Berdajs Denis, Mosbahi Selim, Ferrari Enrico, Charbonnier Dominique, von Segesser Ludwig K
Department of Cardiac Surgery, University Hospital Basel, Basel; Department of Surgery and Anesthesiology, Cardiovascular Research, University Hospital Lausanne, Lausanne.
Department of Surgery and Anesthesiology, Cardiovascular Research, University Hospital Lausanne, Lausanne.
Ann Thorac Surg. 2017 Oct;104(4):1340-1348. doi: 10.1016/j.athoracsur.2017.02.076. Epub 2017 Jun 3.
In this study, the effect of aortic valve (AV) pathology on local hemodynamic conditions was evaluated as a potential trigger for the onset of acute type A and B aortic dissection.
A time- and pressure-related four-dimensional (4-D) computed fluid dynamic model of the aorta was established. In an experimental setup, AV stenosis and AV insufficiency were created. 4-D pressure-related geometry of the aortic root (AR) with valve insufficiency and valve stenosis were determined by high-fidelity (200 Hz) microsonometric crystals. Flow and pressure were obtained at the left ventricle, ascending aorta, and aortic arch.
Expansion of the AR in AV insufficiency was higher with expansion in AV stenosis, at peak ejection, and at the end of systole. In AV insufficiency, there was low shear stress (0 to 0.6 Pa), turbulent flow, and high pressure (80 to 95 mm Hg) at the anterior wall of the ascending aorta, at the proximal aortic arch, and at the aortic isthmus. In stenosis, high shear stress (>2 Pa) and high pressure (>95 mm Hg) were found at the ascending aorta and at the bifurcation of the brachiocephalic trunk.
In AV insufficiency, low shear stresses and turbulent flow regions were documented at the traditional levels of entry tears for acute type A and B dissection. In AV stenosis, high shear stress with elevated pressure at the ascending aorta may be a trigger element for vessel dilatation, aneurysm formation, and intimal tear, which is typical for type A aortic dissection.
在本研究中，评估了主动脉瓣（AV）病变对局部血流动力学状况的影响，将其作为急性A型和B型主动脉夹层发病的潜在触发因素。
建立了一个与时间和压力相关的主动脉四维（4-D）计算流体动力学模型。在实验装置中，制造了AV狭窄和AV关闭不全。通过高保真（200Hz）微声晶体确定了伴有瓣膜关闭不全和瓣膜狭窄的主动脉根部（AR）的4-D压力相关几何形状。在左心室、升主动脉和主动脉弓处获取血流和压力数据。
在射血峰值和收缩期末，AV关闭不全时AR的扩张高于AV狭窄时的扩张。在AV关闭不全时，升主动脉前壁、主动脉弓近端和主动脉峡部存在低剪切应力（0至0.6Pa）、湍流和高压（80至95mmHg）。在狭窄时，升主动脉和头臂干分叉处存在高剪切应力（>2Pa）和高压（>95mmHg）。
在AV关闭不全时，在急性A型和B型夹层的传统入口撕裂水平记录到低剪切应力和湍流区域。在AV狭窄时，升主动脉处的高剪切应力和升高的压力可能是血管扩张、动脉瘤形成和内膜撕裂的触发因素，这是A型主动脉夹层的典型表现。
