Left ventricular dyssynchrony as marker of early dysfunction in premature ventricular contraction-induced cardiomyopathy.

Left ventricular dyssynchrony as marker of early dysfunction in premature ventricular contraction-induced cardiomyopathy.
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左心室异位障碍作为早期功能障碍的标志性,在室性过早收缩引起的心肌病中。

DOI:
10.3389/fcvm.2022.978341
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发表时间:
2022
影响因子:
3.6
通讯作者:
Huizar, Jose F.
Huizar, Jose F.
中科院分区:
医学3区
文献类型:
--
作者:
Kowlgi, Gurukripa N.;Tan, Alex Y.;Kaszala, Karoly;Kontos, Michael C.;Lozano, Pedro;Ellenbogen, Kenneth A.;Huizar, Jose F.

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应变成像被认为是检测左室射血分数(EF)保留患者频繁室性早搏(PVCs)导致的早期左室(LV)功能障碍的工具。然而,室性心肌病(CM)的室内非同步化(IVD),径向和周向应变(RS, CS)的进展尚不清楚。本研究的目的是阐明PVC-CM的CS, IVD和机电延迟(EML)的进展模式。在20只狗体内植入起搏器,在200毫秒时复制心室双裂(室性早搏n = 11),持续12周,并与假手术组(n = 9)进行比较。我们分别在基线、4周、8周和12周获得超声心动图。左腔中腔水平RS和CS。IVD定义为最早与最晚RS峰之间的时间,EML定义为QRS发生与最早RS峰之间的时间,LVEF(62±5 ~ 42±7%,p < 0.01)、CS(-18±3 ~ -12±3,p < 0.01)、EML(219±37 ~ 283±46ms, p = 0.02)在PVC组发生显著变化。尽管保留了51±5%的LVEF,但4周时,峰值CS(-18±3至-14±4,p = 0.02)和IVD(49±31至122±103,p = 0.05)有显著变化。第8周和第12周,IVD恢复正常,EML升高。我们的发现巩固了现有的理论,即应变的变化先于PVC-CM的LVEF的变化。虽然IVD在PVC-CM的早期发展中出现异常,但由于EML的进一步增加提示心脏收缩性重构,它在晚期伪正常化。这些发现与最近发表的数据一致,即异常的左室力学可能是导致室性早搏-心肌病预后更差的底物的一部分。
Strain imaging has been suggested as a tool to detect early left ventricular (LV) dysfunction due to frequent premature ventricular contractions (PVCs) in patients with preserved LV ejection fraction (EF). However, the progression of intraventricular dyssynchrony (IVD), radial, and circumferential strain (RS, CS) in PVC-cardiomyopathy (CM) are unknown. The aim of this study was to elucidate the progression patterns of CS, IVD, and electro-mechanical latency (EML) in PVC-CM. Pacemakers were implanted in 20 canines to reproduce ventricular bigeminy at 200ms (PVCs n = 11) for 12 weeks and compared to a sham group (n = 9). We obtained echocardiograms at baseline, 4-, 8- and 12-weeks. RS and CS were obtained at the LV mid-cavitary level. IVD was defined as the time between the earliest and latest peak RS. EML was defined as the time between the onset of QRS and the earliest peak RS. LVEF (62 ± 5 to 42 ± 7%, p < 0.01), CS (–18 ± 3 to –12 ± 3, p < 0.01), and EML (219 ± 37 to 283 ± 46ms, p = 0.02) changed significantly in the PVC group. Peak CS (–18 ± 3 to –14 ± 4, p = 0.02) and IVD (49 ± 31 to 122 ± 103, p = 0.05) had a significant change at 4-weeks despite preserved LVEF (51 ± 5%). IVD normalized while EML increased at weeks 8 and 12. Our findings consolidate the existing theory that changes in strain precede changes in LVEF in PVC-CM. While IVD becomes abnormal early in the development of PVC-CM, it pseudo-normalizes at advanced stages due to further increases in EML suggestive of cardiac contractility remodeling. These findings are consistent with recent published data where abnormal LV mechanics could be part of a substrate that can predispose to worse outcome in PVC-Cardiomyopathy.
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