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Heart doi:10.1136/heartjnl-2012-302489
  • Heart failure
  • Original Article

Exercise-induced torsional dyssynchrony relates to impaired functional capacity in patients with heart failure and normal ejection fraction

  1. Francisco Leyva1
  1. 1Department of Cardiovascular Medicine, University of Birmingham, Birmingham, UK
  2. 2University Hospital of North Staffordshire and Institute for Science and Technology in Medicine, Keele University, Stoke-on-Trent, UK
  3. 3Department of Medicine & Therapeutics, The Chinese University of Hong Kong, Shatin, China
  1. Correspondence to Dr Yu Ting Tan, Department of Cardiovascular Medicine, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK; ytingtan99{at}googlemail.com
  • Received 30 May 2012
  • Revised 6 October 2012
  • Accepted 9 October 2012
  • Published Online First 6 December 2012

Abstract

Background Left ventricular (LV) systole and diastole are intimately dependent on myocardial torsion, which involves coupling between myocardial rotation (twisting in systole and untwisting in diastole) and longitudinal motion. Heart failure with normal ejection fraction (HFNEF) is known to involve exercise-induced wall motion abnormalities, but torsion on exercise has not been explored. We hypothesised that torsional dyssynchrony may also be involved and be exaggerated by exercise.

Methods and Results 67 patients (age 73±7 years, 45 female) with HFNEF and 38 controls underwent cardiopulmonary exercise testing and echocardiography at rest and on supine exercise. Analysis of three plane motions was performed using speckle tracking and tissue Doppler imaging. Torsional dyssynchrony was quantified as the SD of the time to peak systolic motion (SDSM) (basal and apical rotation, longitudinal and radial displacement); the time difference between peak twist and peak longitudinal displacement (twist-longitudinal motion delay, TLMD) and the ratio of untwist to longitudinal extension (UT:LE). At rest, HFNEF patients had similar SDSM, TLMD and UT:LE compared with controls. Exercise was associated with significantly more dyssynchrony in the HFNEF patients (SDSM 38.8±27.6 ms vs 25.9±15.5 ms, p=0.02; TLMD 28.4±46.2 ms vs 2.9±31.2 ms, p=0.005 and UT:LE 10.4±15.3 vs 3.3±3.8, p=0.022). The SDSM correlated positively with LV wall thickness (r=0.31, p=0.015) and negatively with peak oxygen consumption (r=−0.299, p=0.01) and changes in stroke volume on exercise (r=−0.371, p=0.001).

Conclusions HFNEF involves exercise-induced torsional dyssynchrony in systole and diastole, which relates to LV hypertrophy as well as exercise capacity.

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