Volume 11 Supplement 1

Abstracts of the 12th Annual SCMR Scientific Sessions – 2009

Open Access

Increased left ventricular torsion in hypertrophic cardiomyopathy mutation carriers with normal wall thickness

  • Iris Rüssel1,
  • Wessel P Brouwer1,
  • Tjeerd Germans1,
  • Tim Marcus1,
  • Marco Götte1 and
  • Albert van Rossum1
Journal of Cardiovascular Magnetic Resonance200911(Suppl 1):P201

DOI: 10.1186/1532-429X-11-S1-P201

Published: 28 January 2009

Objective

To determine the amount of left ventricular (LV) torsion in hypertrophic cardiomyopathy (HCM) mutation carriers (carriers) with normal wall thickness.

Background

Increased LV torsion has been observed in HCM and is thought to be caused by wall thickening [1]. However, structural abnormalities that precede the development of hypertrophy in HCM may also cause alterations in LV torsion in carriers with normal wall thickness [2].

Methods

Ten carriers with an LV wall thickness <10 mm, and ten age and gender matched controls underwent CMR cine imaging and tissue tagging. LV volumes were calculated from the cine images. Basal and apical rotations and LV torsion, defined as the circumferential-longitudinal shear angle [3], were determined from tissue tagging. Counterclockwise rotation as seen from the apex was considered positive. LV volumes, peak rotation and torsion were compared between both groups using Student's T-test. A p-value < 0.05 was considered significant.

Results

LV end-diastolic and end-systolic volumes were not significantly different between both groups (p = 0.79 and p = 0.36, resp.), whereas EF was significantly larger in the carriers (63.2 ± 3.2% vs. 59.7 ± 2.8%, p = 0.02). Peak apical rotation and peak torsion were significantly larger in the carriers (14.6 ± 3.2° vs. 10.3 ± 3.3°, p = 0.01, and 10.2 ± 2.3° vs. 7.1 ± 1.0°, p = 0.001, resp.), while peak basal rotation was significantly smaller (-2.5 ± 2.2° vs. -4.6 ± 1.7°, p = 0.03).

Conclusion

HCM mutation carriers with normal wall thickness demonstrate increased LV torsion. Underlying altered myocardial architecture might be responsible for this finding.

Authors’ Affiliations

(1)
VU Medical Center

References

  1. Circ. 1994, 90: 854-867.
  2. Circ. 2007, 115: e610-1. 10.1161/CIRCULATIONAHA.106.685180.
  3. J Cardiovasc Magn Reson. 2008, 10: 26-10.1186/1532-429X-10-26.

Copyright

© Rüssel et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.

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