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Heart 2010;96:49-55 doi:10.1136/hrt.2009.166629
  • Original article
  • Heart failure and cardiomyopathy

Left ventricular twist mechanics in patients with apical hypertrophic cardiomyopathy: assessment with 2D speckle tracking echocardiography

  1. S-A Chang1,
  2. H-K Kim2,
  3. D-H Kim2,
  4. J-C Kim3,
  5. Y-J Kim2,
  6. H-C Kim3,
  7. D-W Sohn2,
  8. B-H Oh2,
  9. Y-B Park2
  1. 1
    Department of Cardiology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Korea
  2. 2
    Department of Internal Medicine, Cardiovascular Center, Seoul National University Hospital, Korea
  3. 3
    Department of Bioengineering, Seoul National University Hospital, Seoul, Korea
  1. Correspondence to Dr Hyung-Kwan Kim, Division of Cardiology, Department of Internal Medicine, Cardiovascular Center, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul, 110-744, Korea; hkkim73{at}snu.ac.kr
  • Accepted 5 October 2009
  • Published Online First 26 October 2009

Abstract

Objective: Left ventricular (LV) apical rotation significantly contributes to LV twist, which has been reported to have a vital role in maintaining LV systolic and diastolic function. Apical hypertrophic cardiomyopathy (ApHCM) is a unique disease with pathological LV hypertrophy at the apex. We aimed (1) to evaluate LV twist mechanics in ApHCM and (2) to demonstrate the influence of predominantly local, pathological involvement of the apical myocardium on LV twist mechanics.

Methods: 21 patients diagnosed with ApHCM were consecutively enrolled and compared with normal controls. After a standard echocardiographic examination, we scanned parasternal basal and apical short-axis planes to quantify LV rotations and LV twist using the speckle tracking technique. For better understanding of LV twist mechanics in ApHCM, LV radial and biplanar strains and LV twist-volume curve were also evaluated.

Results: Compared with the normal controls, apical rotation was markedly decreased in ApHCM patients (p<0.001), but the decreases in basal rotation were not significant. As a consequence, LV twist was significantly lower in ApHCM patients (p = 0.007). Apical radial (p = 0.01) and biplanar (p<0.001) strains in ApHCM were also significantly decreased. Compared to normal controls, LV twist-volume and twist-radial displacement curves clearly showed a decrement in the slope of the linear systolic phase and a loss of an inflection point separating the early from late untwisting phase in ApHCM patients.

Conclusion: LV twist in ApHCM was significantly decreased due to a reduction in apical rotation, suggesting that regional myocardial changes in ApHCM can modify the global LV twist mechanics. Given the close interconnection between LV systolic and diastolic function, impairment of LV twist may lead to the loss of early diastolic suction and finally generate diastolic dysfunction in ApHCM.

Footnotes

  • Competing interests None.

  • Provenance and Peer review Not commissioned; externally peer reviewed.

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