Pulsatile flow simulation of patent ductus arteriosus to evaluate thrombosis factors on closure device


  • Nurulnatisya Ahmad Universiti Teknologi Mara
  • Ishkrizat Taib Universiti Tun Hussein Onn
  • Kahar Osman Universiti Teknologi Malaysia
  • Ahmad Zahran Md Khudzari Universiti Teknologi Malaysia




Patent Ductus Arteriosus 1, Flow analysis 2, CFD 3, Thrombosis 4, Closure devices 5, Haemodynamic 6


Transcatheter treatment using occlusion devices is the most common treatment used to treat the Patent Ductus Arteriosus (PDA). The occlusion device act as a physical barrier to blood flow in the duct which facilitates thrombogenesis and occludes the duct. Over the past 15 years, there have been significant developments in the devices used to close PDA. Various design of occlusion device affects the flow of blood in the duct. To improve the efficiency of the thrombogenesis on the surface of occlusion device and estimate the time needed to occludes the duct, it is important to simulate blood flow through different design of occlusion device. Two design was used which is the concave and convex shape of the occlusion device. Blood was simulated as Newtonian with the incompressible and laminar flow. A computational fluid dynamics (CFD) study has been done in pulsatile blood flow through the aortic arch and the occlusion device. The hemodynamic parameters that contribute to the thrombosis formation have been studied and showed that the convex shape yielded more TAWSSlow (< 0.5 Pa) magnitude (65.72%), generated 51.84% areas that exposed to high OSI and calculated 14.46% areas that exposed to RRT ≥ 10 Pa-1. While, concave shape yielded 13.21% of TAWSSlow (< 0.5 Pa), generated only 47.84% of areas that exposed to high OSI and calculated 14.46% areas that exposed to RRT ≥ 10 Pa-1. Therefore, from the preliminary work on PDA occlusion device, it is suggested that to promote thrombosis, the convex shape was much better compared to concave shape.


Asakura T., Karino T. 1990. Flow patterns and spatial distribution of atherosclerotic lesions in human coronary arteries. Circ. Res. 66, 1045-1066.

Bengt A., Ronnie A., Love H., Mikael M., Rahman S., Berend V. W. 2012. Computational fluid dynamics for engineers. New York. Cambridge University Press.

Benitz W. E. and Committee on Fetus and Newborn 2016. Patent ductus arteriosus in preterm infants. Pediatrics.137(1): e20153730.

Carlgren L. E. 1959. The incidence of congenital heart disease in children born in Gothenburg 1941–1950. Br. Heart J. 21, 40–50.

Douglas J., Schneider, M. D. 2012. The patent ductus arteriosus in term infants, children, and adults. Semin Perinatol 36, 146-153.

Forbes T., Turner D. 2012. What is the optimal device for closure of a persistently patent ductus arteriosus? Prog Pediatr Cardiol 33, 125-129.

Pennati G., Belloti M., Fumero R. 1997. Mathematical modelling of the human foetal cardiovascular system based on Doppler ultrasound data. Med. Eng. Phys. 19(4), 327-335.

Haruguchi H., Teraoka S. 2003. Intimal hyperplasia and hemodynamic factors in arterial bypass and arteriovenous grafts: A review. J. Artif. Organs 6, 227-235.

Juan M. J., Peter F. D. 2009. Hemodynamically Driven Stent Strut Design. Ann Biomed Eng. 37, 1486-1494.

Krichenko A., Benson L. N., Burrows P, et al. 1989. Angiographic classification of the isolated, persistently patent ductus arteriosus and implications for percutaneous catheter occlusion. Am. J. Cardiol. 63, 877-879.

Ku D. N., Giddens D. P., Zarins C. K., Glagov S. 1985. Pulsatile flow and artherosclerosis in the human carotid bifurcation. Positive correlation between plaque location and low oscillating shear stress. Arterioscler. Thromb. Vasc. Biol. 5, 293-302.

Liddy S., Oslizlok P., Walsh K. P. 2013. Comparison of the results of transcatheter closure of patent ductus arteriosus with newer amplatzer devices.

Catheter Cardiovasc Interv. 82, 253-259.

Moore J. W., Levi D. S., Moore S. D., et al. 2005. Interventional treatment of patent ductus arteriosus in 2004. Catheter. Cardiovasc. Interv. 64, 91–101.

Portsman W., Wierny L., Warnke H. 1967. Closure of persistent ductus arteriousus without thoracotomy. Ger. Med. Mon. 15, 109-203.

Vaibhavi A. S., Jayesh R. B. 2014. Flow simulation of cardiac defects to evaluate effectiveness of occlusion devices. J Med Devices 8, 020940:1-3.

Vaibhavi A. S., Jayesh R. B. 2015. Simulation of pulsatile blood flow through various cardiac defects and quantitative measurements of shunted blood volume. Procedia Mater Sci. 10, 706-713.

Vaibhavi A. S., Jayesh R. B. 2016. Mathematical modeling and simulation of an occlusion device in a blood vessel. Cardiovasc Eng Technol. 7(4), 420-431.

Yingying H., Jen F. K., Subbu S. V. 2014. Biomaterials and design in occlusion devices for cardiac defects: A review. Acta Biomater. 10, 1088-1101.

Thomas K., Christian J. K., Manuela A., Eva B., Emanuela R. B. 2008. Normal values for aortic diameters in children and adolescents – assessment in vivo by contrast-enhanced CMR-angiography. J. Cardiovasc. Magn. Reson. 10: 56.

Zarins C. K., Giddens D. P., Bharadvaj B. K., Sottiurai V. S., Mabon R. F., Glagov S. 1983. Carotid bifircation artherosclerosis. Quantative correlation of pluque localization with flow velocity profiles and wall shear stress. Circ. Res. 53, 502-514.