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Articles in PresS, published online ahead of print June 20, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00239.2002
Submitted on March 20, 2002
Accepted on June 12, 2002
1 Biophysics, Maastricht University, Maastricht, The Netherlands
2 Cardio Thoracic Surgery, Academic Hospital Maastricht, Maastricht, The Netherlands
3 Radiology, Academic Hospital Maastricht, Maastricht, The Netherlands
4 Physiology, Maastricht University, Maastricht, The Netherlands
* To whom correspondence should be addressed. E-mail: t.arts{at}bf.unimaas.nl.
Aortic valve stenosis impairs subendocardial perfusion with a risk of irreversible subendocardial tissue damage. A likely precursor of damage is subendocardial contractile dysfunction, expressed by parameter TransDif that is defined as epicardial minus endocardial myofiber shortening, normalized to the mean value. Using Magnetic Resonance tagging in two short axis slices of the left ventricle (LV), TransDif was derived from LV torsion and contraction during ejection. TransDif was determined in healthy volunteers (Control, n=9) and in patients with aortic valve stenosis before (AVSten, n=9) and three months after valve replacement (AVRepl, n=7). In Control TransDif was 0.00±0.14 (mean ± sd). In AVSten TransDif increased to 0.96±0.62, suggesting impairment of subendocardial myofiber shortening. In AVRepl TransDif decreased to 0.37±0.20, but was still elevated. In 8 out of 9 AVSten patients the TransDif value was elevated individually (p<0.001), suggesting that the non-invasively determined parameter TransDif may provide important information in planning of treatment of aortic valve stenosis.
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