期刊
CIRCULATION
卷 118, 期 7, 页码 713-721出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCULATIONAHA.107.744623
关键词
myocardial contraction; fibers and sheets; strain; wall thickening; ventricles; systole; mechanics
资金
- NHLBI NIH HHS [R01 HL067025-05, R01 HL029589, HL-29589, R01 HL029589-25, HL-67025, R01 HL067025] Funding Source: Medline
Background-Myocardial fibers are grouped into lamina (or sheets) 3 to 4 cells thick. Fiber shortening produces systolic left ventricular (LV) wall thickening primarily by laminar extension, thickening, and shear, but the regional variability and transmural distribution of these 3 mechanisms are incompletely understood. Methods and Results-Nine sheep had transmural radiopaque markers inserted into the anterior basal and lateral equatorial LV. Four-dimensional marker dynamics were studied with biplane videofluoroscopy to measure circumferential, longitudinal, and radial systolic strains in the epicardium, midwall, and endocardium. Fiber and sheet angles from quantitative histology allowed transformation of these strains into transmural contributions of sheet extension, thickening, and shear to systolic wall thickening. At all depths, systolic wall thickening in the anterior basal region was 1.6 to 1.9 times that in the lateral equatorial region. Interestingly, however, systolic fiber shortening was identical at each transmural depth in these regions. Endocardial anterior basal sheet thickening was >2 times greater than in the lateral equatorial region (epicardium, 0.16 +/- 0.15 versus 0.03 +/- 0.06; endocardium, 0.45 +/- 0.40 versus 0.17 +/- 0.09). Midwall sheet extension was >2 times that in the lateral wall (0.22 +/- 0.12 versus 0.09 +/- 0.06). Epicardial and midwall sheet shears in the anterior wall were approximate to 2 times higher than in the lateral wall (epicardium, 0.14 +/- 0.07 versus 0.05 +/- 0.03; midwall, 0.21 +/- 0.12 versus 0.12 +/- 0.06). Conclusions-These data demonstrate fundamentally different regional contributions of laminar mechanisms for amplifying fiber shortening to systolic wall thickening. Systolic fiber shortening was identical at each transmural depth in both the anterior and lateral LV sites. However, systolic wall thickening of the anterior site was much greater than that of the lateral site. Fiber shortening drives systolic wall thickening, but sheet dynamics and orientations are of great importance to systolic wall thickening. LV wall thickening and its clinical implications pivot on different wall thickening mechanisms in various LV regions. Attempts to implant healthy contractile cells into diseased hearts or to surgically manipulate LV geometry need to take into account not only cardiomyocyte contraction but also transmural LV intercellular architecture and geometry.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据