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  • Poster presentation
  • Open Access

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

  • 1,
  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Journal of Cardiovascular Magnetic Resonance200911 (Suppl 1) :P201

https://doi.org/10.1186/1532-429X-11-S1-P201

  • Published:

Keywords

  • Mutation Carrier
  • Hypertrophic Cardiomyopathy
  • Left Ventricular Volume
  • Left Ventricular Wall Thickness
  • Apical Rotation

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, Amsterdam, Netherlands

References

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

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