The motivation of the present study is threefold. Mainly, the etiological explanation of the Womersley number based on physical reasoning. Next, the extension of a previous work [Messaris, Hadjinicolaou, and Karahalios, “Unsteady fluid flow in a slightly curved pipe: A comparative study of a matched asymptotic expansions solution with a single analytical solution,” Phys. Fluids 28, 081901 (2016)] to the annular pipe flow. Finally, the discussion of the effect of the additional stresses generated by a catheter in an artery and exerted on the arterial wall during an in vivo catheterization. As it is known, the square of the Womersley number may be interpreted as an oscillatory Reynolds number which equals to the ratio of the inertial to the viscous forces. The adoption of a modified Womersley number in terms of the annular gap width seems therefore more appropriate to the description of the annular flow than an ordinary Womersley number defined in terms of the pipe radius. On this ground, the non-dimensional equations of motion are approximately solved by two analytical methods: a matched asymptotic expansions method and a single. In the first method, which is valid for very large values of the Womersley number, the flow region consists of the main core and the two boundary layers formed at the inner and outer boundaries. In the second, the fluid is considered as one region and the Womersley number can vary from finite values, such that they fit to the blood flow in the aorta and the main arteries, to infinity. The single solution predicts increasing circumferential and decreasing axial stresses with increasing catheter radius at a prescribed value of the Womersley parameter in agreement with analogous results from other theoretical and numerical solutions. It also predicts the formation of pinches on the secondary flow streamlines and a third boundary layer, additional to those formed at the boundary walls. Finally, we show that the insertion of a catheter in an artery may trigger possible disastrous side effects. It may cause unexpected damage to a predisposed but still dormant location of the arterial wall due to high additional radial pressure that induces an excessive distension of the artery.