Dyssynchronous Left Ventricular Activation is Insufficient for the Breakdown of Wringing Rotation
Status PubMed-not-MEDLINE Language English Country Switzerland Media electronic-ecollection
Document type Journal Article
PubMed
35615669
PubMed Central
PMC9124904
DOI
10.3389/fphys.2022.838038
PII: 838038
Knihovny.cz E-resources
- Keywords
- Lagrangian particle tracking, NOGA XP, cardiac mechanics, electromechanical mapping, finite element simulation, torsion, wringing,
- Publication type
- Journal Article MeSH
Cardiac resynchronization therapy is a valuable tool to restore left ventricular function in patients experiencing dyssynchronous ventricular activation. However, the non-responder rate is still as high as 40%. Recent studies suggest that left ventricular torsion or specifically the lack thereof might be a good predictor for the response of cardiac resynchronization therapy. Since left ventricular torsion is governed by the muscle fiber orientation and the heterogeneous electromechanical activation of the myocardium, understanding the relation between these components and the ability to measure them is vital. To analyze if locally altered electromechanical activation in heart failure patients affects left ventricular torsion, we conducted a simulation study on 27 personalized left ventricular models. Electroanatomical maps and late gadolinium enhanced magnetic resonance imaging data informed our in-silico model cohort. The angle of rotation was evaluated in every material point of the model and averaged values were used to classify the rotation as clockwise or counterclockwise in each segment and sector of the left ventricle. 88% of the patient models (n = 24) were classified as a wringing rotation and 12% (n = 3) as a rigid-body-type rotation. Comparison to classification based on in vivo rotational NOGA XP maps showed no correlation. Thus, isolated changes of the electromechanical activation sequence in the left ventricle are not sufficient to reproduce the rotation pattern changes observed in vivo and suggest that further patho-mechanisms are involved.
Department of Electrocardiology and Heart Failure Medical University of Silesia Katowice Poland
Department of Electrocardiology Upper Silesian Heart Center Katowice Poland
Division of Cardiology and Structural Heart Diseases Medical University of Silesia Katowice Poland
Institute of Biomedical Engineering Karlsruhe Institute of Technology Karlsruhe Germany
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