AIM To investigate wall shear stress(WSS) magnitude and distribution in cirrhotic patients with portal hypertension using computational fluid dynamics. METHODS Idealized portal vein(PV) system models were reconstructe...AIM To investigate wall shear stress(WSS) magnitude and distribution in cirrhotic patients with portal hypertension using computational fluid dynamics. METHODS Idealized portal vein(PV) system models were reconstructed with different angles of the PV-splenic vein(SV) and superior mesenteric vein(SMV)-SV. Patient-specific models were created according to enhanced computed tomography images. WSS was simulated by using a finite-element analyzer, regarding the blood as a Newtonian fluid and the vessel as a rigid wall. Analysis was carried out to compare the WSSin the portal hypertension group with that in healthy controls.RESULTS For the idealized models, WSS in the portal hypertension group(0-10 dyn/cm2) was significantly lower than that in the healthy controls(10-20 dyn/cm2), and low WSS area(0-1 dyn/cm2) only occurred in the left wall of the PV in the portal hypertension group. Different angles of PV-SV and SMV-SV had different effects on the magnitude and distribution of WSS, and low WSS area often occurred in smaller PV-SV angle and larger SMV-SV angle. In the patient-specific models, WSS in the cirrhotic patients with portal hypertension(10.13 ± 1.34 dyn/cm2) was also significantly lower than that in the healthy controls(P < 0.05). Low WSS area often occurred in the junction area of SV and SMV into the PV, in the area of the division of PV into left and right PV, and in the outer wall of the curving SV in the control group. In the cirrhotic patients with portal hypertension, the low WSS area extended to wider levels and the magnitude of WSS reached lower levels, thereby being more prone to disturbed flow occurrence.CONCLUSION Cirrhotic patients with portal hypertension show dramatic hemodynamic changes with lower WSS and greater potential for disturbed flow, representing a possible causative factor of PV thrombosis.展开更多
基金Supported by the Program for Changjiang Scholars and Innovative Research Team in Universities,No.PCSIRT-1171National Natural Science Foundation of China,No.81270504Fundamental Research Funds for the Central Universities,No.xjj20100209
文摘AIM To investigate wall shear stress(WSS) magnitude and distribution in cirrhotic patients with portal hypertension using computational fluid dynamics. METHODS Idealized portal vein(PV) system models were reconstructed with different angles of the PV-splenic vein(SV) and superior mesenteric vein(SMV)-SV. Patient-specific models were created according to enhanced computed tomography images. WSS was simulated by using a finite-element analyzer, regarding the blood as a Newtonian fluid and the vessel as a rigid wall. Analysis was carried out to compare the WSSin the portal hypertension group with that in healthy controls.RESULTS For the idealized models, WSS in the portal hypertension group(0-10 dyn/cm2) was significantly lower than that in the healthy controls(10-20 dyn/cm2), and low WSS area(0-1 dyn/cm2) only occurred in the left wall of the PV in the portal hypertension group. Different angles of PV-SV and SMV-SV had different effects on the magnitude and distribution of WSS, and low WSS area often occurred in smaller PV-SV angle and larger SMV-SV angle. In the patient-specific models, WSS in the cirrhotic patients with portal hypertension(10.13 ± 1.34 dyn/cm2) was also significantly lower than that in the healthy controls(P < 0.05). Low WSS area often occurred in the junction area of SV and SMV into the PV, in the area of the division of PV into left and right PV, and in the outer wall of the curving SV in the control group. In the cirrhotic patients with portal hypertension, the low WSS area extended to wider levels and the magnitude of WSS reached lower levels, thereby being more prone to disturbed flow occurrence.CONCLUSION Cirrhotic patients with portal hypertension show dramatic hemodynamic changes with lower WSS and greater potential for disturbed flow, representing a possible causative factor of PV thrombosis.