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This Article Full Text Full Text (PDF) All Versions of this Article: 288/4/H1546    most recent 00716.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (16) Citing Articles via Google Scholar Google Scholar Articles by Cheng, A. Articles by Ingels, N. B. Search for Related Content PubMed PubMed Citation Articles by Cheng, A. Articles by Ingels, N. B., Jr.

Transmural cardiac strains in the lateral wall of the ovine left ventricle

¹Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford; ³Laboratory of Cardiovascular Physiology and Biophysics, Research Institute of the Palo Alto Medical Foundation, Palo Alto, California; and ²Department of Biomedical Engineering, Texas A&M University, College Station, Texas

Submitted 19 July 2004 ; accepted in final form 2 December 2004

The constant-volume property of contracting cardiac muscle has been invoked in models of heart wall mechanics that predict that systolic subendocardial left ventricular (LV) wall thickening must significantly exceed subepicardial thickening. To examine this prediction, we implanted arrays of radiopaque markers to measure lateral equatorial wall transmural strains and global and regional LV geometry in seven sheep and studied the four-dimensional dynamics of these arrays using biplane videofluoroscopy (60 Hz) in anesthetized intact animals 1 and 8 wk after surgery. A transmural gradient of systolic lateral wall thickening was observed at 1 wk (P = 0.009; linear regression) but was no longer present at 8 wk (P = 0.243). Referenced to end diastole, group mean (±SD) end-systolic radial subepicardial, midwall, and subendocardial wall thickening strains were, respectively, 0.08 ± 0.08, 0.14 ± 0.08, and 0.22 ± 0.12 at 1 wk and 0.19 ± 0.07 (P = 0.02; 1 vs. 8 wk), 0.20 ± 0.04, and 0.23 ± 0.07 at 8 wk. With the exception of an 8-ml (7%) increase in end-diastolic volume (P = 0.04) from 1 to 8 wk, LV shape and hemodynamics were otherwise unchanged. We conclude that equivalent hemodynamics can be generated by the left ventricle with or without a transmural gradient of systolic wall thickening in this region; thus such a gradient is unlikely to be a fundamental property of the contracting LV myocardium. We discuss some implications of these findings regarding mechanisms involved in systolic wall thickening.

wall thickening; left ventricle myocardium; systolic function

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