Denis Berdajs1, Selim Mosbahi2, Enrico Ferrari2, Dominique Charbonnier3, Ludwig K von Segesser2. 1. Department of Cardiac Surgery, University Hospital Basel, Basel; Department of Surgery and Anesthesiology, Cardiovascular Research, University Hospital Lausanne, Lausanne. Electronic address: denis.berdajs@bluewin.ch. 2. Department of Surgery and Anesthesiology, Cardiovascular Research, University Hospital Lausanne, Lausanne. 3. CFS Engineering, Lausanne, Switzerland.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.