Longitudinal strain delay index by speckle tracking imaging - A new marker of response to cardiac resynchronization therapy
Longitudinal strain delay index by speckle tracking imaging - A new marker of response to cardiac resynchronization therapy
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DOI：
10.1161/circulationaha.107.750190
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发表时间：
2008-09-09
期刊：
影响因子：
37.8
通讯作者：
Grimm, Richard A.
中科院分区：
文献类型：
--
作者：
Lim, Pascal;Buakhamsri, Adisai;Grimm, Richard A.
背景--在伴有左心室不同步的心力衰竭患者中，延迟节段的收缩能力并不能完全影响收缩末期功能。我们通过应变延迟指数来量化与机械不同步相关的收缩储备，以预测心脏再同步治疗的反应，应变延迟指数被定义为16个节段峰值和收缩末期应变之和。方法和结果-在100例心力衰竭患者(射血分数=26+/-9%，QRS=154+/-29ms，纽约心脏协会III级94%)中，我们研究了心脏再同步治疗前，通过2D散斑追踪使用纵向应变的应变延迟指数和12个节段心肌峰值速度的时间标准差。在回顾组(n=65)中确定了预测心脏再同步化治疗反应的应变延迟指数的最佳截断值，然后在验证组(n=35)中进行了确认。100例患者中，在3个月时出现左心室收缩末期容量减少15%(有效)。在回顾组中，应答者(n=42/65)的应变期延迟指数大于无应答者(35+/-8%对19+/-7%，P=25%)，应答者为82%(18/22)，无应答者为92%(12/13)。在整个人群中(n=100)，应变延迟指数与两个缺血区的反向重构相关(r=-0.68，P
Background-In heart failure patients with left ventricular dyssynchrony, contractility in delayed segments does not fully contribute to end-systolic function. We quantified this reserve of contraction related to mechanical dyssynchrony to predict response to cardiac resynchronization therapy by the strain delay index, which was defined as the sum of the difference between peak and end-systolic strain across 16 segments.Methods and Results-In 100 heart failure patients (ejection fraction=26 +/- 9%, QRS=154 +/- 29 ms, 94% in New York Heart Association class III), we studied left ventricular dyssynchrony before cardiac resynchronization therapy by the strain delay index using longitudinal strain by 2D speckle tracking and by the SD of time to peak myocardial velocity in 12 segments. The optimal cutoff value of the strain delay index to predict response to cardiac resynchronization therapy was determined in a retrospective group (n = 65) and then confirmed in a validation group (n = 35). Left ventricular end-systolic volume reduction at 3 months >15% (responder) occurred in 64 of 100 patients. In the retrospective group, the strain delay index but not the SD of time to peak myocardial velocity was greater in responders (n = 42/65) than nonresponders (35 +/- 8% versus 19 +/- 7%, P= 25% identified 82% (18/22) of responders and 92% (12/13) of nonresponders. Among the entire population (n=100), strain delay index correlated with reverse remodeling in both the ischemic (r=-0.68, P