High shear stress. wait wait wait, no. Low shear stress. Wait wait. Low then high shear stress. Oh, okay high shear stress too.

The problem is that you don't have high shear stress WITHOUT high tensile strain, all while disregarding oscillatory tensile strain, pulsatile acceleration between peak systole and diastole, as well as vortice formation.

In my own opinion after carefully digesting all viewpoints, it seems that tensile stress and vortice formation are the most important damaging forces upon an artery.  Shear stress is most contradictory if you disregard vortical turbulence/stagnation, and once again, tensile strain.

Shear stress is basically "drag."  Like a hand in the wind palm forward, the drag on it is higher than when the hand is held parallel to the wind, creating less drag.  How high drag is better for the artery than low drag is explained by the high drag drawing the endothelium tight, like a comb over a dogs' fur in a straight, undeviating stroke.  Low drag is supposedly bad for an artery because it doesn't pull the cells tight.  To me that doesn't make a lot of sense, but when pulsatile flow (a slight backwards flow on diastole with a majority forward flow on systole) is taken account, that makes sense.  Also, vortical formation, is important, but these things are never mentioned in one sentence, causing major confusion.  It is not that hard to understand together, it makes it more confusing and ambiguous not to talk about all these things at once.  Low shear stress + pulsatile flow caused by a local pressure differential + vortices (tornados of the blood) cause the endothelium to become dissheveled.  Like taking your hand and making random circles in your pet's fur, this will cause the once linearly oriented cells to become haphazardly arranged rather than in the direction of the laminar flow.

It is counterintuitive.  LOW SHEAR STRESS causes atherosclerosis not high shear stress.  Studies in coronary arteries show a precise opposition between high shear areas free of plaque and the low shear area laden with plaque.  The problem most have is to confuse shear stress with tensile stress (combined radial, circumferential, longitudinal).  Like the thumb and the toe, they are absolutely different things.  But more confusing, when there is a big plaque, there is high shear stress in the throat it makes with lumenal occlusion. Then, high shear stress may rip open the plaque, causing thrombosis and downstream ischemia.  All the while, tensile stress is proportional to shear stress, and higher tensile stress causes more load on the force bearing elements of the arterial ECM, which invariably only causes one thing:  wear and tear (literally).

With venous systolic pressure up to ten times lower than arterial systolic pressure, it is not difficult to understand why arteries always endure more tensile strain.  Whatever the shear stress condition, tensile strain in the artery is always higher than in a vein, partially explaining why only thrombosis is found in veins but no plaque.  It is interesting to note that a vein placed in the coronary bed for bypass does then suffer plaque stenosis when it never did before.  What is the sudden difference?  Systolic pressure and tensile strain is much higher in the arterial bed.

Yet there are instances when high shear stress contributes to arterial damage, such as a biscupid aortic valve.

You'll see above, that the high shear stress area (which is invariably a zone of high tensile strain) coincides perfectly with proximal aortic dissection, the Stanford Type A, Debakey Type II dissection, as well as a frequent site of aortic root (not sinus) plaques.

Valve-Related Hemodynamics Mediate Human Bicuspid Aortopathy