Biomedical and Metabolic Imaging Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA.
J Cardiovasc Magn Reson. 2012 Jan 6;14(1):1. doi: 10.1186/1532-429X-14-1.
We sought to investigate the relationship between infarct and dyssynchrony post- myocardial infarct (MI), in a porcine model. Mechanical dyssynchrony post-MI is associated with left ventricular (LV) remodeling and increased mortality.
Cine, gadolinium-contrast, and tagged cardiovascular magnetic resonance (CMR) were performed pre-MI, 9 ± 2 days (early post-MI), and 33 ± 10 days (late post-MI) post-MI in 6 pigs to characterize cardiac morphology, location and extent of MI, and regional mechanics. LV mechanics were assessed by circumferential strain (eC). Electro-anatomic mapping (EAM) was performed within 24 hrs of CMR and prior to sacrifice.
Mean infarct size was 21 ± 4% of LV volume with evidence of post-MI remodeling. Global eC significantly decreased post MI (-27 ± 1.6% vs. -18 ± 2.5% (early) and -17 ± 2.7% (late), p < 0.0001) with no significant change in peri-MI and MI segments between early and late time-points. Time to peak strain (TTP) was significantly longer in MI, compared to normal and peri-MI segments, both early (440 ± 40 ms vs. 329 ± 40 ms and 332 ± 36 ms, respectively; p = 0.0002) and late post-MI (442 ± 63 ms vs. 321 ± 40 ms and 355 ± 61 ms, respectively; p = 0.012). The standard deviation of TTP in 16 segments (SD16) significantly increased post-MI: 28 ± 7 ms to 50 ± 10 ms (early, p = 0.012) to 54 ± 19 ms (late, p = 0.004), with no change between early and late post-MI time-points (p = 0.56). TTP was not related to reduction of segmental contractility. EAM revealed late electrical activation and greatly diminished conduction velocity in the infarct (5.7 ± 2.4 cm/s), when compared to peri-infarct (18.7 ± 10.3 cm/s) and remote myocardium (39 ± 20.5 cm/s).
Mechanical dyssynchrony occurs early after MI and is the result of delayed electrical and mechanical activation in the infarct.
我们旨在研究心肌梗死后梗死和不同步性之间的关系，为此构建了猪模型。心肌梗死后的机械不同步与左心室（LV）重构和死亡率增加有关。
在 6 头猪中，在心肌梗死前（MI）、9±2 天（早期 MI）和 33±10 天（晚期 MI）进行心脏电影、钆对比和标记心血管磁共振（CMR），以描述心脏形态、MI 的位置和范围以及局部力学。通过周向应变（eC）评估 LV 力学。CMR 后 24 小时内进行电解剖映射（EAM）并在牺牲前进行。
平均梗死面积为 LV 体积的 21±4%，伴有梗死后重构的证据。MI 后，整体 eC 明显降低（-27±1.6%比-18±2.5%（早期）和-17±2.7%（晚期），p<0.0001），但早期和晚期之间 MI 段和周边段的 eC 无显著变化。MI 段达峰时间（TTP）明显长于正常和周边段，无论是在早期（440±40 ms 比 329±40 ms 和 332±36 ms，分别；p=0.0002）还是晚期 MI（442±63 ms 比 321±40 ms 和 355±61 ms，分别；p=0.012）。16 个节段 TTP 的标准差（SD16）在 MI 后明显增加：从 28±7 ms 增加到 50±10 ms（早期，p=0.012）到 54±19 ms（晚期，p=0.004），早期和晚期 MI 之间无变化（p=0.56）。TTP 与节段收缩力降低无关。EAM 显示，与周边梗死区（18.7±10.3 cm/s）和远隔心肌（39±20.5 cm/s）相比，梗死区晚期电活动和传导速度明显降低（5.7±2.4 cm/s）。
机械不同步在 MI 后早期发生，是梗死区延迟电和机械激活的结果。
