Johnson Lauren, Lamia Bouchra, Kim Hyung Kook, Tanabe Masaki, Gorcsan John, Schwartzman David, Shroff Sanjeev G, Pinsky Michael R
Cardiovascular Systems Laboratory, Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Pacing Clin Electrophysiol. 2012 Feb;35(2):174-87. doi: 10.1111/j.1540-8159.2011.03246.x. Epub 2011 Oct 20.
Most current indices of synchrony quantify left ventricular (LV) contraction pattern in terms of a single, global (integrated) measure. We report the development and physiological relevance of a novel method to quantify LV segmental contraction synchrony.
LV pressure-volume and echocardiographic data were collected in seven anesthetized, opened-chest dogs under several pacing modes: right atrial (RA) (control), right ventricular (RV) (dyssynchrony), and additional LV pacing at either apex (CRTa) or free wall (CRTf). Cross-correlation-based integrated (CCSI(int) ) and segmental (CCSI(seg) ) measures of synchrony were calculated from speckle-tracking derived radial strain, along with a commonly used index (maximum time delay). LV contractility was quantified using either E(es) (ESPVR slope) or ESPVR(area) (defined in the manuscript).
RV pacing decreased CCSI(int) at LV base (0.95 ± 0.02 [RA] vs 0.64 ± 0.14 [RV]; P < 0.05) and only CRTa improved it (0.93 ± 0.03; P < 0.05 vs RV). The CCSI(seg) analysis identified anteroseptal and septal segments as being responsible for the low CCSI(int) during RV pacing and inferior segment for poor resynchronization with CRTf. Changes in ESPVR(area) , and not in E(es) , indicated depressed LV contractility with RV pacing, an observation consistent with significantly decreased global LV performance (stroke work [SW]: 252 ± 23 [RA] vs 151 ± 24 [RV] mJ; P < 0.05). Only CRTa improved SW and contractility (SW: 240 ± 19 mJ; ESPVR(area) : 545 ± 175 mmHg•mL; both P < 0.01 vs RV). Only changes in CCSI(seg) and global LV contractility were strongly correlated (R(2) = 0.698, P = 0.005).
CCSI(seg) provided insights into the changes in LV integrated contraction pattern and a better link to global LV contractility changes.
目前大多数同步性指标是通过单一的整体(综合)测量来量化左心室(LV)收缩模式。我们报告了一种量化左心室节段性收缩同步性的新方法的开发及其生理相关性。
在七种起搏模式下收集了七只麻醉开胸犬的左心室压力 - 容积和超声心动图数据:右心房(RA)(对照)、右心室(RV)(不同步),以及在 apex 或游离壁进行额外的左心室起搏(CRTa 或 CRTf)。基于互相关的同步性综合(CCSI(int))和节段性(CCSI(seg))测量是根据散斑追踪得出的径向应变计算的,同时还有一个常用指标(最大时间延迟)。使用 E(es)(ESPVR 斜率)或 ESPVR(area)(在手稿中定义)来量化左心室收缩性。
右心室起搏降低了左心室底部的 CCSI(int)(0.95 ± 0.02 [RA] 对 0.64 ± 0.14 [RV];P < 0.05),只有 CRTa 改善了它(0.93 ± 0.03;与 RV 相比 P < 0.05)。CCSI(seg)分析确定前间隔和间隔节段是右心室起搏期间 CCSI(int)低的原因,而下节段是 CRTf 再同步不良的原因。ESPVR(area)的变化而非 E(es)的变化表明右心室起搏时左心室收缩性降低,这一观察结果与左心室整体性能显著下降一致(每搏功[SW]:252 ± 23 [RA] 对 151 ± 24 [RV] mJ;P < 0.05)。只有 CRTa 改善了 SW 和收缩性(SW:240 ± 19 mJ;ESPVR(area):545 ± 175 mmHg•mL;两者与 RV 相比 P < 0.01)。只有 CCSI(seg)的变化与左心室整体收缩性变化密切相关(R(2)=0.698,P = 0.005)。
CCSI(seg)提供了对左心室综合收缩模式变化的见解,并与左心室整体收缩性变化有更好的关联。