Marta Cvijic1,2, Jürgen Duchenne1, Serkan Ünlü1,3,4, Blazej Michalski1,5, Marit Aarones6, Stefan Winter7, Svend Aakhus6,8, Wolfgang Fehske7, Ivan Stankovic9, Jens-Uwe Voigt1. 1. Department of Cardiovascular Diseases, University Hospital Leuven, Herestraat 49, 3000 Leuven, Belgium. 2. Department of Cardiology, University Medical Centre Ljubljana, Ljubljana, Slovenia. 3. Department of Pharmacology, Gazi University Institute of Health Sciences, Ankara, Turkey. 4. Atatürk Chest Diseases and Chest Surgery Education and Research Hospital, Ankara, Turkey. 5. Department of Cardiology, Medical University of Łodz, Łodz, Poland. 6. Department of Cardiology, Oslo University Hospital, Oslo, Norway. 7. Klinik für Innere Medizin und Kardiologie, St. Vinzenz Hospital, Cologne, Germany. 8. Department of Circulation and Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway. 9. Department of Cardiology, University Clinical Hospital Centre Zemun, University of Belgrade, Serbia.
Abstract
Aims: The interaction between asynchronous regional myocardial activation and left ventricular (LV) wall remodelling has not been well established. We investigated the relationship between time of onset of longitudinal shortening (Tonset), regional myocardial work, and segmental LV wall thickness (SWT) in patients treated with cardiac resynchronization therapy (CRT). Methods and results: We analysed 26 patients with sinus rhythm, non-ischaemic cardiomyopathy (63 ± 9 years, 69% male, QRS duration 174 ± 18 ms) and positive response to CRT (15% reduction in end-systolic volume). Longitudinal strain was obtained by 2D speckle-tracking echocardiography before and after [14.5 (7-29) months] CRT. Tonset and SWT were measured in 18 segments per LV. Segmental myocardial work was calculated from non-invasive segmental stress-strain loop area. Before CRT, Tonset was the shortest in septal and anteroseptal and the longest in lateral and posterior walls (P < 0.001) and not different after CRT (P = 0.733). Before CRT, septal and anteroseptal walls were significantly thinner than lateral and posterior. After CRT, reverse remodelling increased thickness in septal and anteroseptal and thinned lateral and posterior segments (P < 0.001). Before CRT, non-uniformity in work distribution with reduced work in septal and anteroseptal and increased work in lateral and posterior walls (P < 0.001) was observed. After CRT, distribution of myocardial work was uniform (P = 0.215). Conclusion: Dys-synchronous myocardial shortening is related to thinning of early and thickening of late activated segments in heart failure with conduction delay. Correction of dys-synchrony leads to regression of inhomogeneity towards more evenly distributed wall thickness. Regional differences in myocardial work load that are homogenized by successful CRT are considered as the underlying pathophysiological mechanism.
Aims: The interaction between asynchronous regional myocardial activation and left ventricular (LV) wall remodelling has not been well established. We investigated the relationship between time of onset of longitudinal shortening (Tonset), regional myocardial work, and segmental LV wall thickness (SWT) in patients treated with cardiac resynchronization therapy (CRT). Methods and results: We analysed 26 patients with sinus rhythm, non-ischaemic cardiomyopathy (63 ± 9 years, 69% male, QRS duration 174 ± 18 ms) and positive response to CRT (15% reduction in end-systolic volume). Longitudinal strain was obtained by 2D speckle-tracking echocardiography before and after [14.5 (7-29) months] CRT. Tonset and SWT were measured in 18 segments per LV. Segmental myocardial work was calculated from non-invasive segmental stress-strain loop area. Before CRT, Tonset was the shortest in septal and anteroseptal and the longest in lateral and posterior walls (P < 0.001) and not different after CRT (P = 0.733). Before CRT, septal and anteroseptal walls were significantly thinner than lateral and posterior. After CRT, reverse remodelling increased thickness in septal and anteroseptal and thinned lateral and posterior segments (P < 0.001). Before CRT, non-uniformity in work distribution with reduced work in septal and anteroseptal and increased work in lateral and posterior walls (P < 0.001) was observed. After CRT, distribution of myocardial work was uniform (P = 0.215). Conclusion: Dys-synchronous myocardial shortening is related to thinning of early and thickening of late activated segments in heart failure with conduction delay. Correction of dys-synchrony leads to regression of inhomogeneity towards more evenly distributed wall thickness. Regional differences in myocardial work load that are homogenized by successful CRT are considered as the underlying pathophysiological mechanism.
Authors: Alwin Zweerink; Robin Nijveldt; Natalia J Braams; Alexander H Maass; Kevin Vernooy; Frederik J de Lange; Mathias Meine; Bastiaan Geelhoed; Michiel Rienstra; Isabelle C van Gelder; Marc A Vos; Albert C van Rossum; Cornelis P Allaart Journal: J Cardiovasc Magn Reson Date: 2021-01-11 Impact factor: 5.364
Authors: Ganna Degtiarova; Piet Claus; Jürgen Duchenne; Marta Cvijic; Georg Schramm; Johan Nuyts; Jens-Uwe Voigt; Olivier Gheysens Journal: EJNMMI Res Date: 2019-12-09 Impact factor: 3.138