Are intramural suction-squeezing effects generated by the variations in radial wall stress during each heart beat the motor of atherosclerosis? A new concept.
In the early sixties, the existence of predilection sites for atherosclerotic lesions inside the arterial circulation led to the concept that low wall shear stress (WSS) was responsible, together with systemic factors like high blood pressure, hypercholesterolemia, or diabetes, for the genesis and progression of atherosclerosis. It was found later that oscillating WSS and high WSS gradients could also be incriminated. Yet, this concept, which is broadly accepted today, fails to explains several facts, for instance that some arteries (e.g. epicardial coronary arteries) are more prone to become atherosclerotic than other ones exposed to the same systemic factors (e.g. hepatic and brain arteries). In this paper, we present a quite different concept. It is based on the fact that the increase in intravascular pressure and flow that occur in the arteries during systole generates, at the predilection sites of atherosclerotic lesions (bends, bifurcations, and branchings), an increase of radial wall stress in the outer layers of the arterial wall so that this stress becomes momentarily tensile. These cyclic stress increases have a suction effect that is likely to facilitate the diffusion of atherogenic cells and substances inside the wall. Furthermore, since arteries are not primarily structured to resist inversions of radial stress, they may also create damages (e.g. disruptions of cell membranes and elastic lamellae) followed by inflammations and micro-haemorrhages in the wall. This new concept may provide a complementary (or possibly alternative) explanation of atherosclerosis.
Doriot
P-A
PA
Cardiology Division, University Hospital of Geneva, Micheli-du-Crest 24, CH-1211, Geneva, Switzerland. pierre-andre.doriot@hcuge.ch <pierre-andre.doriot@hcuge.ch>
D000818:Animals; D050197:Atherosclerosis / Q000175:diagnosis* / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D001808:Blood Vessels / Q000473:pathology; D002320:Cardiovascular Physiological Phenomena; D003331:Coronary Vessels / Q000033:anatomy & histology / Q000473:pathology*; D004730:Endothelium, Vascular / Q000473:pathology; D006801:Humans; D008954:Models, Biological; D008955:Models, Cardiovascular; D015233:Models, Statistical; D008962:Models, Theoretical; D011312:Pressure