Left ventricle, LV wringing wall motion relies on physiological muscle fiber orientation, fibrotic status, and electromechanics (EM). The loss of proper EM activation can lead to rigid-body-type (RBT) LV rotation, which is associated with advanced heart failure (HF) and challenges in resynchronization. To describe the EM coupling and scar tissue burden with respect to rotational patterns observed on the LV in patients with ischemic heart failure with reduced ejection fraction (HFrEF) left bundle branch block (LBBB). Thirty patients with HFrEF/LBBB underwent EM analysis of the left ventricle using an invasive electro-mechanical catheter mapping system (NOGA XP, Biosense Webster). The following parameters were evaluated: rotation angle; rotation velocity; unipolar/bipolar voltage; local activation time, LAT; local electro-mechanical delay, LEMD; total electro-mechanical delay, TEMD. Patients underwent late-gadolinium enhancement cMRI when possible. The different LV rotation pattern served as sole parameter for patients' grouping into two categories: wringing rotation (Group A, n = 6) and RBT rotation (Group B, n = 24). All parameters were aggregated into a nine segment, three sector and whole LV models, and compared at multiple scales. Segmental statistical analysis in Group B revealed significant inhomogeneities, across the LV, regarding voltage level, scar burdening, and LEMD changes: correlation analysis showed correspondently a loss of synchronization between electrical (LAT) and mechanical activation (TEMD). On contrary, Group A (relatively low number of patients) did not present significant differences in LEMD across LV segments, therefore electrical (LAT) and mechanical (TEMD) activation were well synchronized. Fibrosis burden was in general associated with areas of low voltage. The rotational behavior of LV in HF/LBBB patients is determined by the local alteration of EM coupling. These findings serve as a strong basic groundwork for a hypothesis that EM analysis may predict CRT response.Clinical trial registration: SUM No. KNW/0022/KB1/17/15.
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http://dx.doi.org/10.1038/s41598-021-82793-1 | DOI Listing |
Brain Res Bull
January 2025
School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, China; Department of Rehabilitation Medicine, Huashan Hospital, Fudan University, Shanghai, China; National Center for Neurological Disorders, Huashan Hospital, Fudan University, Shanghai, China; National Clinical Research Center for Geriatric Diseases, Huashan Hospital, Fudan University, Shanghai, China. Electronic address:
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Prog Cardiovasc Dis
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Department of Internal Medicine, Section on Internal Medicine C, University of Verona, Italy. Electronic address:
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January 2025
Department of Child Psychology, The Children's Hospital, National Clinical Research Center for Child Health, Zhejiang University School of Medicine, National Children's Regional Medical Center, Hangzhou, Zhejiang, China. Electronic address:
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Cardiology A Department, Ibn Sina Hospital, Mohammed V University, Faculty of Medicine and Pharmacy, Rabat, Morocco.
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Anzhen Hospital, Capital Medical University, Beijing 100029, China; Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing 100029, China. Electronic address:
Pyruvate Dehydrogenase Kinase1 (PDK1) belongs to the family of kinases, regulates diverse metabolic processes. PDK1 is a susceptibility locus for heart failure via thinning of ventricle walls, and enlarged atria and ventricles. We successfully developed a PDK1 knockout (PDK1/) human embryonic stem cell (hESC) line using an episomal vector-based CRISPR/Cas9 system explore the role of PDK in human heart development.
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