Cardiovascular Research Center, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
J Appl Physiol (1985). 2012 Oct 15;113(8):1267-84. doi: 10.1152/japplphysiol.00785.2012. Epub 2012 Aug 23.
Load-adjusted measures of left ventricle (LV) systolic performance are limited by dependence on LV stiffness and afterload. To our knowledge, no stiffness-adjusted and afterload-adjusted indicator was tested in models of pressure (POH) and volume overload hypertrophy (VOH). We hypothesized that wall stress reflects changes in loading, incorporating chamber stiffness and afterload; therefore, stroke volume-to-wall stress ratio more accurately reflects systolic performance. We used rat models of POH (ascending aortic banding) and VOH (aorto-cava shunt). Animals underwent echocardiography and pressure-volume analysis at baseline and dobutamine challenge. We achieved extreme bidirectional alterations in LV systolic performance, end-systolic elastance (Ees), passive stiffness, and arterial elastance (Ea). In POH with LV dilatation and failure, some load-independent indicators of systolic performance remained elevated compared with controls, while some others failed to decrease with wide variability. In VOH, most, but not all indicators, including LV ejection fraction, were significantly reduced compared with controls, despite hyperdynamic circulation, lack of heart failure, and preserved contractile reserve. We related systolic performance to Ees adjusted for Ea and LV passive stiffness in multivariate models. Calculated residual Ees was not reduced in POH with heart failure and was reduced in VOH, while it positively correlated to dobutamine dose. Conversely, stroke volume-to-wall stress ratio was normal in compensated POH, markedly decreased in POH with heart failure, and, in contrast with LV ejection fraction, normal in VOH. Our results support stroke volume-to-wall stress ratio as a load-adjusted and stiffness-adjusted indicator of systolic function in models of POH and VOH.
左心室(LV)收缩功能的负荷调整指标受到 LV 僵硬度和后负荷的影响。据我们所知,在压力(POH)和容量超负荷肥厚(VOH)模型中,尚未测试过任何僵硬度和后负荷调整的指标。我们假设壁应力反映了负荷的变化,包含了心室僵硬度和后负荷;因此,每搏量与壁应力比更能准确反映收缩功能。我们使用 POH(升主动脉缩窄)和 VOH(腔静脉分流)的大鼠模型。动物在基线和多巴酚丁胺挑战时接受超声心动图和压力-容积分析。我们实现了 LV 收缩性能、收缩末期弹性(Ees)、被动僵硬度和动脉弹性(Ea)的双向极端变化。在 LV 扩张和衰竭的 POH 中,与对照组相比,一些收缩性能的独立于负荷的指标仍然升高,而其他一些指标则因变异性较大而未能降低。在 VOH 中,尽管存在高动力循环、无心力衰竭和保留收缩储备,与对照组相比,大多数但不是所有指标,包括 LV 射血分数,均显著降低。我们在多变量模型中将收缩性能与 Ea 和 LV 被动僵硬度调整后的 Ees 相关联。在心力衰竭的 POH 中,计算出的残余 Ees 没有降低,而在 VOH 中则降低,而与多巴酚丁胺剂量呈正相关。相反,在代偿性 POH 中,每搏量与壁应力比正常,在心力衰竭的 POH 中明显降低,并且与 LV 射血分数相反,在 VOH 中正常。我们的结果支持每搏量与壁应力比作为 POH 和 VOH 模型中收缩功能的负荷调整和僵硬度调整指标。