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Left Ventricular Twists Mechanics in Patients with Apical Hypertrophic Cardiomyopathy
  1. Sung-A Chang1,
  2. Hyung-Kwan Kim2,*,
  3. Dae-Hee Kim2,
  4. Yong-Jin Kim2,
  5. Dae-Won Sohn2,
  6. Byung-Hee Oh2,
  7. Young-Bae Park2
  1. 1 Department of Cardiology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea, Republic of;
  2. 2 Department of Internal Medicine, Cardiovascular Center, Seoul National University Hospital, Seoul, Korea, Republic of
  1. Correspondence to: Hyung-Kwan Kim, Internal Medicine, Seoul National University Hospital, Department of Internal Medicine, Seoul National University College of Medicine,28 Yongon-dong, Chongno-gu, Seoul, 110-744 Korea, Seoul, 110-744, Korea, Republic of; cardiman{at}


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

Methods: Twenty-one patients diagnosed with ApHCM were consecutively enrolled and was 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 speckle tracking technique. For better understanding of LV twist mechanics in ApHCM, LV radial and bi-planar strains, and LV twist-volume curve was also evaluated.

Results: Compared with the normal controls, apical rotation was markedly decreased in ApHCM patients(p<0.001), but 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 bi-planar(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 slope of linear systolic phase and a loss of inflection point separating 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.

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