Abstract
Aims
Postsystolic wall thickening (PSWT) occurs after aortic valve closure. We investigated the influence of ischemia location and wall interactions on PSWT in normal and stunned myocardium.
Methods and results
Twenty-two dogs were studied. Seven chronically instrumented dogs (sonomicrometry) underwent 10-min coronary artery occlusion (CAO) of left circumflex artery (“LCX stunning”) and seven other dogs underwent 10-min CAO of the anterior descending artery (“LAD stunning”) followed by reperfusion. At baseline, there was no PSWT in the anterior wall whereas posterior wall started and finished to thicken after the anterior wall, demonstrating PSWT. With LCX stunning, PSWT was observed in the posterior wall without affecting the remote anterior wall. With LAD stunning, PSWT in the anterior wall was transient and of lower magnitude Vs. posterior wall; in the remote posterior wall, PSWT previously observed at baseline, almost vanished. Postsystolic to systolic wall thickening ratio identified (ROC analysis) normal, ischemic and stunned myocardium with different amplitudes between walls. Tissue Doppler Imaging demonstrated similar pattern in basal, mid and apical segments (additional n = 4 for both LCX and LAD stunning).
Conclusion
The present study demonstrates that location of ischemia and wall interactions produce discrepancies in PSWT between anterior and posterior walls in stunned myocardium.
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Acknowledgments
Laurence Lucats was supported by a fellowship from INSERM (“poste d’accueil”) and a grant from the Académie Nationale de Médecine. The authors are greatly indebted to Dr. Guy Heyndrickx for fruitful discussion during the elaboration of this manuscript.
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Returned for 1. Revision: 23 October 2007 1. Revision received: 19 December 2007
Returned for 2. Revision: 7 January 2008 2. Revision received: 10 January 2007
Returned for 3. Revision: 14 January 2008 3. Revision received: 22 January 2008
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Lucats, L., Monnet, X., Bizé, A. et al. Regional and temporal heterogeneity of postsystolic wall thickening is associated with left ventricular asynchrony in normal and experimental stunned myocardium. Basic Res Cardiol 103, 385–396 (2008). https://doi.org/10.1007/s00395-008-0716-1
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DOI: https://doi.org/10.1007/s00395-008-0716-1