Marcus J Tim, Gan C Tji-Joong, Zwanenburg Jaco J M, Boonstra Anco, Allaart Cor P, Götte Marco J W, Vonk-Noordegraaf Anton
Department of Physics and Medical Technology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, the Netherlands.
J Am Coll Cardiol. 2008 Feb 19;51(7):750-7. doi: 10.1016/j.jacc.2007.10.041.
The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening.
In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening.
In 21 PAH patients (mean pulmonary arterial pressure 55 +/- 13 mm Hg and electrocardiogram-QRS width 100 +/- 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T(onset)) and peak time (T(peak)) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law.
The T(onset) was 51 +/- 23 ms, 65 +/- 4 ms, and 52 +/- 22 ms for LV, septum, and RV, respectively. The T(peak) was 293 +/- 58 ms, 267 +/- 22 ms, and 387 +/- 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 +/- 45 ms, coinciding with septal overstretch and RV T(peak). The L-R delay in T(onset) was -1 +/- 16 ms (p = 0.84), and the L-R delay in T(peak) was 94 +/- 41 ms (p < 0.001). The L-R delay in T(peak) was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T(peak) correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05).
In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.
本研究旨在探讨肺动脉高压（PAH）患者心室间不同步的原因是缩短起始时间还是缩短持续时间。
在PAH中，室间隔向左弯曲（LVSB）可能是由于心肌缩短存在从左到右（L-R）延迟所致。
对21例PAH患者（平均肺动脉压55±13mmHg，心电图QRS波宽度100±16ms）应用磁共振成像心肌标记技术（时间分辨率14ms）。计算左心室（LV）游离壁、室间隔和右心室（RV）游离壁圆周缩短的起始时间（T(onset)）和峰值时间（T(peak)）。根据拉普拉斯定律估算RV壁张力。
LV、室间隔和RV的T(onset)分别为51±23ms、65±4ms和52±22ms。LV、室间隔和RV的T(peak)分别为293±58ms、267±22ms和387±50ms。最大LVSB出现在395±45ms，与室间隔过度伸展和RV的T(peak)一致。T(onset)的L-R延迟为-1±16ms（p = 0.84），T(peak)的L-R延迟为94±41ms（p < 0.001）。T(peak)的L-R延迟与QRS波宽度无关，但与RV壁张力相关（p < 0.05）。T(peak)的L-R延迟与室间隔向左弯曲相关（p < 0.05），与LV舒张末期容积呈负相关（p < 0.05），与每搏输出量呈负相关（p < 0.05）。
在PAH中，心肌缩短峰值的L-R延迟是由RV缩短持续时间延长引起的。这种L-R延迟与LVSB、LV充盈减少和每搏输出量减少有关。
