Zhang Yongxue, Lu Qingsheng, Feng Jiaxuan, Yu Peng, Zhang Suming, Teng Zhongzhao, Gillard Jonathan H, Song Runze, Jing Zaiping
Division of Vascular Surgery, Changhai Hospital, Shanghai, PR China.
Cardiology. 2014;128(2):220-5. doi: 10.1159/000358041. Epub 2014 Apr 24.
This study sought to elucidate the underlying hemodynamic mechanisms involved in the longitudinal propagation of acute, type-B aortic dissections.
Three-dimensional patient-specific aortic geometry was reconstructed from computed tomography images of 3 cases, followed by computational fluid dynamic analysis using finite-element analysis modeling. Three models were reconstructed; the normal-aortic model (from a healthy volunteer), the visceral-involvement model (from a patient whose visceral arteries were involved) and the progression model (from a patient whose visceral arteries were intact at admission). Wall pressure distribution was analyzed in all three models.
In the systolic phase of a cardiac cycle, the wall pressure dropped from the proximal to the distal aorta within the true lumen. This pressure gradient was observed in all three models. A milder pressure gradient was seen in the false lumen in the visceral-involvement model, whereas the pressure in the false lumen remained almost constant in the progression model. The dyssynchrony of the pressure gradients in the true and false lumens caused an imbalance in pressure between the two lumens.
The interluminal pressure differential may be a contributing factor in the compression of the true lumen and the cleavage force of the aortic wall, leading to the longitudinal propagation of the dissection.
