Impact of pulmonary vascular stiffness and vasodilator treatment in pediatric pulmonary hypertension: 21 patient-specific fluid-structure interaction studies.
Impact of pulmonary vascular stiffness and vasodilator treatment in pediatric pulmonary hypertension: 21 patient-specific fluid-structure interaction studies.
复制标题
DOI：
10.1016/j.cmpb.2011.09.002
复制
发表时间：
2012-11
影响因子：
6.1
通讯作者：
Shandas R
中科院分区：
文献类型：
--
作者：
Su Z;Hunter KS;Shandas R
最近肺动脉高压（PAH）的临床研究发现肺血管僵硬度（PVS）增加与疾病预后不良之间存在相关性。然而，在进展性PAH的情况下，PVS、RV功率和血管血流动力学之间的关系仍然存在机制问题，这些问题很难或不可能通过直接测量来回答。经过临床验证的患者特异性计算模型可以通过基于微扰的预测测试来探索这些问题。在这里，我们使用一个简单的患者特异性模型来回答四个问题：当PAH恶化时血流动力学是如何改变的？增加pv如何影响血流动力学和RV功率？对于中度PAH患者，如果压力适度增加，但足以使血管中的胶原蛋白参与其中，后果是什么？降压血管扩张剂治疗对血流动力学有什么影响？21组模型预测的阻抗和平均PA压（mPAP）与临床测量结果吻合良好，从而验证了模型的有效性。使用三个PAH结局组的数据对病情恶化进行建模；这不仅表明了预期的mPAP增加，而且表明了压力脉动性的增加。有趣的是，长期增加的mPAP降低了WSS，这表明PA横截面积增加对WSS的影响大于PVS增加。对于以弹性蛋白为基础的上游血管重构的中度高PVR （12.7 WU）患者，从弹性蛋白为主的血管行为转变为胶原为主的血管行为导致mPAP、压力和WSS脉搏度大幅增加。对于同一例患者，通过模拟血管扩张剂将PVR降低到与轻度PAH相当的值，并没有降低压力脉动性，却显著增加了WSS脉动性。总之，这些结果表明PVS与血流动力学密切相关，血流动力学可能在PAH进展中起重要作用。这些结果支持了一种假设，即除了降低平均压力外，治疗还应以减少或逆转上游血管重构为目标。
Recent clinical studies of pulmonary arterial hypertension (PAH) have found correlations between increased pulmonary vascular stiffness (PVS) and poorer disease outcomes. However, mechanistic questions remain about the relationships amongst PVS, RV power, and vascular hemodynamics in the setting of progressive PAH that are difficult or impossible to answer using direct measurements. Clinically-validated patient-specific computational modeling may allow exploration of these issues through perturbation-based predictive testing. Here we use a simple patient-specific model to answer four questions: how do hemodynamics change as PAH worsens? How does increasing PVS impact hemodynamics and RV power? For a patient with moderate PAH, what are the consequences if the pressures increase modestly yet sufficiently to engage collagen in those vessels? What impact does pressure-reducing vasodilator treatment have on hemodynamics? Twenty-one sets of model-predicted impedance and mean PA pressure (mPAP) show good agreement with clinical measurements, thereby validating the model. Worsening was modeled using data from three PAH outcomes groups; these show not only the expected increase in mPAP, but also an increase in pressure pulsatility. Interestingly, chronically increasing mPAP decreased WSS, suggesting that increased PA cross-sectional area affected WSS greater than increased PVS. For a patient with moderately high PVR (12.7 WU) with elastin-based upstream vascular remodeling, moving from elastin-dominant vessel behavior to collagen-dominant behavior caused substantial increases in mPAP, pressure and WSS pulsatility. For the same patient, reducing PVR through a simulated vasodilator to a value equivalent to mild PAH did not decrease pressure pulsatility and dramatically increased WSS pulsatility. Overall, these results suggest a close association between PVS and hemodynamics and that hemodynamics may play an important role in progressing PAH. These support the hypothesis that treatments should target decreasing or reversing upstream vascular remodeling in addition to decreasing mean pressures.
登录
查看更多内容
DOI：
10.1115/1.2206202
发表时间：
2006-08-01
影响因子：
1.7
作者：
Hunter, Kendall S.;Lanning, Craig J.;Shandas, Robin
通讯作者：
Shandas, Robin
影响因子：
24
作者：
Kaiser, DR;Billups, K;Bank, AJ
通讯作者：
Bank, AJ
DOI：
10.1016/0735-1097(93)90682-q
发表时间：
1993-02-01
影响因子：
24
作者：
LASKEY, WK;FERRARI, VA;KUSSMAUL, WG
通讯作者：
KUSSMAUL, WG
影响因子：
24.3
作者：
Dartevelle, P;Fadel, E;Simonneau, G
通讯作者：
Simonneau, G
影响因子：
20.1
作者：
MILNOR, WR;BERGEL, DH;BARGAINE.JD
通讯作者：
BARGAINE.JD