Heterogeneity of left ventricular wall thickening mechanisms.
Heterogeneity of left ventricular wall thickening mechanisms.
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DOI：
10.1161/circulationaha.107.744623
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发表时间：
2008-08-12
期刊：
影响因子：
37.8
通讯作者：
Ingels NB Jr
中科院分区：
文献类型：
--
作者：
Cheng A;Nguyen TC;Malinowski M;Daughters GT;Miller DC;Ingels NB Jr
心肌纤维分为3-4个细胞厚的层（或片）。纤维缩短主要通过层流伸展、增厚和剪切产生收缩期左室壁增厚，但这三种机制的区域变异性和透壁分布尚不完全清楚。9只绵羊的前基底和外侧赤道LV中插入了透壁不透射线标记。使用双平面视频荧光透视研究4D标记动力学，以测量心外膜、中壁和内膜的周向、纵向和径向收缩应变。定量组织学的纤维和片材角度允许将这些应变转化为片材延伸、增厚和剪切对收缩期壁增厚的透壁贡献。在所有深度，收缩期壁增厚的前基底区是1.6-1.9倍，在外侧赤道区。然而，有趣的是，收缩期纤维缩短在这些区域的每个透壁深度是相同的。心内膜前基底膜增厚大于外侧赤道区的2倍（心外膜：0.16±0.15 vs. 0.03±0.06;心内膜：0.45±0.40 vs. 0.17±0.09）。中壁片材延伸是侧壁片材延伸的2倍（0.22±0.12 vs. 0.09±0.06）。前壁中的心外膜和中壁片状剪比侧壁中的片状剪高102倍（心外膜：0.14±0.07 vs. 0.05±0.03;中壁：0.21±0.12 vs. 0.12±0.06）。这些数据表明，从根本上不同的区域贡献的层流机制放大纤维缩短收缩期壁增厚。左心室前部和外侧部位的每个透壁深度处的突触纤维缩短是相同的。然而，收缩期室壁增厚的前部网站远远大于外侧网站。纤维缩短驱动收缩期壁增厚，但片层动力学和取向对收缩期壁增厚非常重要。左室壁增厚及其临床意义取决于不同左室区域的不同壁增厚机制。将健康的收缩细胞植入病变心脏或手术操纵LV几何形状的尝试不仅需要考虑心肌细胞收缩，还需要考虑透壁LV细胞间的结构和几何形状。
Myocardial fibers are grouped into lamina (or sheets) 3-4 cells thick. Fiber shortening produces systolic LV wall thickening primarily by laminar extension, thickening and shear, but the regional variability and transmural distribution of these three mechanisms are incompletely understood. Nine sheep had transmural radiopaque markers inserted into the anterior basal and lateral equatorial LV. 4D 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 1.6-1.9 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 were >2x greater than in the lateral equatorial region (epicardium: 0.16±0.15 vs. 0.03±0.06; endocardium: 0.45±0.40 vs. 0.17±0.09). Midwall sheet extension was >2x that in the lateral wall (0.22±0.12 vs. 0.09±0.06). Epicardial and midwall sheet shears in the anterior wall were ∼2x higher than in the lateral wall (epicardium: 0.14±0.07 vs. 0.05±0.03; midwall: 0.21±0.12 vs. 0.12±0.06). 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 surgically manipulate LV geometry will need to take into account not only cardiomyocyte contraction, but also transmural LV intercellular architecture and geometry.