Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, PO Box 616, Maastricht, 6200 MD, The Netherlands.
Cardiovasc Res. 2012 Nov 1;96(2):286-95. doi: 10.1093/cvr/cvs251. Epub 2012 Aug 8.
In chronic pulmonary hypertension (PH), right ventricular (RV) failure is associated with shortening of the RV free wall (RVFW) beyond pulmonary valve closure, temporarily paralleled by pronounced lengthening of the left ventricular free wall (LVFW). We hypothesized that this early-diastolic LVFW lengthening is caused by altered RVFW myofibre function and may therefore serve as a non-invasive measure of PH-induced RV (dys)function.
In 22 idiopathic pulmonary arterial hypertension (IPAH) patients, five chronic thrombo-embolic PH (CTEPH) patients, and six healthy subjects, ventricular volumes and circumferential strains were obtained using magnetic resonance imaging. RV ejection fraction (RVEF) and stroke volume index (RVSVI) were smaller in IPAH and CTEPH patients than in normals (RVEF: 32 ± 12 and 23 ± 19 vs. 59 ± 14%, respectively, both P < 0.01; RVSVI: 32 ± 9 and 23 ± 9 vs. 47 ± 6 mL/m(2), both P < 0.001). LV early-diastolic strain index (LVEDSI), defined as LVFW strain in the period between LVFW and RVFW peak shortening normalized for total systolic LVFW shortening, was larger in IPAH and CTEPH patients (0.52 ± 0.33 and 0.55 ± 0.40, both P < 0.01) than in normals (-0.03 ± 0.03). LVEDSI correlated negatively with RVEF (R = -0.74, P < 0.0001) and RVSVI (R = -0.69, P < 0.0001). Three multi-scale computer simulations of PH (all with mean pulmonary artery pressure = 55 mmHg) with complete, incomplete, and no structural adaptation of ventricular walls to local myofibre load showed that LVEDSI increased with deficiency of cardiac adaptation to PH (0.01, 0.52, and 0.84, respectively).
Early-diastolic LV lengthening reflects inadequate structural adaptation of the RVFW to increased myofibre load and is therefore a useful, non-invasive, and easily obtainable predictor of PH-induced RV dysfunction.
在慢性肺动脉高压（PH）中，右心室（RV）衰竭与 RV 游离壁（RVFW）在肺动脉瓣关闭后的缩短有关，同时左心室游离壁（LVFW）明显延长。我们假设这种早期舒张期 LVFW 延长是由 RVFW 肌纤维功能改变引起的，因此可以作为 PH 引起的 RV（功能障碍）的非侵入性测量。
在 22 例特发性肺动脉高压（IPAH）患者、5 例慢性血栓栓塞性 PH（CTEPH）患者和 6 例健康受试者中，使用磁共振成像获得心室容积和周向应变。与正常组相比，IPAH 和 CTEPH 患者的 RV 射血分数（RVEF）和每搏量指数（RVSVI）较小（RVEF：32±12 和 23±19 与 59±14%，均 P<0.01；RVSVI：32±9 和 23±9 与 47±6 mL/m²，均 P<0.001）。LV 早期舒张应变指数（LVEDSI）定义为 LVFW 应变在 LVFW 和 RVFW 峰值缩短之间的时间段内，归一化为总收缩期 LVFW 缩短，在 IPAH 和 CTEPH 患者中较大（0.52±0.33 和 0.55±0.40，均 P<0.01）比正常组（-0.03±0.03）。LVEDSI 与 RVEF（R=-0.74，P<0.0001）和 RVSVI（R=-0.69，P<0.0001）呈负相关。三个 PH 的多尺度计算机模拟（平均肺动脉压=55mmHg），心室壁完全、不完全和没有适应局部肌纤维负荷的结构性适应，显示 LVEDSI 随着心脏对 PH 的适应不足而增加（分别为 0.01、0.52 和 0.84）。
早期舒张期 LV 延长反映了 RVFW 对增加的肌纤维负荷的结构性适应不足，因此是一种有用的、非侵入性的和容易获得的 PH 引起的 RV 功能障碍的预测指标。
