Petter Storsten1, John M Aalen1, Espen Boe2, Espen W Remme3, Ola Gjesdal4, Camilla Kjellstad Larsen1, Øyvind Senstad Andersen1, Morten Eriksen3, Erik Kongsgaard5, Jürgen Duchenne6, Jens-Uwe Voigt6, Otto A Smiseth7, Helge Skulstad8. 1. Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 2. Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 3. Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 4. Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 5. Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway. 6. Department of Cardiovascular Sciences, KU Leuven - University of Leuven, Leuven, Belgium; Department of Cardiovascular Diseases, University Hospitals Leuven, Leuven, Belgium. 7. Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. 8. Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Center for Cardiological Innovation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. Electronic address: helsku@ous-hf.no.
Abstract
OBJECTIVES: The purpose of this study was to investigate how LBBB and CRT modify RV free wall function by direct ventricular interaction. BACKGROUND: Right ventricular (RV) function influences prognosis in patients with left bundle branch block (LBBB) and cardiac resynchronization therapy (CRT). There is, however, limited insight into how LBBB and CRT affect RV function. METHODS: In 24 patients with LBBB with nonischemic cardiomyopathy, RV and left ventricular (LV) strain by speckle-tracking echocardiography was measured before and after CRT. Underlying mechanisms were studied in 16 anesthetized dogs with ultrasonic dimension crystals and micromanometers. RESULTS: Patients with LBBB demonstrated distinct early systolic shortening in the RV free wall, which coincided with the typical abnormal early systolic septal shortening. In animals, this RV free wall contraction pattern resulted in reduced myocardial work as a large portion of the shortening occurred against low pressure during early systole, coinciding with abnormal leftward septal motion. RV systolic function was maintained by vigorous contraction in the late-activated LV lateral wall, which pushed the septum toward the RV. CRT reduced abnormal septal motion and increased RV free wall work because there was less inefficient shortening against low pressure. CONCLUSIONS: LBBB reduces workload on the RV free wall because of abnormal septal motion and delayed activation of the LV lateral wall. Restoring septal and LV function by CRT increases workload in RV free wall and may explain why patients with RV failure respond poorly to CRT. (Contractile Reserve in Dyssynchrony: A Novel Principle to Identify Candidates for Cardiac Resynchronization Therapy [CRID-CRT]; NCT02525185).
OBJECTIVES: The purpose of this study was to investigate how LBBB and CRT modify RV free wall function by direct ventricular interaction. BACKGROUND: Right ventricular (RV) function influences prognosis in patients with left bundle branch block (LBBB) and cardiac resynchronization therapy (CRT). There is, however, limited insight into how LBBB and CRT affect RV function. METHODS: In 24 patients with LBBB with nonischemic cardiomyopathy, RV and left ventricular (LV) strain by speckle-tracking echocardiography was measured before and after CRT. Underlying mechanisms were studied in 16 anesthetized dogs with ultrasonic dimension crystals and micromanometers. RESULTS:Patients with LBBB demonstrated distinct early systolic shortening in the RV free wall, which coincided with the typical abnormal early systolic septal shortening. In animals, this RV free wall contraction pattern resulted in reduced myocardial work as a large portion of the shortening occurred against low pressure during early systole, coinciding with abnormal leftward septal motion. RV systolic function was maintained by vigorous contraction in the late-activated LV lateral wall, which pushed the septum toward the RV. CRT reduced abnormal septal motion and increased RV free wall work because there was less inefficient shortening against low pressure. CONCLUSIONS:LBBB reduces workload on the RV free wall because of abnormal septal motion and delayed activation of the LV lateral wall. Restoring septal and LV function by CRT increases workload in RV free wall and may explain why patients with RV failure respond poorly to CRT. (Contractile Reserve in Dyssynchrony: A Novel Principle to Identify Candidates for Cardiac Resynchronization Therapy [CRID-CRT]; NCT02525185).
Authors: Silvia Deaconu; Alexandru Deaconu; Alina Scarlatescu; Ioana Petre; Sebastian Onciul; Aura Vijiiac; Diana Zamfir; Gabriela Marascu; Corneliu Iorgulescu; Andrei Dan Radu; Stefan Bogdan; Radu Vatasescu Journal: J Clin Med Date: 2021-05-31 Impact factor: 4.241