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16 results on '"Amin Youssef, G."'

1. Hypertensive disorders in women with peripartum cardiomyopathy: insights from the ESC EORP PPCM Registry

Author

Jackson, Alice M., Petrie, Mark C., Frogoudaki, Alexandra, Laroche, Cécile, Gustafsson, Finn, Ibrahim, Bassem, Mebazaa, Alexandre, Johnson, Mark R., Seferovic, Petar M., Regitz‐Zagrosek, Vera, Mbakwem, Amam, Böhm, Michael, Prameswari, Hawani Sasmaya, Abdel Gawad, Doaa Ahmed Fouad, Goland, Sorel, Damasceno, Albertino, Karaye, Kamilu, Farhan, Hasan Ali, Hamdan, Righab, Maggioni, Aldo P., Sliwa, Karen, Bauersachs, Johann, Meer, Peter, Favaloro, R., Favaloro, L., Carballo, M., Peradejordi, M., Renedo, M.F., Absi, D., Bertolotti, A., Ratto, R., Talavera, M.L., Gomez, R., Lockwood, S., Barton, T., Austin, M‐A., Arstall, M., Aldridge, E., Chow, Y.Y., Dekker, G., Mahadavan, G., Rose, J., Wittwer, M., Hoppe, U., Sandhofer, A., Bahshaliyev, A., Gasimov, Z., Babayev, A., Niftiyev, P., Hasanova, I., AlBannay, R., AlHaiki, W., Husain, A., Mahdi, N., Kurlianskaya, A., Lukyanchyk, M., Shatova, O., Troyanova‐Shchutskaia, T., Anghel, L., De Pauw, M., Gevaert, S., De Backer, J., De Hosson, M., Vervaet, P., Timmermans, P.J., Janssen, A., Yameogo, N.V., Kagambega, L.J., Cumyn, A., Caron, N., Cote, A‐M., Sauve, N., Nkulu, D. Ngoy, Lez, D. Malamba, Yolola, E. Ngoy, Krejci, J., Poloczkova, H., Ersboll, A., Gustafsson, F., Elrakshy, Y., Hassanein, M., Hammad, B., Eldin, O. Nour, Fouad, D., Salman, S., Zareh, Z., Abdeall, D., Elenin, H. Abo, Ebaid, H., El Nagar, A., Farag, S., Saed, M., El Rahman, Y H Abd, Ibrahim, B.S., Abdelhamid, M., Hanna, R.N. W., Youssef, G., Awad, R., Botrous, O.L. I., Halawa, S. Ibrahim, Nasr, G., Saad, A., El Tahlawi, M., Abdelbaset, M., El‐saadawy, M., El‐shorbagy, A., Shalaby, G., Anttonen, O., Tolppanen, H., Hamekoski, S., Menez, T., Noel, A., Lamblin, N., Mouquet, F., Coulon, C., Groote, P., Langlois, S., Schurtz, G., Cohen‐Solal, A., Mebazaa, A., Fournier, M‐C., Louadah, B., Akrout, N., Logeart, D., Leurent, G., Jovanova, S., Arnaudova‐Dezulovicj, F., Livrinova, V., Bauersachs, J., Hilfiker‐Kleiner, D., Berliner, D., Jungesblut, M., Koenig, T., Moulig, V.A., Pfeffer, T.J., Böhm, M., Kindermann, I., Schwarz, V., Schmitt, C., Swojanowsky, P., Pettit, S., Petrie, M., McAdam, M., Patton, D., Bakhai, A., Krishnamurthy, V., Lim, L., Clifford, P., Bowers, N., Clark, A. L., Witte, K., Cullington, D., Oliver, J., Simms, A., Mcginlay, M., McDonagh, T., Shah, A. M., Amin‐Youssef, G., De Courcey, J., Martin, K., Shaw, S., Vause, S., Wallace, S., Malin, G., Wick, C., Nikolaou, M., Rentoukas, I., Chinchilla, H., Andino, L., Iyengar, S., Chandra, S., Yadav, D.K., Babu, R. Ravi, Singh, A.K., Kumar, S., Karunamay, B.B., Chaubey, S.K., Dhiman, S.R., Jha, V.C., Singh, S.K., Kodati, D., Dasari, R., Sultana, S., Dewi, T.I., Prameswari, H. Sasmaya, Al‐Farhan, H.A., Al‐Hussein, A., Yaseen, I.F., Al‐Azzawi, Falah, Al‐Saedi, Ghazi, Mahmood, G.M., Mohammed, M.K., Ridha, A.F., Shotan, A., Vazan, A., Goland, S., Biener, M., Senni, M., Grosu, A., Martin, E., Esposti, D. Degli, Bacchelli, S., Borghi, C., Metra, M., Sciatti, E., Orabona, R., Sani, F., Brunetti, N.D., Sinagra, G., Bobbo, M., D'Agata Mottolese, B., Gesuete, V., Rakar, S., Ramani, F., Kamiya, C., Barasa, A., Ngunga, M., Bajraktari, G., Hyseni, V., Lleshi, D., Pllana, E., Pllana, T., Noruzbaeva, A., Ismailov, F., Mirrakhimov, E., Abilova, S., Lunegova, O., Kerimkulova, A., Osmankulova, G., Duishenalieva, M., Kurmanbekova, B., Turgunov, M., Mamasaidova, S., Bektasheva, E., Kavoliuniene, A., Muckiene, G., Vaitiekiene, A., Celutkiene, J., Balkevicine, L., Barysiene, J., Chee, K.H., Damasceno, A., Machava, M., Veldhuisen, D.J., Meer, P., Berg, M., Roos‐Hesselink, J., Hagen, I., Baris, L., Hurtado, P., Ezeonu, P., Isiguzo, G., Obeka, N., Onoh, R., Asogwa, F., Onyema, C., Otti, K., Ojji, D., Odili, A., Nwankwo, A., Karaye, K., Ishaq, N., Sanni, B., Abubakar, H., Mohammed, B., Sani, M., Kehinde, M., Mbakwem, A., Afolabi, B., Amadi, C., Kilasho, M., Qamar, N., Furnaz, S., Gurmani, S., Kayani, M.G.A. Mahmood, Munir, R., Hussain, S., Malik, S., Mumtaz, S., Saligan, J.R., Rubis, P., Biernacka‐Fijalkowska, B., Lesniak‐Sobelga, A., Wisniowska‐Smialek, S., Kasprzak, J.D., Lelonek, M., Zycinski, P., Jankowski, L., Grajek, S., Oko‐Sarnowska, Z., Rutkowska, A. Bartczak, Kaluzna‐Oleksy, M., Plaskota, K., Demkow, M., Dzielinska, Z., Henzel, J., Kryczka, K., Moiseeva, O., Irtyuga, O., Karelkina, E., Zazerskaya, I., Seferovic, P.M., Milinkovic, I., Živkovic, I., Ristic, A.D., Milasinovic, D., Kong, W. KF, Tan, L.K., Tan, J.L., Thain, S., Poh, K.K., Yip, J., Sliwa, K., Azibani, F., Hovelmann, J., Viljoen, C., Briton, O., Zamora, E., Orcajo, N. Alonso, Carbonell, R., Pascual, C., Muncharaz, J. Farre, Alonso‐Pulpon, L., Cubero, J. Segovia, Urquia, M. Taibo, Garcia‐Pavia, P., Gomez‐Bueno, M., Cobo‐Marcos, M., Briceno, A., Galvan, E. De Teresa, Garcia‐Pinilla, J.M., Robles‐Mezcua, A., Morcillo‐Hildalgo, L., Elbushi, A., Suliman, A., Ahamed, N., Jazzar, K., Murtada, M., Schaufelberger, M., Goloskokova, V., Hullin, R., Yarol, N., Arrigo, M., Cavusoglu, Y., Eraslan, S., Fak, A.S., Enar, S. Catirli, Sarac, L., Cankurtaran, B., Gumrukcuoglu, H., Ozturk, F., Omagino, J., Mondo, C., Lwabi, P., Ingabire, P., Nabbaale, J., Nyakoojo, W., Okello, E., Sebatta, E., Ssinabulya, I., Atukunda, E., Kitooleko, S., Semu, T., Salih, B.T., Komaranchath, A.M., Almahmeed, W.A.R., Gerges, F., Farook, F.S. Mohamed, Albakshy, F., Mahmood, N., Wani, S., Freudenberger, R., Islam, N., Quinones, J., Sundlof, D., Beitler, C., Centolanza, L., Cornell, K., Huffaker, S., Matos, L., Marzo, K., Paruchuri, V., Patel, D., Abdullaev, T., Alyavi, B., Mirzarakhimova, S., Tsoy, I., Bekbulatova, R., and Uzokov, J.

Abstract

Aims: \ud Hypertensive disorders occur in women with peripartum cardiomyopathy (PPCM). How often hypertensive disorders co-exist, and to what extent they impact outcomes, is less clear. We describe differences in phenotype and outcomes in women with PPCM with and without hypertensive disorders during pregnancy.\ud \ud Methods: \ud The European Society of Cardiology PPCM Registry enrolled women with PPCM from 2012-2018. Three groups were examined: 1) women without hypertension (‘PPCM-noHTN’); 2) women with hypertension but without pre-eclampsia (‘PPCM-HTN’); 3) women with pre-eclampsia (‘PPCM-PE’). Maternal (6-month) and neonatal outcomes were compared.\ud \ud Results: \ud Of 735 women included, 452 (61.5%) had PPCM-noHTN, 99 (13.5%) had PPCM-HTN and 184 (25.0%) had PPCM-PE. Compared to women with PPCM-noHTN, women with PPCM-PE had more severe symptoms (NYHA IV in 44.4% and 29.9%, p

Published
2021

4. Cardiopoietic cell therapy for advanced ischemic heart failure : results at 39 weeks of the prospective, randomized, double blind, sham-controlled CHART-1 clinical trial

Author

Bartunek, Jozef, Terzic, Andre, Davison, Beth A, Filippatos, Gerasimos S, Radovanovic, Slavica, Beleslin, Branko, Merkely, Bela, Musialek, Piotr, Wojakowski, Wojciech, Andreka, Peter, Horvath, Ivan G, Katz, Amos, Dolatabadi, Dariouch, El Nakadi, Badih, Arandjelovic, Aleksandra, Edes, Istvan, Seferovic, Petar M, Obradovic, Slobodan, Vanderheyden, Marc, Jagic, Nikola, Petrov, Ivo, Atar, Shaul, Halabi, Majdi, Gelev, Valeri L, Shochat, Michael K, Kasprzak, Jaroslaw D, Sanz Ruiz, Ricardo, Heyndrickx, Guy R, Nyolczas, Noémi, Legrand, Victor, Guédès, Antoine, Heyse, Alex, Moccetti, Tiziano, Fernandez Aviles, Francisco, Jimenez Quevedo, Pilar, Bayes Genis, Antoni, Hernandez Garcia, Jose Maria, Ribichini, Flavio, Gruchala, Marcin, Waldman, Scott A, Teerlink, John R, Gersh, Bernard J, Povsic, Thomas J, Henry, Timothy D, Metra, Marco, Hajjar, Roger J, Tendera, Michal, Behfar, Atta, Alexandre, Bertrand, Seron, Aymeric, Stough, Wendy Gattis, Sherman, Warren, Cotter, Gad, Wijns, W. i. l. l. i. a. m. Collaborators Clinical investigators, Dens, sites Belgium: Ziekenhuis Oost Limburg: J., Dupont, M., Mullens, W., Janssens, M., Dolatabadi, Hoˆpital Civil de Charleroi: D., De Bruyne, Y., Lalmand, J., Dubois, P., El Nakadi, B., Aminian, A., De Vuyst, E., Gurnet, P., Gujic, M., Blankoff, I., Guedes, CHU Mont Godinne UCL: A., Gabriel, L., Seldrum, S., Doyen, C., Andre´, M., Heyse, AZ Glorieux: A., Van Durme, F., Verschuere, J., Legrand, Domaine Universitaire du Sart Tilman: V., Gach, O., D’Orio, V., Davin, L., Lancellotti, P., Baudoux, E., Ancion, A., Dulgheru, R., Vanderheyden, OLV Ziekenhuis Aalst – Cardiologie: M., Bartunek, J., Wijns, W., Verstreken, S., Penicka, . M., Gelev, P. Meeus Bulgaria: Tokuda Hospital Sofia: V., Zheleva Kichukova, I., Parapunova, R., Melamed, R., Sardovski, S., Radev, O., Yordanov, A., Radinov, A., Nenov, D., Amine, I., Petrov, City Hospital Clinic Cardiology Center: I., Kichukov, K., Nikitasov, L., Stankov, Z., Stoyanov, H., Tasheva Dimitrova, I., Angelova, M., Dimitrov, E., Minchev, M., Garvanski, I., Botev, C., Polomski, P., Alexandrovska University Hospital, Vassilev, Sofia: D., Karamfiloff, K., Tarnovska Kadreva, R., Vladimirova, L., Dimitrov, G., Hadzhiev, E., Tzvetkova, G., Andreka, . M. Atanasova Hungary: Gottsegen Gyo¨ rgy Orszagos Kardiologiai Inte´zet: P., Fontos, G., Fabian, J., Csepregi, A., Uzonyi, G., Gelei, A., Edes, Debreceni Egyetem Orvos e´s Ege´szse´gtudomanyi Centrum Altalanos Orvostudomanyi Kar Kardiologia Inte´zet: I., Balogh, L., Vajda, G., Darago, A., Gergely, S., Fulop, T., Jenei, C., Horvath, Pe´csi Tudomanyegyetem Klinikai Ko¨zpont Szıvgyogyaszati Klinika: I., Magyari, B., Nagy, A., Cziraki, A., Faludi, R., Kittka, B., Alizadeh, H., Merkely, Semmelweis Egyetem Varosmajori Szıv e´s Ergyogyaszati Klinika: B., Geller, L., Farkas, P., Szombath, G., Foldes, G., Skopal, J., Kovacs, A., Kosztin, A., Gara, E., Sydo, N., Nyolczas, MH Ege´szse´gu¨gyi Ko¨zpont Kardiologiai Osztaly: N., Kerecsen, G., Korda, A., Kiss, . M., Borsanyi, T., Polgar, B., Muk, B., Sharif, Z. Bari Ireland: HRB Clinical Research Facility: F., Atar, Y. M. Smyth Israel:Western Galilee Hospital: S., Shturman, A., Akria, L., Kilimnik, M., Brezins, M., Halabi, Ziv Medical Center: M., Dally, N., Goldberg, A., Aehab, K., Rosenfeld, I., Levinas, T., Saleem, D., Katz, Barzilai Medical Center: A., Plaev, T., Drogenikov, T., Nemetz, A., Barshay, Y., Jafari, J., Orlov, I., Nazareth Hospital EMMS: M. Omory, N. Kogan Nielsen, Shochat, Hillel Yaffe Medical Center: M., Shotan, A., Frimerman, A., Meisel, S., Asif, A., Sofer, O., Blondheim, D. S., Vazan, A., Metra, L. Arobov Italy: A. O. Spedali Civili di Brescia: M., Bonadei, I., Inama, L., Chiari, E., Lombardi, C., Magatelli, M., Russo, D., Lazzarini, V., Carubelli, V., Vassanelli, AOUI Verona – Borgo Trento Hospital: C., Ribichini, Flavio Luciano, Bergamini, C., Krampera, Mauro, Cicoria, M. A., Zanolla, L., Dalla Mura, D., Gambaro, A., Rossi, A., Pesarini Poland: Jagiellonian University Department of Cardiac, G., Musialek, Vascular Diseases at John Paul II Hospital in Krakow: P., Mazurek, A., Drabik, L., Ka˛dzielski, A., Walter, Z., Dzieciuch Rojek, M., Rubis, P., Plazak, . W., Tekieli, L., Podolec, J., Orczyk, W., Sutor, U., Zmudka, K., Olszowska, M., Podolec, P., Gruchala, Uniwersyteckie Centrum Kliniczne: M., Ciecwierz, D., Mielczarek, M., Burakowski, S., Chmielecki, M., Zielinska, M., Frankiewicz, A., Wdowczyk, J., Stopczynska, I., Bellwon, J., Mosakowska, K., Nadolna, R., Wroblewska, J., Rozmyslowska, M., Rynkiewicz, M., Marciniak, I., Raczak, G., Tarnawska, M., Taszner, M., Kasprzak, Bieganski Hospital: J., Plewka, M., Fiutowska, D., Rechcinski, T., Lipiec, P., Sobczak, M., Weijner Mik, P., Wraga, M., Krecki, R., Markiewicz, M., Haval Qawoq, D., Wojakowski, Gornosla˛skie Centrum Medyczne Sla˛skie j. Akademii Medycznej: W., Ciosek, J., Dworowy, S., Gaszewska Zurek, E., Ochala, A., Cybulski, W., Jadczyk, T., Wanha, W., Parma, Z., Kozlowski, M., Dzierzak, M., Markiewicz Serbia: Clinical Hospital Center Zvezdara, M., Arandjelovic, Cardiology Clinic: A., Sekularac, N., Boljevic, D., Bogdanovic, A., Zivkovic, S., Cvetinovic, N., Loncar, G., Clinical Centre of Serbia, Beleslin, Cardiology Clinic: B., Nedeljkovic, M., Trifunovic, D., Giga, V., Banovic, M., Nedeljkovic, I., Stepanovic, J., Vukcevic, V., Djordjevic Dikic, A., Dobric, M., Obrenovic Kircanski, B., Seferovic, Cardiology Clinic: P., Orlic, D., Tesic, M., Petrovic, O., Milinkovic, I., Simeunovic, D., Jagic, Clinical Center of Kragujevac: N., Tasic, M., Nikolic, D., Miloradovic, V., Djurdjevic, P., Sreckovic, M., Zornic, N., Clinical Hospital Center Bezanijska Kosa, Radovanovic, Cardiology Department: S., Saric, J., Hinic, S., Djokovic, A., Ðordevic, S., Bisenic, V., Markovic, O., Stamenkovic, S., Malenkovic, V., Tresnjak, J., Misic, G., Cotra, D., Tomovic, L., Vuckovic, V., Clinic of Emergency Internal Medicine, Obradovic, Military Medical Academy: S., Jovic, Z., Vukotic, S., Markovic, D., Djenic, N., Ristic Andjelkov, A., Bayes Genis, D. Ljubinka Spain: Hospital Universitario Germans Trias I. Pujol: A., Rodriguez Leor, O., Labata, C., Vallejo, N., Ferrer, E., Batlle, M., Fernandez Aviles, Hospital General Universitario Gregorio Mara~non: F., Sanz Ruiz, R., Casado, A., Loughlin, G., Zatarain, E., Anguita, J., Ferna ndez Santos, M. E., Pascual, C., Bermejo, J., Hernandez Garcia, Hospital Clinico Universitario Virgen de la Victoria: J. M., Jimenez Navarro, M., Dominguez, A., Carrasco, F., Mu~noz, A., Garcia Pinilla, J. M., Ruiz, J., Queipo de Llano, M. P., Hernandez, A., Fernandez, A., Jimenez Quevedo, Hospital Clinico San Carlos: P., Guerra, R., Biagioni, C., Gonzalez, R. A., Gomez deDiego, J. J., Mansson Broberg, L. Perez de Isla Sweden: Karolinska University Hospital: A., Sylve´n, C., Leblanc, K., Winter, R., Blomberg, P., Gunyeli, E., Ruck, A., Silva, C., Fo¨rstedt Switzerland: CardioCentro Ticino, J., Moccetti, Switzerland: T., Rossi, M., Pasotti, E., Petrova, I., Crljenica, C., Monti, C., Murzilli, R., Su¨rder, D., Moccetti, M., Turchetto, L., Locicero, V., Chiumiento, L., Maspoli, S., Mombelli, M., Anesini, A., Biggiogero, M., Ponti, G., Camporini, C., Polledri, S., Hill, G. Dolci United Kingdom: Kings College Hospital: J., Plymen, C., Amin Youssef, G., Mcdonagh, T., Drasar, E., Mijovic, A., Jouhra, F., Mcloman, D., Dworakowski, R., Webb, I., Byrne, J., and Potter, V.

Subjects
0301 basic medicine, Male, Cardiopoiesis, Cardiovascular disease, Disease severity, Marker, Precision medicine, Regenerative medicine, Stem cell, Target population, Adult, Aged, Double-Blind Method, Female, Heart Failure, Humans, Mesenchymal Stem Cell Transplantation, Middle Aged, Myocardial Ischemia, Prospective Studies, Treatment Outcome, Young Adult, Cardiology and Cardiovascular Medicine, Cell- and Tissue-Based Therapy, mesenchymal stem-cells, 030204 cardiovascular system & hematology, Cardiorespiratory Medicine and Haematology, outcomes, Fast-Track Clinical Research, Sudden cardiac death, 0302 clinical medicine, Ischemia, cardiovascular disease, Clinical endpoint, target population, CHART Program, Ejection fraction, bone-marrow, Heart Failure/Cardiomyopathy, 3. Good health, Cohort, Cardiology, Fast Track, disease severity, delivery, medicine.medical_specialty, precision medicine, Clinical Sciences, regenerative medicine, 03 medical and health sciences, cardiopoiesis, Internal medicine, medicine, Adverse effect, marker, disease, business.industry, medicine.disease, mortality, Confidence interval, Clinical trial, stem cell, Editor's Choice, 030104 developmental biology, predictors, Cardiovascular System & Hematology, Heart failure, business
Abstract

Altres ajuts: This work was supported by Celyad, SA (Mont-Saint-Guibert, Belgium). Celyad has received research grants from the Walloon Region (Belgium, DG06 funding). Cardiopoietic cells, produced through cardiogenic conditioning of patients' mesenchymal stem cells, have shown preliminary efficacy. The Congestive Heart Failure Cardiopoietic Regenerative Therapy (CHART-1) trial aimed to validate cardiopoiesis-based biotherapy in a larger heart failure cohort. This multinational, randomized, double-blind, sham-controlled study was conducted in 39 hospitals. Patients with symptomatic ischaemic heart failure on guideline-directed therapy (n = 484) were screened; n = 348 underwent bone marrow harvest and mesenchymal stem cell expansion. Those achieving > 24 million mesenchymal stem cells (n = 315) were randomized to cardiopoietic cells delivered endomyocardially with a retention-enhanced catheter (n = 157) or sham procedure (n = 158). Procedures were performed as randomized in 271 patients (n = 120 cardiopoietic cells, n = 151 sham). The primary efficacy endpoint was a Finkelstein–Schoenfeld hierarchical composite (all-cause mortality, worsening heart failure, Minnesota Living with Heart Failure Questionnaire score, 6-min walk distance, left ventricular end-systolic volume, and ejection fraction) at 39 weeks. The primary outcome was neutral (Mann–Whitney estimator 0.54, 95% confidence interval [CI] 0.47–0.61 [value > 0.5 favours cell treatment], P = 0.27). Exploratory analyses suggested a benefit of cell treatment on the primary composite in patients with baseline left ventricular end-diastolic volume 200–370 mL (60% of patients) (Mann–Whitney estimator 0.61, 95% CI 0.52–0.70, P = 0.015). No difference was observed in serious adverse events. One (0.9%) cardiopoietic cell patient and 9 (5.4%) sham patients experienced aborted or sudden cardiac death. The primary endpoint was neutral, with safety demonstrated across the cohort. Further evaluation of cardiopoietic cell therapy in patients with elevated end-diastolic volume is warranted.

Published
2017

5. Thromboembolic events in peripartum cardiomyopathy: results from the ESC EORP PPCM registry

Author

Tromp, Jasper, Jackson, Alice M, Abdelhamid, Magdy, Fouad, Doaa, Youssef, Ghada, Petrie, Mark C, Bauersachs, Johann, Sliwa, Karen, van der Meer, Peter, Gale, C P, Beleslin, B., Budaj, A., Chioncel, O., Dagres, N., Danchin, N., Emberson, J., Erlinge, D., Glikson, M., Gray, A., Kayikcioglu, M., Maggioni, A P, Nagy, V K, Nedoshivin, A., Petronio, A-S, Roos-Hesselink, J., Wallentin, L., Zeymer, U., Bauersachs, J., Sliwa, K., Boehm, M., Johnson, M., Hilfiker-Kleiner, D., Mbakwem, A., Mebazaa, A., Mouquet, F., Petrie, M., Pieske, B., Regitz-Zagrosek, V., Schaufelberger, M., Seferovic, P M, Tavazzi, L., van der Meer, P., Van Spaendonck-Zwarts, K., Favaloro, R., Favaloro, L., Carballo, M., Peradejordi, M., Renedo, M F, Absi, D., Bertolotti, A., Ratto, R., Talavera, M L, Gomez, R., Lockwood, S., Barton, T., Austin, M-A, Arstall, M., Aldridge, E., Chow, Y Y, Dekker, G., Mahadavan, G., Rose, J., Wittwer, M., Hoppe, U., Sandhofer, A., Bahshaliyev, A., Gasimov, Z., Babayev, A., Niftiyev, P., Hasanova, I., AlBannay, R., AlHaiki, W., Husain, A., Mahdi, N., Kurlianskaya, A., Lukyanchyk, M., Shatova, O., Troyanova-Shchutskaia, T., Anghel, L., De Pauw, M., Gevaert, S., De Backer, J., De Hosson, M., Vervaet, P., Timmermans, P J, Janssen, A., Yameogo, N V, Kagambega, L J, Cumyn, A., Caron, N., Cote, A-M, Sauve, N., Nkulu, D Ngoy, Lez, D Malamba, Yolola, E Ngoy, Krejci, J., Poloczkova, H., Ersboll, A., Gustafsson, F., Elrakshy, Y., Hassanein, M., Hammad, B., Eldin, O Nour, Fouad, D., Salman, S., Zareh, Z., Abdeall, D., Elenin, H Abo, Ebaid, H., El Nagar, A., Farag, S., Saed, M., El Rahman, Y H Abd, Ibrahim, B S, Abdelhamid, M., Hanna, R N W, Youssef, G., Awad, R., Botrous, O L I, Halawa, S Ibrahim, Nasr, G., Saad, A., El Tahlawi, M., Abdelbaset, M., El-Saadawy, M., El-Shorbagy, A., Shalaby, G., Anttonen, O., Tolppanen, H., Hamekoski, S., Menez, T., Noel, A., Lamblin, N., Coulon, C., de Groote, P., Langlois, S., Schurtz, G., Cohen-Solal, A., Fournier, M-C, Louadah, B., Akrout, N., Logeart, D., Leurent, G., Jovanova, S., Arnaudova-Dezulovicj, F., Livrinova, V., Berliner, D., Jungesblut, M., Koenig, T., Moulig, V A, Pfeffer, T J, Böhm, M., Kindermann, I., Schwarz, V., Schmitt, C., Swojanowsky, P., Pettit, S., McAdam, M., Patton, D., Bakhai, A., Krishnamurthy, V., Lim, L., Clifford, P., Bowers, N., Clark, A L, Witte, K., Cullington, D., Oliver, J., Simms, A., Mcginlay, M., McDonagh, T., Shah, A M, Amin-Youssef, G., De Courcey, J., Martin, K., Shaw, S., Vause, S., Wallace, S., Malin, G., Wick, C., Nikolaou, M., Rentoukas, I., Chinchilla, H., Andino, L., Iyengar, S., Chandra, S., Yadav, D K, Babu, R Ravi, Singh, A K, Kumar, S., Karunamay, B B, Chaubey, S K, Dhiman, S R, Jha, V C, Singh, S K, Kodati, D., Dasari, R., Sultana, S., Dewi, T I, Prameswari, H Sasmaya, Al-Farhan, H A, Al-Hussein, A., Yaseen, I F, Al-Azzawi, Falah, Al-Saedi, Ghazi, Mahmood, G M, Mohammed, M K, Ridha, A F, Shotan, A., Vazan, A., Goland, S., Biener, M., Senni, M., Grosu, A., Martin, E., Esposti, D Degli, Bacchelli, S., Borghi, C., Metra, M., Sciatti, E., Orabona, R., Sani, F., Brunetti, N D, Sinagra, G., Bobbo, M., D'Agata Mottolese, B., Gesuete, V., Rakar, S., Ramani, F., Kamiya, C., Barasa, A., Ngunga, M., Bajraktari, G., Hyseni, V., Lleshi, D., Pllana, E., Pllana, T., Noruzbaeva, A., Ismailov, F., Mirrakhimov, E., Abilova, S., Lunegova, O., Kerimkulova, A., Osmankulova, G., Duishenalieva, M., Kurmanbekova, B., Turgunov, M., Mamasaidova, S., Bektasheva, E., Kavoliūnienė, Aušra, Muckienė, Gintarė, Vaitiekienė, Audronė, Čelutkienė, Jelena, Balkevičienė, Laura, Barysienė, Jūratė, Chee, K H, Damasceno, A., Machava, M., van Veldhuisen, D J, van den Berg, M., van Hagen, I., Baris, L., Hurtado, P., Ezeonu, P., Isiguzo, G., Obeka, N., Onoh, R., Asogwa, F., Onyema, C., Otti, K., Ojji, D., Odili, A., Nwankwo, A., Karaye, K., Ishaq, N., Sanni, B., Abubakar, H., Mohammed, B., Sani, M., Kehinde, M., Afolabi, B., Amadi, C., Kilasho, M., Qamar, N., Furnaz, S., Gurmani, S., Kayani, M G A Mahmood, Munir, R., Hussain, S., Malik, S., Mumtaz, S., Saligan, J R, Rubis, P., Biernacka-Fijalkowska, B., Lesniak-Sobelga, A., Wisniowska-Smialek, S., Kasprzak, J D, Lelonek, M., Zycinski, P., Jankowski, L., Grajek, S., Oko-Sarnowska, Z., Rutkowska, A Bartczak, Kaluzna-Oleksy, M., Plaskota, K., Demkow, M., Dzielinska, Z., Henzel, J., Kryczka, K., Moiseeva, O., Irtyuga, O., Karelkina, E., Zazerskaya, I., Milinkovic, I., Živkovic, I., Ristic, A D, Milasinovic, D., Kong, W Kf, Tan, L K, Tan, J L, Thain, S., Poh, K K, Yip, J., Azibani, F., Hovelmann, J., Viljoen, C., Briton, O., Zamora, E., Orcajo, N Alonso, Carbonell, R., Pascual, C., Muncharaz, J Farre, Alonso-Pulpon, L., Cubero, J Segovia, Urquia, M Taibo, Garcia-Pavia, P., Gomez-Bueno, M., Cobo-Marcos, M., Briceno, A., Galvan, E De Teresa, Garcia-Pinilla, J M, Robles-Mezcua, A., Morcillo-Hildalgo, L., Elbushi, A., Suliman, A., Ahamed, N., Jazzar, K., Murtada, M., Goloskokova, V., Hullin, R., Yarol, N., Arrigo, M., Cavusoglu, Y., Eraslan, S., Fak, A S, Enar, S Catirli, Sarac, L., Cankurtaran, B., Gumrukcuoglu, H., Ozturk, F., Omagino, J., Mondo, C., Lwabi, P., Ingabire, P., Nabbaale, J., Nyakoojo, W., Okello, E., Sebatta, E., Ssinabulya, I., Atukunda, E., Kitooleko, S., Semu, T., Salih, B T, Komaranchath, A M, Almahmeed, W A R, Gerges, F., Farook, F S Mohamed, Albakshy, F., Mahmood, N., Wani, S., Freudenberger, R., Islam, N., Quinones, J., Sundlof, D., Beitler, C., Centolanza, L., Cornell, K., Huffaker, S., Matos, L., Marzo, K., Paruchuri, V., Patel, D., Abdullaev, T., Alyavi, B., Mirzarakhimova, S., Tsoy, I., Bekbulatova, R., and Uzokov, J.

Published
2023

6. Arrhythmia and Death Following Percutaneous Revascularization in Ischemic Left Ventricular Dysfunction: Prespecified Analyses From the REVIVED-BCIS2 Trial.

Author

Perera D, Morgan HP, Ryan M, Dodd M, Clayton T, O'Kane PD, Greenwood JP, Walsh SJ, Weerackody R, McDiarmid A, Amin-Youssef G, Strange J, Modi B, Lockie T, Hogrefe K, Ahmed FZ, Behan M, Jenkins N, Abdelaal E, Anderson M, Watkins S, Evans R, Rinaldi CA, and Petrie MC

Subjects
Humans, Male, Aged, Female, Stroke Volume, Death, Sudden, Cardiac epidemiology, Death, Sudden, Cardiac etiology, Death, Sudden, Cardiac prevention & control, Ventricular Function, Left, Arrhythmias, Cardiac etiology, Treatment Outcome, Ventricular Dysfunction, Left etiology, Defibrillators, Implantable adverse effects
Abstract

Background: Ventricular arrhythmia is an important cause of mortality in patients with ischemic left ventricular dysfunction. Revascularization with coronary artery bypass graft or percutaneous coronary intervention is often recommended for these patients before implantation of a cardiac defibrillator because it is assumed that this may reduce the incidence of fatal and potentially fatal ventricular arrhythmias, although this premise has not been evaluated in a randomized trial to date., Methods: Patients with severe left ventricular dysfunction, extensive coronary disease, and viable myocardium were randomly assigned to receive either percutaneous coronary intervention (PCI) plus optimal medical and device therapy (OMT) or OMT alone. The composite primary outcome was all-cause death or aborted sudden death (defined as an appropriate implantable cardioverter defibrillator therapy or a resuscitated cardiac arrest) at a minimum of 24 months, analyzed as time to first event on an intention-to-treat basis. Secondary outcomes included cardiovascular death or aborted sudden death, appropriate implantable cardioverter defibrillator (ICD) therapy or sustained ventricular arrhythmia, and number of appropriate ICD therapies., Results: Between August 28, 2013, and March 19, 2020, 700 patients were enrolled across 40 centers in the United Kingdom. A total of 347 patients were assigned to the PCI+OMT group and 353 to the OMT alone group. The mean age of participants was 69 years; 88% were male; 56% had hypertension; 41% had diabetes; and 53% had a clinical history of myocardial infarction. The median left ventricular ejection fraction was 28%; 53.1% had an implantable defibrillator inserted before randomization or during follow-up. All-cause death or aborted sudden death occurred in 144 patients (41.6%) in the PCI group and 142 patients (40.2%) in the OMT group (hazard ratio, 1.03 [95% CI, 0.82-1.30]; P =0.80). There was no between-group difference in the occurrence of any of the secondary outcomes., Conclusions: PCI was not associated with a reduction in all-cause mortality or aborted sudden death. In patients with ischemic cardiomyopathy, PCI is not beneficial solely for the purpose of reducing potentially fatal ventricular arrhythmias., Registration: URL: https://www., Clinicaltrials: gov; Unique identifier: NCT01920048., Competing Interests: Disclosures None.

Published
2023
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8. Diagnostic value of 18 F-FDG PET/CT in infective endocarditis.

Author

Anton-Vazquez V, Cannata A, Amin-Youssef G, Watson S, Fife A, Mulholland N, Gunning M, Papachristidis A, MacCarthy P, Baghai M, Deshpande R, Khan H, Byrne J, and Dworakowski R

Subjects
Fluorodeoxyglucose F18, Humans, Positron Emission Tomography Computed Tomography methods, Positron-Emission Tomography adverse effects, Radiopharmaceuticals pharmacology, Retrospective Studies, Endocarditis diagnostic imaging, Endocarditis etiology, Endocarditis, Bacterial
Abstract

Introduction: 18F-fluorodeoxyglucose positron emission tomography ( 18 F-FDG-PET/CT) is not routinely recommended for the diagnosis of infective endocarditis (IE) due to the lack of clinical impact., Materials and Methods: Between January 2016 and January 2020, clinical data from patients with a possible diagnosis of IE were reviewed retrospectively to evaluate the value of 18 F-FDG-PET/CT in the diagnosis of IE. 18 F-FDG PET/CT scan was performed as an additional diagnostic tool in possible IE when echocardiography was inconclusive or in patients with definite IE to identify extracardiac complications. Cases were classified according to modified Duke criteria as rejected, definite or possible., Results: 313 patients with suspected IE were included. 72 (23%) patients underwent 18F-FDG PET/CT. 18 F-FDG PET/CT resulted in a reclassification of Duke criteria in 29/72 (40%) patients, from "possible" to "definite" (n, 10) and to "rejected" (n, 19). Patients who benefited from a Duke criteria reclassification following 18 F-FDG PET/CT were more frequently classified as possible IE at inclusion or had a non-conclusive baseline echocardiography (100% vs 58%; p 0.001) and had more likely a prosthetic metallic valve replacement (59% vs 21%; p 0.001). Abnormal perivalvular uptake was identified in 46 patients (71% prosthetic vs 50% native; p 0.118). 18 F-FDG PET/CT identified extracardiac uptake consistent with septic emboli in 14/72 (19%) patients. In addition, extracardiac uptake indicative of an alternative diagnosis was identified in 5 patients (2% prosthetic vs 17% native; p 0.039)., Conclusion: The use of 18 F-FDG-PET/CT has shown to be useful in the diagnosis of IE, particularly in prosthetic IE and may provide additional value in the detection of septic emboli and/or the identification of an alternative diagnosis different from IE., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

Published
2022
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9. Cardiac energetics in patients with chronic heart failure and iron deficiency: an in-vivo  31 P magnetic resonance spectroscopy study.

Author

Papalia F, Jouhra F, Amin-Youssef G, Shah AM, Charles-Edwards G, and Okonko DO

Subjects
Adenosine Triphosphate, Chronic Disease, Humans, Magnetic Resonance Spectroscopy, Anemia complications, Anemia, Iron-Deficiency complications, Heart Failure, Iron Deficiencies
Abstract

Aims: Iron deficiency (ID) is prevalent and adverse in chronic heart failure (CHF) but few human studies have explored the myocardial mechanism(s) that potentially underlie this adversity. Because mitochondrial oxidative phosphorylation (OXPHOS) provides over 90% of the hearts adenosine triphosphate (ATP), and iron is critical for OXPHOS, we hypothesized that patients with CHF and ID would harbour greater cardiac energetic impairments than patients without ID., Methods and Results: Phosphorus magnetic resonance spectroscopy was used to quantify the phosphocreatine (PCr) to ATP (PCr/ATP) ratio, an index of in-vivo cardiac energetics, in CHF patients and healthy volunteers. Cardiac structure and function was assessed from magnetic resonance short stack cines. Patients with (n = 27) and without (n = 12) ID, and healthy volunteers (n = 11), were similar with respect to age and gender. The PCr/ATP ratio was lower in patients with ID (1.03 [0.83-1.38]) compared to those without ID (1.72 [1.51-2.26], p < 0.01) and healthy volunteers (1.39 [1.10-3.68], p < 0.05). This was despite no difference in cardiac structure and function between patients with and without ID, and despite adjustment for the presence of anaemia, haemoglobin levels, cardiac rhythm, or New York Heart Association (NYHA) class. In the total CHF cohort, the PCr/ATP ratio correlated with ferritin levels (rho = 0.4, p < 0.01), and was higher in NYHA class I than class II or III patients (p = 0.02)., Conclusion: Iron deficiency is associated with greater cardiac energetic impairment in patients with CHF irrespective of anaemia and cardiac structure and function. Suppression of cardiac mitochondrial function might therefore be a mechanism via which ID worsens human CHF., (© 2022 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Published
2022
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10. 16S rDNA PCR for the aetiological diagnosis of culture-negative infective endocarditis.

Author

Anton-Vazquez V, Dworakowski R, Cannata A, Amin-Youssef G, Gunning M, Papachristidis A, MacCarthy P, Baghai M, Deshpande R, Khan H, Byrne J, and Fife A

Subjects
DNA, Ribosomal genetics, Humans, Male, Middle Aged, Polymerase Chain Reaction, RNA, Ribosomal, 16S genetics, Retrospective Studies, Endocarditis diagnosis, Endocarditis, Bacterial diagnosis
Abstract

Introduction: Culture-negative infective endocarditis (IE) accounts for 7-31% of all cases. Metagenomics has contributed to improving the aetiological diagnosis of IE patients undergoing valve surgery. We assessed the impact of 16S ribosomal DNA gene polymerase chain reaction (16S rDNA PCR) in the aetiological diagnosis of culture-negative IE., Methods: Between January 2016 and January 2020, clinical data from culture-negative IE patients were reviewed retrospectively. Identification of bacteria was performed using 16S rDNA PCR in heart valve specimens., Results: 36 out of 313 patients (12%) with culture-negative IE had their valve tissue specimens submitted for 16S rDNA PCR. 16S rDNA PCR detected and identified bacterial nucleic acid in heart valve tissue significantly more frequently compared to valve culture alone 25(70%) vs 5(12%); p < 0.05. Mean age was 57 years (SD 18) and 80% were male. Native and aortic valve were involved in 76% and 52% of cases, respectively. Streptococcus spp. (n 15) were the most commonly detected organisms, followed by bacteria of the HACEK group (Haemophilus parainfluenzae 2, Aggregatibacter actinomycetemcomitans 1), nutritionally variant streptococci (Abiotrophia defectiva 2), and one each of Staphylococcus aureus, Corynebacterium pseudodiphtheriticum, Helcococcus kunzii, Neisseria gonorrhoeae, Tropheryma whipplei., Conclusion: 16S rDNA PCR may be a useful diagnostic tool for the identification of the causative organism in culture-negative IE. Efforts towards a shorter turnaround time for results should be consider and further studies assessing the clinical impact of this technique in culture-negative IE are needed., (© 2021. Springer-Verlag GmbH Germany, part of Springer Nature.)

Published
2022
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11. Collateral implications of the COVID-19 pandemic: belated presentation of infective endocarditis in a young patient.

Author

Toth E, Dancy L, Amin-Youssef G, Papachristidis A, and Dworakowski R

Subjects
Abscess, Adult, Aortic Valve diagnostic imaging, Aortic Valve pathology, Aortic Valve physiopathology, Aortic Valve Insufficiency, COVID-19 diagnosis, COVID-19 physiopathology, Electrocardiography, Fatal Outcome, Humans, Male, Pandemics, SARS-CoV-2, Young Adult, COVID-19 complications, Endocarditis diagnosis, Endocarditis physiopathology, Endocarditis virology
Published
2020
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12. Tissue Doppler-Derived Left Ventricular Systolic Velocity Is Associated with Lethal Arrhythmias in Cardiac Device Recipients Irrespective of Left Ventricular Ejection Fraction.

Author

Barakat MF, Chehab O, Kaura A, Sunderland N, Hayat S, Dhillon PS, Gall N, Monaghan MJ, Amin-Youssef G, Mayet J, Shah AM, Scott PA, and Okonko DO

Subjects
Aged, Death, Sudden, Cardiac, Female, Humans, Male, Retrospective Studies, Risk Factors, Stroke Volume, Treatment Outcome, Ventricular Function, Left, Defibrillators, Implantable, Tachycardia, Ventricular
Abstract

Background: Life-threatening arrhythmias (LTAs) can trigger sudden cardiac death or provoke implantable cardioverter-defibrillator (ICD) discharges that escalate morbidity and mortality. Longitudinal myofibrils predominate in the subendocardium, which is uniquely sensitive to arrhythmogenic triggers. In this study, we test the hypothesis that mitral annular systolic velocity (S'), a simple routinely obtained tissue Doppler index of LV long-axis systolic function, might predict lethal arrhythmias irrespective of left ventricular ejection fraction (LVEF)., Methods: This is a retrospective analysis of data from 302 patients (mean age, 68 years; LVEF, 32%; 77% male; 52% ischemic; 35% primary prevention; and 53% cardiac resynchronization therapy defibrillator [CRT-D]) who were followed up (median, 15 months) at two centers after receipt of an ICD or CRT-D for diverse indications. S', averaged from tissue Doppler-derived medial and lateral mitral annular velocities, was correlated with the primary outcome of time to sustained ventricular tachycardia (VT) or fibrillation (VF) needing device therapy., Results: The median S' was 5.1 (interquartile range, 4.0-6.2) cm/sec and lower in CRT-D than ICD subjects (4.5 [3.8-5.6] cm/sec vs 5.5 [4.8-6.8] cm/sec, P < .001). Fifty-six (19%) subjects had LTA. Each 1 cm/sec higher S' correlated to a 30% decreased risk of LTA (hazard ratio = 0.70; 95% CI, 0.57-0.87; P = .001) independently of age, sex, β-blocker use, center, ICD use, and LVEF. Adding S' to the baseline Cox model improved net reclassification (P = .02). An S' > 5.6 cm/sec was the best cutoff and linked to a 58% lower LTA risk than an S' ≤ 5.6 cm/sec (95% CI, 0.23-0.85; P = .02)., Conclusions: A higher S' is associated with a reduced probability of LTA in cardiac device recipients irrespective of LVEF and may have the potential to be used clinically to titrate medical, device, and ablative therapies to mitigate future arrhythmic risk., (Copyright © 2020 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.)

Published
2020
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13. Isolated papillary muscle rupture with nonobstructive coronary artery disease, minimal myocardial infarction, and normal wall motion.

Author

Nakou ES, Theodoropoulos KC, Shaikh H, Amin-Youssef G, Monaghan MJ, and Papachristidis A

Subjects
Humans, Papillary Muscles diagnostic imaging, Coronary Artery Disease, Heart Rupture, Post-Infarction diagnostic imaging, Mitral Valve Insufficiency complications, Mitral Valve Insufficiency diagnostic imaging, Myocardial Infarction diagnostic imaging
Abstract

Papillary muscle (PM) rupture can usually complicate inferior or posterior myocardial infarctions, but selective PM infarction is extremely rare, and the exact underlying pathophysiological mechanism is not entirely clear. We present a case of PM rupture due to isolated PM infarction in a patient with unobstructed coronary arteries, which could be misdiagnosed as a vegetation or other mass given the absence of regional wall motion abnormalities (RWMAs) on transthoracic echocardiogram. Our case highlights that in patients with severe mitral regurgitation and associated mitral valve mass, the absence of RWMAs should not exclude ischemic PM rupture from differential diagnosis., (© 2020 Wiley Periodicals LLC.)

Published
2020
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14. Calculated plasma volume status and outcomes in patients undergoing coronary bypass graft surgery.

Author

Maznyczka AM, Barakat MF, Ussen B, Kaura A, Abu-Own H, Jouhra F, Jaumdally H, Amin-Youssef G, Nicou N, Baghai M, Deshpande R, Wendler O, Kolvekar S, and Okonko DO

Subjects
Aged, Aged, 80 and over, Cohort Studies, Female, Humans, Male, Middle Aged, Preoperative Period, Prognosis, Retrospective Studies, Treatment Outcome, Coronary Artery Bypass, Plasma Volume
Abstract

Objectives: Congestion is associated with worse outcomes in critically ill surgical patients but can be difficult to quantify noninvasively. We hypothesised that plasma volume status (PVS), estimated preoperatively using a validated formula that enumerates percentage change from ideal plasma volume (PV), would provide incremental prognostic utility after coronary artery bypass graft (CABG) surgery., Methods: In this retrospective cohort study, patients who underwent CABG surgery (1999-2010) were identified from a prospectively collected database. Actual ([1-haematocrit] x [a+(b x weight [kg])]) and ideal (c x weight [kg]) PV were obtained from equations where a, b and c are sex-dependent constants. Calculated PVS was then derived (100% x [(actual-ideal)/ideal])., Results: In 1887 patients (mean age 67±10 years; 79% male; median European System for Cardiac Operative Risk Evaluation [EuroSCORE] 4), mean PVS was -8.2±9%. While 8% of subjects had clinical evidence of congestion, a relatively increased PV (PVS >0%) was estimated in 17% and correlated with lower serum sodium, higher EuroSCORE and a diagnosis of diabetes mellitus. A PVS≥5.6% was optimally prognostic and associated with greater mortality (HR: 2.31, p=0.009), independently of, and incremental to, EuroSCORE, New York Heart Association class and serum sodium. A PVS≥5.6% also independently predicted longer intensive care (β: 0.65, p=0.007) and hospital (β: 2.01, p=0.006) stays, and greater postoperative renal (OR: 1.61, p=0.008) and arrhythmic (OR: 1.29, p=0.03) complications., Conclusions: Higher PVS values, calculated simply from weight and haematocrit, are associated with worse inpatient outcomes after CABG. PVS could help refine risk stratification and further investigations are warranted to evaluate the potential clinical utility of PVS-guided management in patients undergoing CABG., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Published
2019
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15. Effect of Iron Isomaltoside on Skeletal Muscle Energetics in Patients With Chronic Heart Failure and Iron Deficiency.

Author

Charles-Edwards G, Amaral N, Sleigh A, Ayis S, Catibog N, McDonagh T, Monaghan M, Amin-Youssef G, Kemp GJ, Shah AM, and Okonko DO

Subjects
Aged, Aged, 80 and over, Anemia, Iron-Deficiency blood, Anemia, Iron-Deficiency diagnosis, Biomarkers blood, Disaccharides adverse effects, Double-Blind Method, Female, Ferric Compounds adverse effects, Heart Failure diagnosis, Heart Failure physiopathology, Hematinics adverse effects, Humans, Iron blood, London, Magnetic Resonance Spectroscopy, Male, Middle Aged, Muscle, Skeletal metabolism, Muscle, Skeletal physiopathology, Phosphocreatine metabolism, Recovery of Function, Time Factors, Treatment Outcome, Anemia, Iron-Deficiency drug therapy, Disaccharides therapeutic use, Energy Metabolism drug effects, Exercise Tolerance drug effects, Ferric Compounds therapeutic use, Heart Failure drug therapy, Hematinics therapeutic use, Iron Deficiencies, Muscle, Skeletal drug effects
Abstract

Background: Iron repletion augments exercise capacity in chronic heart failure (HF), but there is a lack of mechanistic data explaining how iron could augment exercise performance despite minimal changes in hemoglobin (Hb). Besides Hb, iron is an obligate component of mitochondrial enzymes that generate cellular energy in the form of adenosine triphosphate and phosphocreatine (PCr). Dynamic phosphorus magnetic resonance spectroscopy is a noninvasive tool that quantifies in vivo muscle energetics by measuring the kinetics of PCr recovery after exertion. We tested the hypothesis that intravenous iron repletion in chronic HF enhances skeletal muscle energetics as reflected by shorter PCr recovery half-times (PCr t 1/2 ) on phosphorus magnetic resonance spectroscopy., Methods: We enrolled 40 patients (50% anemic) with chronic HF, New York Heart Association class ≥II, left ventricular ejection fraction ≤45%, and iron deficiency (ferritin<100 μg/L or 100-300 μg/L with transferrin saturation <20%). Subjects underwent stratified (anemic versus nonanemic) randomization (1:1) to a single, double-blinded, total dose infusion of iron isomaltoside or saline placebo with end points reassessed early at 2 weeks posttreatment to minimize confounding from exercise adaptation. The primary end point was PCr t 1/2 at 2 weeks. Secondary end points included ADP recovery half-time (ADP t 1/2; energetic marker), iron status, symptoms, Hb, exercise capacity, and safety., Results: In the total population, treatment groups were similar at baseline. At 2 weeks, iron isomaltoside improved PCr t 1/2 (adjusted difference, -6.8 s; 95% CI, 11.5 to -2.1; P=0.006), ADP t 1/2 (-5.3 s; 95% CI, -9.7 to -0.9; P=0.02), ferritin (304 ng/mL; 95% CI, 217-391; P<0.0001), transferrin saturation (6.8%; 95% CI, 2.7-10.8; P=0.002), New York Heart Association class (-0.23; 95% CI, -0.46 to -0.01; P=0.04), resting respiratory rate (-0.7 breaths/min; 95% CI, -1.2 to -0.2; P=0.009), and postexercise Borg dyspnea score (-2.0; 95% CI, -3.7 to -0.3; P=0.04), but not Hb (2.4 g/L; 95% CI, -3.5 to 8.4; P=0.41). Adverse events were similar between groups. In subgroup analyses, iron isomaltoside improved PCr t 1/2 in anemic (-8.4 s; 95% CI, -16.7 to -0.2; P=0.04) and nonanemic (-5.2 s; 95% CI, -10.6 to 0.2; P=0.06) cohorts., Conclusions: In patients with chronic HF and iron deficiency, a total repletion dose of iron isomaltoside given at a single sitting is well tolerated and associated with faster skeletal muscle PCr t 1/2 at 2 weeks, implying better mitochondrial function. Augmented skeletal muscle energetics might therefore be an important mechanism via which iron repletion confers benefits in chronic HF despite minimal Hb changes., Clinical Trial Registration: URL: https://www.clinicaltrialsregister.eu/ctr-search/trial/2012-005592-13/GB . Unique identifier: EudraCT 2012-005592-13.

Published
2019
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16. Biologic Variability of Soluble ST2 in Patients With Stable Chronic Heart Failure and Implications for Monitoring.

Author

Piper S, deCourcey J, Sherwood R, Amin-Youssef G, and McDonagh T

Subjects
Aged, Aged, 80 and over, Biomarkers blood, Chronic Disease, Cohort Studies, Female, Humans, Male, Middle Aged, Natriuretic Peptide, Brain blood, Peptide Fragments blood, Stroke Volume, Time Factors, Heart Failure blood, Interleukin-1 Receptor-Like 1 Protein blood
Abstract

Soluble ST2 (sST2) is a novel biomarker implicated in myocardial remodeling and fibrosis. Recent studies in normal subjects have suggested that the biologic variability (BV) of sST2 is significantly lower than that of the B-type natriuretic peptides and N-terminal pro B-type natriuretic peptide (NTproBNP). It may, consequently, be a better biomarker for monitoring patients with chronic heart failure (CHF). To date, no published studies have examined the BV of sST2 in a heart failure population. Blood samples from 50 outpatients with pharmacologically optimized stable CHF and persistent left ventricular dysfunction (ejection fraction <40%) were collected at baseline, 1 hour, 1 month, 3 months, and 6 months. Using log-transformed data, mean intra-individual coefficients of variation (CVI) and subsequent reference change values were calculated for both NTproBNP and sST2. Results demonstrate significantly lower CVI and reference change values for sST2 compared with NTproBNP at 1 month (12.02 [36%] vs 36.75 [103%]), p <0.001, 3 months (12.23 [36%] vs 40.98 [114%]), p <0.001, and 6 months (16.41 [47%] vs 46.02 [128%]), p <0.001. In conclusion, the BV of sST2 is significantly lower than that of NTproBNP in patients with CHF. These results support previous indications that sST2 may be a better biomarker for monitoring such patients., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Published
2016
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