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Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice
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Opposite effects of coronary artery disease and hypertrophic cardiomyopathy on left ventricular long axis function

Waleed Arshad1, Alison M Duncan, Darrel P Francis

  • 1Department of Cardiology, Royal Brompton Hospital, Sydney Street, London SW3 6NP, United Kingdom. waleedarshad@aol.com

International Journal of Cardiology
|April 30, 2005
PubMed

Insights

Reduced early diastolic lengthening velocity is seen in hypertrophic cardiomyopathy (HCM) and coronary artery disease (CAD). However, HCM shows increased velocity with stress, unlike CAD, suggesting HCM’s issue is muscle stiffness, not ischemia.

Area of Science:

  • Cardiology
  • Cardiac Physiology
  • Echocardiography

Background:

  • The underlying mechanism for diminished early diastolic long axis lengthening velocity in hypertrophic cardiomyopathy (HCM) remains unclear.
  • This study investigates the mechanisms behind reduced diastolic function in HCM.

Purpose of the Study:

  • To differentiate the causes of reduced early diastolic long axis lengthening velocity in hypertrophic cardiomyopathy (HCM).
  • To compare HCM with coronary artery disease (CAD) and normal subjects.

Main Methods:

  • Simultaneous measurement of septal long axis amplitude and early lengthening velocity.
  • Utilized dobutamine stress echocardiography.
  • Compared 23 HCM patients, 23 normal subjects, and 22 CAD patients.

Main Results:

  • Resting lengthening velocity was reduced in both HCM and CAD compared to normals.
  • Dobutamine stress increased lengthening velocity in HCM and normals, but not in CAD.
  • HCM showed increased recoil velocity per unit deformation with stress, unlike CAD, and no worsening of post-ejection shortening.

Conclusions:

  • Reduced peak early lengthening velocity is not exclusive to HCM, also appearing in CAD.
  • Increased lengthening velocity with stress in HCM, without worsening post-ejection shortening, suggests abnormal relaxation is not due to subendocardial ischemia.
  • The data indicate an elastic mechanism with increased passive muscle stiffness, potentially due to fibrosis or fiber disarray, in HCM.
Abstract

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