated diagnostic imaging, Cross-Sectional Studies, Female, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Phenotype, Retrospective Studies, Risk Assessment, Risk Factors, Severity of Illness Index, Systole, Ventricular Dysfunction, Left diagnostic imaging, Ventricular Dysfunction, Left physiopathology, Cardiomyopathy, Dilated genetics, Cardiomyopathy, Dilated physiopathology, Exercise, Habits, Lamin Type A genetics, Ventricular Dysfunction, Left genetics, Ventricular Function, Left genetics
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Background Lamin A/C cardiomyopathy is a malignant and highly penetrant inheritable cardiomyopathy. Competitive sports have been associated with adverse events in these patients, but data on recreational exercise are lacking. We aimed to explore associations between exercise exposure and disease severity in patients with lamin A/C genotype. Methods and Results Lamin A/C genotype positive patients answered a questionnaire on exercise habits from age 7 years until genetic diagnosis. We recorded exercise hours >3 metabolic equivalents and calculated cumulative lifetime exercise. Patients were grouped in active or sedate based on lifetime exercise hours above or below median. We performed echocardiography, 12-lead ECG, Holter monitoring, and biomarkers including NT-proBNP (N-terminal pro-B-type natriuretic peptide). We defined left ventricular ejection fraction <45% as a clinically significant impairment of left ventricular function. We included 69 patients (age 42±14 years, 41% probands, 46% women) with median lifetime exercise 4160 (interquartile range 1041-6924) hours. Active patients were more frequently probands (53% versus 29%, P =0.04), had lower left ventricular ejection fraction (43±13% versus 51±11%, P =0.006), and higher NT-proBNP (78 [interquartile range 32-219] pmol/L versus 30 [interquartile range 13-64] pmol/L, P =0.03) compared with sedate, while age did not differ (45±13 years versus 40±16 years, P =0.16). The decrease in left ventricular ejection fraction per tertile increment in lifetime exercise was 4% (95% CI -7% to -0.4%, P =0.03), adjusted for age and sex and accounting for dependence within families. Left ventricular ejection fraction <45% was observed at a younger age in active patients (log rank P =0.007). Conclusions Active lamin A/C patients had worse systolic function compared with sedate which occurred at younger age. Our findings may improve exercise recommendations in patients with lamin A/C.
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- 2020
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35. Global Left Ventricular Strain at Presentation Is Associated with Subsequent Recovery in Patients with Peripartum Cardiomyopathy.
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Sugahara M, Kagiyama N, Hasselberg NE, Blauwet LA, Briller J, Cooper L, Fett JD, Hsich E, Wells G, McNamara D, and Gorcsan J 3rd
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- Adult, Cardiomyopathies diagnosis, Echocardiography, Female, Follow-Up Studies, Humans, Pregnancy, Prognosis, Prospective Studies, Cardiomyopathies physiopathology, Heart Ventricles diagnostic imaging, Myocardial Contraction physiology, Peripartum Period, Stroke Volume physiology, Ventricular Function, Left physiology
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Background: Peripartum cardiomyopathy (PPCM) is a serious complication of pregnancy associated with variable degrees of left ventricular (LV) recovery. The aim of this study was to test the hypothesis that global LV strain at presentation has prognostic value in patients with PPCM., Methods: One hundred patients with PPCM aged 30 ± 6 years were enrolled in the multicenter Investigation in Pregnancy Associated Cardiomyopathy study along with 21 normal female control subjects. Speckle-tracking global longitudinal strain (GLS) and global circumferential strain (GCS) analysis was performed. The predefined primary combined outcome variable was death, transplantation, LV assist device implantation, or evidence of persistent LV dysfunction (LV ejection fraction [LVEF] < 50%) at 1 year., Results: GLS measurement was feasible in 110 subjects: 89 of 90 patients with PPCM (99%) with echocardiographic data and all 21 control subjects. Of 84 patients (94%) with 1-year follow-up, 21 (25%) had unfavorable primary outcomes: four LV assist device placements, two deaths, and 15 patients with persistent LV dysfunction. GLS at presentation with a cutoff of 10.6% (absolute value) was specifically associated with the subsequent primary outcome with 75% sensitivity and 95% specificity. GCS at presentation with a cutoff of 10.1% was associated with the primary outcome with 78% sensitivity and 84% specificity. GLS and GCS remained significantly associated with outcomes after adjusting for LVEF (GLS odds ratio, 2.07; P < .001; GCS odds ratio, 1.37; P = .005). GLS was significantly additive to LVEF (C statistic = 0.76-0.91, net reclassification improvement = 1.32, P < .001)., Conclusions: GLS and GCS in patients with PPCM at presentation were associated with subsequent clinical outcomes, including death, LV assist device implantation, and evidence of persistent LV dysfunction. Strain measures may add prognostic information over LVEF for risk stratification., (Copyright © 2019 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.)
- Published
- 2019
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36. Lamin A/C cardiomyopathy: young onset, high penetrance, and frequent need for heart transplantation.
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Hasselberg NE, Haland TF, Saberniak J, Brekke PH, Berge KE, Leren TP, Edvardsen T, and Haugaa KH
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- Adolescent, Adult, Female, Follow-Up Studies, Humans, Lamin Type A genetics, Male, Middle Aged, Mutation, Prevalence, Young Adult, Cardiomyopathy, Dilated, Heart Transplantation statistics & numerical data
- Abstract
Aims: Lamin A/C (LMNA) mutations cause familial dilated cardiomyopathy (DCM) with frequent conduction blocks and arrhythmias. We explored the prevalence, cardiac penetrance, and expressivity of LMNA mutations among familial DCM in Norway. Furthermore, we explored the risk factors and the outcomes in LMNA patients., Methods and Results: During 2003-15, genetic testing was performed in patients referred for familial DCM. LMNA genotype-positive subjects were examined by electrocardiography, Holter monitoring, cardiac magnetic resonance imaging, and echocardiography. A positive cardiac phenotype was defined as the presence of atrioventricular (AV) block, atrial fibrillation/flutter (AF), ventricular tachycardia (VT), and/or echocardiographic DCM. Heart transplantation was recorded and compared with non-ischaemic DCM of other origin. Of 561 unrelated familial DCM probands, 35 (6.2%) had an LMNA mutation. Family screening diagnosed an additional 93 LMNA genotype-positive family members. We clinically followed up 79 LMNA genotype-positive [age 42 ± 16 years, ejection fraction (EF) 45 ± 13%], including 44 (56%) with VT. Asymptomatic LMNA genotype-positive family members (age 31 ± 15 years) had a 9% annual incidence of a newly documented cardiac phenotype and 61% (19/31) of cardiac penetrance during 4.4 ± 2.9 years of follow-up. Ten (32%) had AV block, 7 (23%) AF, and 12 (39%) non-sustained VT. Heart transplantation was performed in 15 of 79 (19%) LMNA patients during 7.8 ± 6.3 years of follow-up., Conclusion: LMNA mutation prevalence was 6.2% of familial DCM in Norway. Cardiac penetrance was high in young asymptomatic LMNA genotype-positive family members with frequent AV block and VT, highlighting the importance of early family screening and cardiological follow-up. Nearly 20% of the LMNA patients required heart transplantation.
- Published
- 2018
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37. Reply: Interaction Between Longitudinal, Circumferential, and Radial Deformations and Their Contributions to Ejection Fraction.
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Stokke TM, Hasselberg NE, Smedsrud MK, Sarvari SI, Haugaa KH, Smiseth OA, Edvardsen T, and Remme EW
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- Stroke Volume, Systole, Ventricular Function
- Published
- 2018
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38. [Cardiomyopathy in hereditary muscular dystrophies].
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Hasselberg NE, Berge KE, Rasmussen M, Früh A, Ørstavik K, and Haugaa KH
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- Arrhythmias, Cardiac diagnosis, Arrhythmias, Cardiac etiology, Arrhythmias, Cardiac genetics, Cardiomyopathies diagnosis, Cardiomyopathies genetics, Electrocardiography, Humans, Muscle Cells physiology, Muscular Dystrophies, Limb-Girdle complications, Muscular Dystrophies, Limb-Girdle congenital, Muscular Dystrophies, Limb-Girdle diagnosis, Muscular Dystrophies, Limb-Girdle genetics, Muscular Dystrophy, Duchenne complications, Muscular Dystrophy, Duchenne congenital, Muscular Dystrophy, Duchenne diagnosis, Muscular Dystrophy, Duchenne genetics, Muscular Dystrophy, Emery-Dreifuss complications, Muscular Dystrophy, Emery-Dreifuss congenital, Muscular Dystrophy, Emery-Dreifuss diagnosis, Muscular Dystrophy, Emery-Dreifuss genetics, Myotonic Dystrophy complications, Myotonic Dystrophy diagnosis, Myotonic Dystrophy genetics, Cardiomyopathies etiology, Muscular Dystrophies complications, Muscular Dystrophies congenital, Muscular Dystrophies diagnosis, Muscular Dystrophies genetics
- Published
- 2018
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39. Geometry as a Confounder When Assessing Ventricular Systolic Function: Comparison Between Ejection Fraction and Strain.
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Stokke TM, Hasselberg NE, Smedsrud MK, Sarvari SI, Haugaa KH, Smiseth OA, Edvardsen T, and Remme EW
- Subjects
- Adult, Cardiomyopathy, Hypertrophic physiopathology, Echocardiography, Three-Dimensional, Female, Heart Ventricles physiopathology, Humans, Male, Middle Aged, Retrospective Studies, Severity of Illness Index, Systole, Cardiomyopathy, Hypertrophic diagnosis, Heart Ventricles diagnostic imaging, Myocardial Contraction physiology, Stroke Volume physiology, Ventricular Function, Left physiology
- Abstract
Background: Preserved left ventricular (LV) ejection fraction (EF) and reduced myocardial strain are reported in patients with hypertrophic cardiomyopathy, ischemic heart disease, diabetes mellitus, and more., Objectives: The authors performed a combined mathematical and echocardiographic study to understand the inconsistencies between EF and strains., Methods: An analytical equation showing the relationship between EF and the 4 parameters, global longitudinal strain (GLS), global circumferential strain (GCS), wall thickness, and short-axis diameter, was derived from an elliptical LV model. The equation was validated by measuring the 4 parameters by echocardiography in 100 subjects with EF ranging from 16% to 72% and comparing model-predicted EF with measured EF. The effect of the different parameters on EF was explored in the model and compared with findings in the patients., Results: Calculated EF had very good agreement with measured EF (r = 0.95). The model showed that GCS contributes more than twice as much to EF than GLS. A significant reduction of GLS could be compensated by a small increase of GCS or wall thickness or reduced diameter. The model further demonstrated how EF can be maintained in ventricles with increased wall thickness or reduced diameter, despite reductions in both longitudinal and circumferential shortening. This was consistent with similar EF in 20 control subjects and 20 hypertrophic cardiomyopathy patients with increased wall thickness and reductions in both circumferential and longitudinal shortening (all p < 0.01)., Conclusions: Reduced deformation despite preserved EF can be explained through geometric factors. Due to geometric confounders, strain better reflects systolic function in patients with preserved EF., (Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2017
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40. The systolic paradox in hypertrophic cardiomyopathy.
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Haland TF, Hasselberg NE, Almaas VM, Dejgaard LA, Saberniak J, Leren IS, Berge KE, Haugaa KH, and Edvardsen T
- Abstract
Objective: We explored cardiac volumes and the effects on systolic function in hypertrophic cardiomyopathy (HCM) patients with left ventricular hypertrophy (HCM LVH+) and genotype-positive patients without left ventricular hypertrophy (HCM LVH-)., Methods: We included 180 HCM LVH+, 100 HCM LVH- patients and 80 healthy individuals. End-Diastolic Volume Index (EDVI), End-Systolic Volume Index (ESVI) and ejection fraction (EF) were assessed by echocardiography. Left ventricular (LV) global longitudinal strain (GLS) was measured by speckle tracking echocardiography., Results: EDVI and ESVI were significantly smaller in HCM LVH+ compared with HCM LVH- patients (41±14 mL/m
2 vs 49±13 mL/m2 and 16±7 mL/m2 vs 19±6 mL/m2 , respectively, both p<0.001) and in healthy individuals (41±14 mL/m2 vs 57±14 mL/m2 and 16±7 mL/m2 vs 23±9 mL/m2 , respectively, both p<0.001). HCM LVH- patients had significantly lower EDVI and ESVI compared with healthy individuals (49±13 mL/m2 vs 57±14 mL/m2 and 19±6 mL/m2 vs 23±9 mL/m2 , both p<0.001). EF was similar (61%±7% vs 60%±8% vs 61%±6%, p=0.43) in the HCM LVH+, HCM LVH- and healthy individuals, despite significantly worse GLS in the HCM LVH+ (-16.4%±3.7% vs -21.3%±2.4% vs -22.3%±3.7%, p<0.001). GLS was worse in the HCM LVH- compared with healthy individuals in pairwise comparison (p=0.001). Decrease in ESVI was closely related to EF in HCM LVH+ and HCM LVH- (R=0.45, p<0.001 and R=0.43, p<0.001) as expected, but there was no relationship with GLS (R=0.02, p=0.77 and R=0.11, p=0.31). Increased maximal wall thickness (MWT) correlated significantly with worse GLS (R=0.58, p<0.001), but not with EF (R=0.018, p=0.30) in the HCM LVH+ patients., Conclusion: HCM LVH+ had smaller cardiac volumes that could explain the preserved EF, despite worse GLS that was closely related to MWT. HCM LVH- had reduced cardiac volumes and subtle changes in GLS compared with healthy individuals, indicating a continuum of both volumetric and systolic changes present before increased MWT., Competing Interests: Competing interests: None declared.- Published
- 2017
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41. Strain echocardiography is related to fibrosis and ventricular arrhythmias in hypertrophic cardiomyopathy.
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Haland TF, Almaas VM, Hasselberg NE, Saberniak J, Leren IS, Hopp E, Edvardsen T, and Haugaa KH
- Subjects
- Adult, Aged, Cardiomyopathy, Hypertrophic physiopathology, Comorbidity, Cross-Sectional Studies, Electrocardiography, Ambulatory, Female, Fibrosis epidemiology, Fibrosis pathology, Humans, Image Interpretation, Computer-Assisted, Kaplan-Meier Estimate, Magnetic Resonance Imaging, Cine, Male, Middle Aged, Multivariate Analysis, Prognosis, ROC Curve, Reference Values, Risk Assessment, Severity of Illness Index, Survival Analysis, Tachycardia, Ventricular physiopathology, Ultrasonography, Doppler, Cardiomyopathy, Hypertrophic diagnostic imaging, Cardiomyopathy, Hypertrophic epidemiology, Echocardiography, Myocardium pathology, Tachycardia, Ventricular diagnostic imaging, Tachycardia, Ventricular epidemiology
- Abstract
Aims: Hypertrophic cardiomyopathy (HCM) patients are at risk of ventricular arrhythmias (VAs). We aimed to explore whether systolic function by strain echocardiography is related to VAs and to the extent of fibrosis by cardiac magnetic resonance imaging (CMR)., Methods and Results: We included 150 HCM patients and 50 healthy individuals. VAs were defined as non-sustained and sustained ventricular tachycardia and aborted cardiac arrest. Left ventricular function was assessed by ejection fraction (EF) and by global longitudinal strain (GLS) assessed by speckle tracking echocardiography. Mechanical dispersion was calculated as standard deviation (SD) of time from Q/R on ECG to peak longitudinal strain in 16 left ventricular segments. Late gadolinium enhancement (LGE) was assessed by CMR. HCM patients had similar EF (61 ± 5% vs. 61 ± 8%, P = 0.77), but worse GLS (-15.7 ± 3.6% vs. -21.1 ± 1.9%, P < 0.001) and more pronounced mechanical dispersion (64 ± 22 vs. 36 ± 13 ms, P < 0.001) compared with healthy individuals. VAs were documented in 37 (25%) HCM patients. Patients with VAs had worse GLS (-14.1 ± 3.6% vs. -16.3 ± 3.4%, P < 0.01), more pronounced mechanical dispersion (79 ± 27 vs. 59 ± 16 ms, P < 0.001), and higher %LGE (6.1 ± 7.8% vs. 0.5 ± 1.4%, P < 0.001) than patients without VAs. Mechanical dispersion correlated with %LGE (R = 0.52, P < 0.001) and was independently associated with VAs (OR 1.6, 95% CI 1.1-2.3, P = 0.02) and improved risk stratification for VAs., Conclusion: GLS, mechanical dispersion, and LGE were markers of VAs in HCM patients. Mechanical dispersion was a strong independent predictor of VAs and related to the extent of fibrosis. Strain echocardiography may improve risk stratification of VAs in HCM., (© The Author 2016. Published by Oxford University Press on behalf of the European Society of Cardiology.)
- Published
- 2016
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42. Left ventricular markers of mortality and ventricular arrhythmias in heart failure patients with cardiac resynchronization therapy.
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Hasselberg NE, Haugaa KH, Bernard A, Ribe MP, Kongsgaard E, Donal E, and Edvardsen T
- Subjects
- Aged, Arrhythmias, Cardiac physiopathology, Echocardiography, Female, Heart Failure physiopathology, Heart Transplantation, Heart-Assist Devices, Humans, Male, Middle Aged, Prospective Studies, Ventricular Dysfunction, Left physiopathology, Arrhythmias, Cardiac mortality, Cardiac Resynchronization Therapy, Heart Failure mortality, Heart Failure therapy, Ventricular Dysfunction, Left mortality
- Abstract
Aims: Cardiac resynchronization therapy (CRT) reduces morbidity and mortality in heart failure. However, prediction of the outcome remains difficult. We aimed to investigate for echocardiographic predictors of ventricular arrhythmias and fatal outcome and to explore how myocardial function is changed by biventricular pacing in heart failure., Methods and Results: We prospectively included 170 heart failure patients (66 ± 10 years, New York Heart Association class 2.8 ± 0.5, 48% ischaemic cardiomyopathy) and recorded ventricular arrhythmias and fatal end point defined as death, heart transplantation, or left ventricular assist device implantation during 2 years. Two-dimensional echocardiography was performed before and 6 months after CRT implantation. CRT response was defined as ≥15% reduction in end-systolic volume at 6 months. Speckle-tracking technique was performed to assess longitudinal and circumferential left ventricular function, defined as global longitudinal (GLS) and circumferential strain (GCS), and to assess mechanical dyssynchrony, defined as mechanical dispersion. GLS before CRT was a predictor of fatal end point independently of CRT response [hazard ratio, HR 1.14 (1.02-1.27), P = 0.02]. Patients with GLS better than -8.3% showed event-free survival benefit (log rank, P < 0.001). Mechanical dispersion at 6 months was an independent predictor of ventricular arrhythmias [HR 1.20 (1.06-1.35), P = 0.005]. CRT responders (59%) had improvement of both GLS and GCS., Conclusion: In heart failure patients with CRT, worse longitudinal function before CRT was an important predictor of fatal outcome during 2 years, independently of CRT response. Mechanical dispersion at 6 months was a strong predictor of ventricular arrhythmias. CRT response by reverse remodelling was dependent on improvement of both longitudinal and circumferential function., (© The Author 2015. Published by Oxford University Press on behalf of the European Society of Cardiology.)
- Published
- 2016
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43. Cardiac Mechanical Alterations and Genotype Specific Differences in Subjects With Long QT Syndrome.
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Leren IS, Hasselberg NE, Saberniak J, Håland TF, Kongsgård E, Smiseth OA, Edvardsen T, and Haugaa KH
- Subjects
- Adult, Biomechanical Phenomena, Case-Control Studies, Cross-Sectional Studies, ERG1 Potassium Channel, Echocardiography, Doppler, Electrocardiography, Genetic Predisposition to Disease, Humans, Long QT Syndrome diagnostic imaging, Long QT Syndrome physiopathology, Middle Aged, Phenotype, Romano-Ward Syndrome diagnostic imaging, Romano-Ward Syndrome physiopathology, Time Factors, Young Adult, Ether-A-Go-Go Potassium Channels genetics, KCNQ1 Potassium Channel genetics, Long QT Syndrome genetics, Mutation, Myocardial Contraction genetics, Romano-Ward Syndrome genetics, Stroke Volume genetics, Ventricular Function, Left genetics
- Abstract
Objectives: This study aimed to explore systolic and diastolic function and to investigate genotype-specific differences in subjects with long QT syndrome (LQTS)., Background: LQTS is an arrhythmogenic cardiac ion channelopathy that traditionally has been considered a purely electrical disease. The most commonly affected ion channels are the slow potassium channel, IKs (KCNQ1 gene/LQT1), and the rapid potassium channel, IKr (KCNH2 gene/LQT2). Recent reports have indicated mechanical abnormalities in patients with LQTS., Methods: We included 192 subjects with genotyped LQTS (139 LQT1, 53 LQT2). Healthy persons of similar age and sex as patients served as controls (n = 60). Using echocardiography, we assessed systolic function by left ventricular (LV) ejection fraction (EF), global longitudinal strain (GLS), and contraction duration (16 LV segments). Mechanical dispersion was calculated as standard deviation of contraction duration. Time difference between contraction duration and QT interval from electrocardiography (ECG) was defined as electromechanical time difference. We assessed diastolic function by transmitral filling velocities, early diastolic myocardial velocity (e'), and left atrial volume index (LAVI). Heart rate corrected QT interval (QTc) was assessed from 12-lead ECG., Results: Systolic function by GLS was reduced in subjects with LQTS compared with healthy controls (-22.1 ± 2.1% vs. -23.0 ± 2.0%, p = 0.01), and GLS was worse in subjects with LQT2 compared with subjects with LQT1 (p = 0.01). Subjects with LQTS had longer contraction duration (426 ± 41 ms vs. 391 ± 36 ms, p < 0.001) and more dispersed contractions (33 ± 14 ms vs. 21 ± 7 ms, p < 0.001) compared with healthy controls. Diastolic function was also reduced in subjects with LQTS compared with healthy controls; e' was lower (10.7 ± 2.7 cm/s vs. 12.5 ± 2.0 cm/s, p < 0.001), and LAVI was increased (30 ± 8 ml/m(2) vs. 26 ± 5 ml/m(2), p = 0.01), also when adjusted for age and other possible confounders., Conclusions: Subjects with LQTS had a consistent reduction in both systolic and diastolic function compared with healthy controls. Differences in myocardial function between subjects with LQT1 and subjects with LQT2 may indicate that mechanical alterations in LQTS are genotype specific., (Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)
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- 2015
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44. Left ventricular global longitudinal strain is associated with exercise capacity in failing hearts with preserved and reduced ejection fraction.
- Author
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Hasselberg NE, Haugaa KH, Sarvari SI, Gullestad L, Andreassen AK, Smiseth OA, and Edvardsen T
- Subjects
- Cross-Sectional Studies, Echocardiography, Exercise Test, Female, Heart Failure diagnostic imaging, Humans, Middle Aged, Oxygen Consumption physiology, Ventricular Dysfunction, Left diagnostic imaging, Heart Failure physiopathology, Stroke Volume physiology, Ventricular Dysfunction, Left physiopathology
- Abstract
Aims: Heart failure patients with reduced and preserved left ventricular (LV) ejection fraction (EF) show reduced exercise capacity. We explored the relationship between exercise capacity and systolic and diastolic myocardial function in heart failure patients., Methods and Results: Exercise capacity, by peak oxygen uptake (VO2), was assessed in 100 patients (56 ± 12 years, NYHA functional class: 2.5 ± 0.9, EF: 42 ± 19%). LV systolic function, as EF and global longitudinal strain (GLS), and right ventricular function were assessed by echocardiography. Left atrial volume index and the ratio of peak early diastolic filling velocity (E) to early diastolic mitral annular velocity (e') were measures of diastolic function. Thirty-seven patients had heart failure with preserved EF (HFpEF), defined as EF ≥50% and echocardiographic diastolic dysfunction. LV GLS and peak pulmonary arterial systolic pressure were independently correlated to peak VO2 in the total study population and in HFpEF separately. LV GLS was superior to EF in identifying patients with impaired peak VO2 <20 mL/kg/min as shown by receiver operating characteristic analyses [areas under curves 0.93 (0.89-0.98) vs. 0.85 (0.77-0.93), P < 0.05]. In patients with HFpEF, GLS was reduced below normal (-17.5 ± 3.2%) and correlated to E/e' (R = 0.45, P = 0.005) and left atrial volume index (R = 0.48, P = 0.003), while EF did not., Conclusion: GLS correlated independently to peak VO2 in patients with reduced and preserved EF and was superior in identifying patients with reduced exercise capacity. In HFpEF, systolic function by GLS was impaired. There was a significant relationship between diastolic function and GLS, confirming a coupling between diastolic and longitudinal systolic function in HFpEF., (© The Author 2014. Published by Oxford University Press on behalf of the European Society of Cardiology.)
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- 2015
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45. Mechanical dispersion by strain echocardiography: a predictor of ventricular arrhythmias in subjects with lamin A/C mutations.
- Author
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Haugaa KH, Hasselberg NE, and Edvardsen T
- Subjects
- Adult, Forecasting, Humans, Arrhythmias, Cardiac diagnosis, Echocardiography, Lamin Type A genetics, Mutation
- Published
- 2015
- Full Text
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46. Vigorous physical activity impairs myocardial function in patients with arrhythmogenic right ventricular cardiomyopathy and in mutation positive family members.
- Author
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Saberniak J, Hasselberg NE, Borgquist R, Platonov PG, Sarvari SI, Smith HJ, Ribe M, Holst AG, Edvardsen T, and Haugaa KH
- Subjects
- Antineoplastic Combined Chemotherapy Protocols, Arrhythmogenic Right Ventricular Dysplasia diagnostic imaging, Athletes, Cross-Sectional Studies, Echocardiography, Female, Genetic Testing methods, Humans, Magnetic Resonance Imaging, Male, Mutation genetics, Stroke Volume physiology, Ventricular Dysfunction, Left diagnostic imaging, Ventricular Dysfunction, Right diagnostic imaging, Arrhythmogenic Right Ventricular Dysplasia genetics, Arrhythmogenic Right Ventricular Dysplasia physiopathology, Exercise physiology, Ventricular Dysfunction, Left physiopathology, Ventricular Dysfunction, Right physiopathology, Ventricular Function, Left physiology, Ventricular Function, Right physiology
- Abstract
Aims: Exercise increases risk of ventricular arrhythmia in subjects with arrhythmogenic right ventricular cardiomyopathy (ARVC). We aimed to investigate the impact of exercise on myocardial function in ARVC subjects., Methods and Results: We included 110 subjects (age 42 ± 17 years), 65 ARVC patients and 45 mutation-positive family members. Athletes were defined as subjects with ≥4 h vigorous exercise/week [≥1440 metabolic equivalents (METs × minutes/week)] during a minimum of 6 years. Athlete definition was fulfilled in 37/110 (34%) subjects. We assessed right ventricular (RV) and left ventricular (LV) myocardial function by echocardiography, and by magnetic resonance imaging (MRI). The RV function by RV fractional area change (FAC), RV global longitudinal strain (GLS) by echocardiography, and RV ejection fraction (EF) by MRI was reduced in athletes compared with non-athletes (FAC 34 ± 9% vs. 40 ± 11%, RVGLS -18.3 ± 6.1% vs. -22.0 ± 4.8%, RVEF 32 ± 8% vs. 43 ± 10%, all P < 0.01). LV function by LVEF and LVGLS was reduced in athletes compared with non-athletes (LVEF by echocardiography 50 ± 10% vs. 57 ± 5%, LVEF by MRI 46 ± 6% vs. 53 ± 8%, and LVGLS -16.7 ± 4.2% vs. -19.4 ± 2.9%, all P < 0.01). The METs × minutes/week correlated with reduced RV and LV function by echocardiography and MRI (all P < 0.01). The LVEF by MRI was also reduced in subgroups of athlete index patients (46 ± 7% vs. 54 ± 10%, P = 0.02) and in athlete family members (47 ± 3% vs. 52 ± 6%, P < 0.05)., Conclusion: Athletes showed reduced biventricular function compared with non-athletes in ARVC patients and in mutation-positive family members. The amount and intensity of exercise activity was associated with impaired LV and RV function. Exercise may aggravate and accelerate myocardial dysfunction in ARVC., (© 2014 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)
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- 2014
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47. Risk prediction of ventricular arrhythmias and myocardial function in Lamin A/C mutation positive subjects.
- Author
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Hasselberg NE, Edvardsen T, Petri H, Berge KE, Leren TP, Bundgaard H, and Haugaa KH
- Subjects
- Adolescent, Adult, Aged, Arrhythmias, Cardiac diagnosis, Arrhythmias, Cardiac physiopathology, Atrioventricular Block genetics, Atrioventricular Block physiopathology, Cardiomyopathy, Dilated diagnosis, Cardiomyopathy, Dilated physiopathology, Child, DNA Mutational Analysis, Denmark, Echocardiography, Doppler, Electrocardiography, Female, Fibrosis, Genetic Predisposition to Disease, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Norway, Phenotype, Predictive Value of Tests, Risk Assessment, Risk Factors, Ventricular Septum pathology, Young Adult, Arrhythmias, Cardiac genetics, Cardiomyopathy, Dilated genetics, Lamin Type A genetics, Mutation, Myocardial Contraction genetics, Stroke Volume genetics, Ventricular Function, Left genetics, Ventricular Septum physiopathology
- Abstract
Aims: Mutations in the Lamin A/C gene may cause atrioventricular block, supraventricular arrhythmias, ventricular arrhythmias (VA), and dilated cardiomyopathy. We aimed to explore the predictors and the mechanisms of VA in Lamin A/C mutation-positive subjects., Methods and Results: We included 41 Lamin A/C mutation-positive subjects. PR-interval and occurrence of VA were recorded. Left ventricular (LV) myocardial function was assessed as ejection fraction and speckle tracking longitudinal strain by echocardiography. Magnetic resonance imaging was performed to assess fibrosis in a selection of subjects. Ventricular arrhythmias were documented in 21 patients (51%). Prolonged PR-interval was the best predictor of VA (P < 0.001). Myocardial function by strain was reduced in the interventricular septum compared with the rest of the LV segments (-16.7% vs. -18.7%, P = 0.001) and correlated to PR-interval (R = 0.41, P = 0.03). Myocardial fibrosis was found exclusively in the interventricular septum and only in patients with VA (P = 0.007). PR-interval was longer in patients with septal fibrosis compared with those without (320 ± 66 vs. 177 ± 40 ms, P < 0.001)., Conclusion: Prolonged PR-interval was the best predictor of VA in Lamin A/C mutation-positive subjects. Electrical, mechanical, and structural cardiac properties were related in these subjects. Myocardial function was most reduced in the interventricular septum and correlated to prolonged PR-interval. Myocardial septal fibrosis was associated with prolonged PR-interval and VA. Localized fibrosis in the interventricular septum may be the mechanism behind reduced septal function, atrioventricular block and VA in Lamin A/C mutation-positive subjects.
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- 2014
- Full Text
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