Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017 Dec 14;19(1):101.
doi: 10.1186/s12968-017-0414-y.

Left ventricular synchrony, torsion, and recoil mechanics in Ebstein's anomaly: insights from cardiovascular magnetic resonance

Michael Steinmetz  1   2 , Simon Usenbenz  3   4 , Johannes Tammo Kowallick  5   4 , Olga Hösch  3 , Wieland Staab  5   4 , Torben Lange  6   4 , Shelby Kutty  7 , Joachim Lotz  5   4 , Gerd Hasenfuß  6   4 , Thomas Paul  3   4 , Andreas Schuster  8   9   10
Affiliations

Left ventricular synchrony, torsion, and recoil mechanics in Ebstein's anomaly: insights from cardiovascular magnetic resonance

Michael Steinmetz et al. J Cardiovasc Magn Reson. .

Abstract

Background: Disease progression and heart failure development in Ebstein's Anomaly (EA) of the tricuspid valve is characterized by both right and left ventricular (LV) deterioration. The mechanisms underlying LV dysfunction and their role in heart failure development are incompletely understood. We hypothesized that LV dyssynchrony and impaired torsion and recoil mechanics induced by paradoxical movement of the basal septum may play a role in heart failure development.

Methods: 31 EA patients and 31 matched controls underwent prospective cardiovascular magnetic resonance (CMR). CMR feature tracking (CMR-FT) was performed on apical, midventricular and basal short-axis and 4D-volume analysis was performed using three long-axis views and a short axis cine stack employing dedicated software. Circumferential uniformity ratio estimates (CURE) time-to-peak-based circumferential systolic dyssynchrony index (C-SDI), 4D volume analysis derived SDI (4D-SDI), torsion (Tor) and systolic (sysTR) and diastolic torsion rate (diasTR) were calculated for the LV. QRS duration, brain natriuretic peptide, NYHA and Total R/L-Volume Index (R/L Index) were obtained.

Results: EA patients (31.5 years; controls 31.4 years) had significantly longer QRS duration (123.35 ms ± 26.36 vs. 97.33 ms ± 11.89 p < 0.01) and showed more LV dyssynchrony (4D-SDI 7.60% ± 4.58 vs. 2.54% ± 0.62, p < 0.001; CURE 0.77 ± 0.05 vs. 0.86 ± 0.03, p < 0.001; C-SDI 7.70 ± 3.38 vs. 3.80 ± 0.91, p = 0.001). There were significant associations of LV dyssynchrony with heart failure parameters and QRS duration. Although torsion and recoil mechanics did not differ significantly (p > 0.05) there was an association of torsion and recoil mechanics with dyssynchrony parameters CURE (sysTR r = -0.426; p = 0.017, diasTR r = 0.419; p = 0.019), 4D-SDI (sysTR r = 0.383; p = 0.044) and C-SDI (diasTR r = -0.364; p = 0.044).

Conclusions: EA is characterized by LV intra-ventricular dyssynchrony, which is associated with heart failure and disease severity parameters. Markers of dyssynchrony can easily be quantified from CMR-FT, and may have a role in the assessment of altered cardiac function, carrying potential management implications for EA patients.

Keywords: CMR feature tracking; Congenital heart disease; Dyssynchrony; Ebstein anomaly; Heart failure; Left ventricle; Torsion and recoil.

PubMed Disclaimer

Conflict of interest statement

Ethics approval and consent to participate

The study was approved by the Ethics Committee of the University Medical Center, Georg-August-University Göttingen, Germany and complies with the declaration of Helsinki and its amendments. Written informed consent was obtained from all participants.

Consent for publication

All authors have read and approved the final version of the manuscript and have consented to submission in its present form

Competing interests

None of the authors has competing interests to report.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Comparison of TPK-values from basal segments showing almost equal TPK values in the control (top) and varying TPK measures in an EA patient (bottom)
Fig. 2
Fig. 2
Comparison of different strains (at a given time point) with spatial position. The 48 hypothetical points show: 1. Complete dyssynchrony (blue dots) where opposite segments exhibit different strain 2. Perfect synchrony (green points) all segments have identical Strain. Modified from Taylor et al. [4]. SSSFP short axis slices with corresponding feature tracking segmentation in an EA patient, from top to bottom: apical, midventricular and basal slice
Fig. 3
Fig. 3
Left: 3D–model of the LV of a patient with EA with segmental subdivision in a three chamber view; Right: Map of myocardial activation representing a delay of the septal segments (blue = activated; red = not yet actived)
See this image and copyright information in PMC

References

    1. Attenhofer Jost CH, Connolly HM, Dearani JA, Edwards WD, Danielson GK. Ebstein’s anomaly. Circulation. 2007;115:277–285. doi: 10.1161/CIRCULATIONAHA.106.619338. - DOI - PubMed
    1. Hosch O, Ngyuen TT, Lauerer P, Schuster A, Kutty S, Staab W, Unterberg-Buchwald C, Sohns JM, Paul T, Lotz J, Steinmetz M. BNP and haematological parameters are markers of severity of Ebstein’s anomaly: correlation with CMR and cardiopulmonary exercise testing. European heart journal cardiovascular Imaging. 2015;16:670–675. - PubMed
    1. Goleski PJ, Sheehan FH, Chen SS, Kilner PJ, Gatzoulis MA. The shape and function of the left ventricle in Ebstein’s anomaly. Int J Cardiol. 2014;171:404–412. doi: 10.1016/j.ijcard.2013.12.037. - DOI - PubMed
    1. Taylor RJ, Umar F, Moody WE, Meyyappan C, Stegemann B, Townend JN, Hor KN, Miszalski-Jamka T, Mazur W, Steeds RP, Leyva F. Feature-tracking cardiovascular magnetic resonance as a novel technique for the assessment of mechanical dyssynchrony. Int J Cardiol. 2014;175:120–125. doi: 10.1016/j.ijcard.2014.04.268. - DOI - PubMed
    1. Deng X, Pan H, Wang J, Wang B, Cheng Z, Cheng L, Zhao L, Li H, Ma X. Functional analysis of two novel mutations in TWIST1 protein motifs found in ventricular Septal defect patients. Pediatr Cardiol. 2015;36:1602–1609. doi: 10.1007/s00246-015-1202-9. - DOI - PubMed

MeSH terms