Search

Your search keyword '"Caliskan K"' showing total 22 results
Start Over Author "Caliskan K" Journal european heart journal
22 results on '"Caliskan K"'

6. P1640Longitudinal patterns of NT-proBNP, troponin T and CRP in relation to the dynamics of echocardiographic parameters in heart failure patients

Author

Klimczak-Tomaniak, D, primary, Van Den Berg, V, additional, Strachinaru, M, additional, Akkerhuis, K M, additional, Baart, S, additional, Caliskan, K, additional, Manintveld, O C, additional, Umans, V, additional, Geleijnse, M L, additional, Boersma, H, additional, Van Dalen, B, additional, and Kardys, I, additional

Published
2019
Full Text
View/download PDF

10. P1675Evolution of lactate dehydrogenase levels in patients with HeartMate II, HeartWare and HeartMate 3 left ventricular assist devices during first-year follow-up

Author

Yalcin, Y C, primary, Muslem, R, additional, Papageorgiou, G, additional, Tedford, R J, additional, Constantinescu, A A, additional, Birim, O C, additional, Brugts, J J, additional, Manintveld, O C, additional, Hsu, S, additional, Leebeek, F W G, additional, Bogers, A J J C, additional, and Caliskan, K, additional

Published
2019
Full Text
View/download PDF

13. P5122A novel method for early identification of cardiac tamponade in patients with continuous flow left ventricular assist devices by use of sublingual microcirculatory imaging

Author

Akin, S, primary, Ince, C, additional, Den Uil, C A, additional, Struijs, A, additional, Muslem, R, additional, Ocak, I, additional, Guven, G, additional, Constantinescu, A A, additional, Soliman, O I, additional, Zijlstra, F, additional, Bogers, A J J C, additional, and Caliskan, K, additional

Published
2018
Full Text
View/download PDF

17. P6174Serial biomarker measurements show that down-titration of RAAS inhibitors and up-titration of diuretics mark progression towards end stage heart failure: Analysis of Bio-SHIFT study

Author

Brankovic, M., primary, Akkerhuis, K.M., additional, Van Boven, N., additional, Manintveld, O., additional, Germans, T., additional, Brugts, J., additional, Caliskan, K., additional, Boersma, E., additional, Umans, V., additional, Constantinescu, A., additional, and Kardys, I., additional

Published
2017
Full Text
View/download PDF

18. 4791Cardiac and genetic features of noncompaction cardiomyopathy and its relation to late outcome: a Dutch multicenter study of 327 pediatric and adult patients

Author

Van Waning, J.I., primary, Caliskan, K., additional, Hoedemaekers, Y.M., additional, Van Spaendonck, K.Y., additional, Baas, A.F., additional, Boekholdt, S.M., additional, Van Melle, J.P., additional, Asselbergs, L.F., additional, Backx, A.P.C.M., additional, Dalinghaus, M., additional, Breur, H., additional, Du Marchie Sarvaas, G.J., additional, Lekanne Dit Deprez, R.H., additional, Jongbloed, J.D.H., additional, and Majoor-Krakauer, D.F., additional

Published
2017
Full Text
View/download PDF

21. Uncertainties and challenges in surgical and transcatheter tricuspid valve therapy: a state-of-the-art expert review.

Author

Chang CC, Veen KM, Hahn RT, Bogers AJJC, Latib A, Oei FBS, Abdelghani M, Modolo R, Ho SY, Abdel-Wahab M, Fattouch K, Bosmans J, Caliskan K, Taramasso M, Serruys PW, Bax JJ, van Mieghem NMDA, Takkenberg JJM, Lurz P, Modine T, and Soliman O

Subjects
Humans, Mitral Valve surgery, Treatment Outcome, Tricuspid Valve surgery, Cardiac Valve Annuloplasty, Heart Valve Prosthesis Implantation, Tricuspid Valve Insufficiency surgery
Abstract

Tricuspid regurgitation (TR) is a frequent and complex problem, commonly combined with left-sided heart disease, such as mitral regurgitation. Significant TR is associated with increased mortality if left untreated or recurrent after therapy. Tricuspid regurgitation was historically often disregarded and remained undertreated. Surgery is currently the only Class I Guideline recommended therapy for TR, in the form of annuloplasty, leaflet repair, or valve replacement. As growing experience of transcatheter therapy in structural heart disease, many dedicated transcatheter tricuspid repair or replacement devices, which mimic well-established surgical techniques, are currently under development. Nevertheless, many aspects of TR are little understood, including the disease process, surgical or interventional risk stratification, and predictors of successful therapy. The optimal treatment timing and the choice of proper surgical or interventional technique for significant TR remain to be elucidated. In this context, we aim to highlight the current evidence, underline major controversial issues in this field and present a future roadmap for TR therapy., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.)

Published
2020
Full Text
View/download PDF

22. Cardiac beta-myosin heavy chain defects in two families with non-compaction cardiomyopathy: linking non-compaction to hypertrophic, restrictive, and dilated cardiomyopathies.

Author

Hoedemaekers YM, Caliskan K, Majoor-Krakauer D, van de Laar I, Michels M, Witsenburg M, ten Cate FJ, Simoons ML, and Dooijes D

Subjects
Adolescent, Adult, Aged, Cardiomyopathy, Dilated diagnostic imaging, Cardiomyopathy, Hypertrophic, Familial diagnostic imaging, Cardiomyopathy, Restrictive diagnostic imaging, Echocardiography methods, Female, Heart Failure diagnostic imaging, Humans, Male, Pedigree, Cardiomyopathy, Dilated genetics, Cardiomyopathy, Hypertrophic, Familial genetics, Cardiomyopathy, Restrictive genetics, Heart Failure genetics, Mutation genetics, Myosin Heavy Chains genetics, Ventricular Myosins genetics
Abstract

Cardiomyopathies are classified according to distinct morphological characteristics. They occur relatively frequent and are an important cause of mortality and morbidity. Isolated ventricular non-compaction or non-compaction cardiomyopathy (NCCM) is characterized by an excessively thickened endocardial layer with deep intertrabecular recesses, reminiscent of the myocardium during early embryogenesis. Aims Autosomal-dominant as well as X-linked inheritance for NCCM has been described and several loci have been associated with the disease. Nevertheless, a major genetic cause for familial NCCM remains to be identified. Methods and Results We describe, in two separate autosomal-dominant NCCM families, the identification of mutations in the sarcomeric cardiac beta-myosin heavy chain gene (MYH7), known to be associated with hypertrophic cardiomyopathy (HCM), restricted cardiomyopathy (RCM), and dilated cardiomyopathy (DCM). Conclusion These results confirm the genetic heterogeneity of NCCM and suggest that the molecular classification of cardiomyopathies includes an MYH7-associated spectrum of NCCM with HCM, RCM, and DCM.

Published
2007
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results