Circulatory disease is the number two cause of death next to cancer in Korea, while the cardiovascular disease alone is the number one cause of death in the US. In the present article, some background, current status and future prospects of biomedical engineering esearch on circulatory disorders are discussed in terms of the origin of atherosclerosis, computational fluid dynamics and medical imaging techniques, clinical treatments and fluid dynamics, advances in stents, hemodynamic analysis of artificial heart, and artificial blood. In particular, the importance of close collaboration of medicine and fluids engineering is emphasized.

Both flow visualizations and computational fluid dynamics were performed to determine hemodynamics in a total cavopulmonary connection (TCPC) model for surgically correcting congenital heart defects. From magnetic resonance images, an anatomically correct glass model was fabricated to visualize steady flow. The total flow rates were 4, 6 and 8L/min and flow rates from SVC and IVC were 40:60. The flow split ratio between LPA and RPA was varied by 70:30, 60:40 and 50:50. A pressure-based finite-volume software was used to solve steady flow dynamics in TCPC models. Results showed that superior vena cava(SVC) and inferior vena cava(IVC) flow merged directly to the intra-atrial conduit, creating two large vortices. Significant swirl motions were observed in the intra-atrial conduit and pulmonary arteries. Flow collision or swirling flow resulted in energy loss in TCPC models. In addition, a large intra-atrial channel or a sharp bend in TCPC geometries could influence on energy losses. Energy conservation was efficient when flow rates in pulmonary branches were balanced. In order to increase energy efficiency in Fontan operations, it is necessary to remove a flow collision in the intra-atrial channel and a sharp bend in the pulmonary bifurcation.

Tumor angiogenesis was simulated using a two-dimensional computational model. The equation that governed angiogenesis comprised a tumor angiogenesis factor (TAF) conservation equation in time and space, which was solved numerically using the Galerkin finite element method. The time derivative in the equation was approximated by a forward Euler scheme. A stochastic process model was used to simulate vessel formation and vessel elongation towards a paracrine site, i.e., tumor-secreted basic fibroblast growth factor (bFGF). In this study, we assumed a two-dimensional model that represented a thin (1.0 mm) slice of the tumor. The growth of the tumor over time was modeled according to the dynamic value of bFGF secreted within the tumor. The data used for the model were based on a previously reported model of a brain tumor in which four distinct stages (namely multicellular spherical, first detectable lesion, diagnosis, and death of the virtual patient) were modeled. In our study, computation was not continued beyond the 'diagnosis' time point to avoid the computational complexity of analyzing numerous vascular branches. The numerical solutions revealed that no bFGF remained within the region in which vessels developed, owing to the uptake of bFGF by endothelial cells. Consequently, a sharp, declining gradient of bFGF existed near the surface of the tumor. The vascular architecture developed numerous branches close to the tumor surface (the brush-border effect). Asymmetrical tumor growth was associated with a greater degree of branching at the tumor surface.

Catheters are used to measure translesional pressure gradients in the stenosed coronary arteries. Uses of catheters during coronary angioplasty cause flow obstructions. A narrowed flow cross section with catheter effectively introduced a tighter stenosis than the enlarged residual stenoses after balloon angiplasty. Catheters in blood vessels cause pressure gradient rise and blood flow drop during the measurements. In this study, three dimensional computer simulations are conducted to investigate the flow blockage effects due to the catheter obstructions during the coronary angioplasty. The computer simulation models are generated by the data, which are measured by coronary angiogram, and the blood is treated as non-Newtonian fluid. The velocity, pressure, and wall shear stress variations are observed for the estimate of damages of blood vessel. This study is also extended to investigate the effects of stenotic vessel size, and shape and catheter size and location.