Load-sensitive measures may overestimate global systolic function in the presence of left ventricular hypertrophy: a comparison with load-insensitive measures

Load-sensitive measures may overestimate global systolic function in the presence of left ventricular hypertrophy: a comparison with load-insensitive measures
复制标题

DOI:
10.1152/ajpheart.00577.2005
复制
发表时间:
2006-04-01
影响因子:
4.8
通讯作者:
Gilbert, RE
Gilbert, RE
中科院分区:
医学2区
文献类型:
--
作者:
Connelly, KA;Prior, DL;Gilbert, RE

文献摘要

被引文献

相似文献

转基因动物模型为心血管疾病的发病机制提供了重要的见解,但功能性心脏评估往往受到高心率和小心脏尺寸的限制。我们假设,在存在同心左心室(LV)肥厚(LVH)的情况下,收缩力的负荷敏感测量可能会被误解为高估整体心脏功能,因为过量肌节的正常功能可能会在收缩期间排出更多的血液。与年龄匹配的 Sprague-Dawley (SD) 对照相比,使用电导导管技术来评估压力-容积 (P-V) 关系,作为评估 18 周龄杂合 (mRen-2)27 转基因大鼠(LVH 模型)体内心脏功能的负荷不敏感方法。对麻醉动物进行超声心动图检查,然后进行 P-V 环分析。 Ren-2 大鼠的血压、体重和心率较高(P < 0.05)。 Ren-2 的收缩功能负荷敏感指标,包括面积变化分数、缩短分数、射血分数和左心室压力发展的正峰值率,均高于对照动物(P < 0.05)。 Ren-2 和 SD 大鼠之间的收缩功能负荷不敏感测量值(包括预负荷可复张卒中做功关系和收缩末期 P-V 关系)没有差异。通过圆周缩短速度评估的区域壁运动表明 Ren-2 大鼠的圆周纤维收缩性增强(P = 0.02),但用于评估纵向功能的组织多普勒成像在组间没有差异。尽管常规测量表明 Ren-2 大鼠的收缩功能增强,但 Ren-2 和 SD 动物之间的负荷不敏感收缩力测量没有差异。这些发现表明,收缩力负荷敏感指数的正常值范围需要根据左心室肥厚程度进行改变。为了准确识别收缩功能的变化,我们建议常规使用超声心动图与负荷不敏感措施评估相结合。
Transgenic animal models have provided a vital insight into the pathogenesis of cardiovascular disease, but functional cardiac assessment is often limited by high heart rates and small heart size. We hypothesized that in the presence of concentric left ventricular (LV) hypertrophy (LVH), load-sensitive measures of contractility may be misinterpreted as overestimating global cardiac function, because the normal function of excess sarcomeres may displace a greater volume of blood during contraction. Conductance catheter technology was used to evaluate pressure-volume (P-V) relationships as a load-insensitive method of assessing cardiac function in vivo in 18-wk-old heterozygous (mRen-2)27 transgenic rats (a model of LVH), compared with age-matched Sprague-Dawley (SD) controls. Anesthetized animals underwent echocardiography followed by P-V loop analysis. Blood pressure, body weight, and heart rate were higher in the Ren-2 rats (P < 0.05). Load-sensitive measures of systolic function, including fractional area change, fractional shortening, ejection fraction, and positive peak rate of LV pressure development, were greater in the Ren-2 than control animals (P < 0.05). Load-insensitive measures of systolic function, including the preload recruitable stroke work relationship and the end-systolic P-V relationship, were not different between Ren-2 and SD rats. Regional wall motion assessed by circumferential shortening velocity suggested enhanced circumferential fiber contractility in the Ren-2 rats (P = 0.02), but tissue Doppler imaging, used to assess longitudinal function, was not different between groups. Although conventional measures suggested enhanced systolic function in the Ren-2 rat, load-insensitive measures of contractility were not different between Ren-2 and SD animals. These findings suggest that the normal range of values for load-sensitive indexes of contractility needs to be altered according to the degree of LVH. To accurately identify changes in systolic function, we suggest that a combination of echocardiography with assessment of load-insensitive measures be used routinely.