Transmural cardiac strains in the lateral wall of the ovine left ventricle.
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.
Cheng
Allen
A
Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford, CA, USA.
Langer
Frank
F
Rodriguez
Filiberto
F
Criscione
John C
JC
Daughters
George T
GT
Miller
D Craig
DC
Ingels
Neil B
NB
D000818:Animals; D004452:Echocardiography; D016014:Linear Models; D008955:Models, Cardiovascular; D009206:Myocardium / Q000473:pathology; D012756:Sheep; D013599:Systole / Q000502:physiology*; D018487:Ventricular Dysfunction, Left / Q000473:pathology / Q000503:physiopathology*; D017725:Ventricular Pressure / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology