Spatial and phasic oscillation of non-Newtonian wall shear stress in human left coronary artery bifurcation: an insight to atherogenesis

Abstract

The lateral walls of the bifurcation, where low and oscillating wall shear stress is observed, are more susceptible to atherosclerosis. The systolic period, rather than the diastolic one, favors the development and progression of atherosclerosis. The blood viscosity properties do not seem to qualitatively affect the spatial and temporal distribution of the wall shear stress.

Elevated heart rate and atherosclerosis: An overview of the pathogenetic mechanisms

“…High heart rate prolongs the exposure of endothelium to low and oscillatory SS By applying sophisticated Computational Fluid Dynamics in realistic arterial models, we and others showed that SS attains a low and oscillatory pattern during systole, whereas in diastole it exhibits an initial steep increment up to its diastolic maximum, and then it slowly declines throughout the rest of diastolic phase until the initiation of the next systole [62,[77][78][79][80] (Fig. 4).…”

“…4). Given the involvement of low and oscillatory SS in atherosclerosis, one could speculate that the systolic period favors the pathophysiological processes responsible for the onset and development of atherosclerosis [77], whereas the steep increase of SS, appearing in diastole, modulates an atheroprotective milieu, compensating for the atherogenic systolic SS values (Fig. 6).…”

“…7). However, as the heart rate increases, the diastolic time gradually decreases, resulting in an increase of the total time spent on systoles per minute relatively to diastole; of note in severe tachycardia the duration of diastole may even become equal to that of systole [74,77]. As a result, in regions susceptible to atherosclerosis high heart rate attenuates the atheroprotective effect of diastole, exposing the endothelium to the atherogenic effect of the systolic low and oscillatory SS for longer periods.…”

Prognostic clinical and angiographic characteristics for the development of a new significant lesion in remote segments after successful percutaneous coronary intervention

“…Davies et al, found a strong correlation between qualitative stenosis morphology and subsequent in-hospital outcome in patients who underwent thrombolysis after acute myocardial infarction [25], supporting the earlier suggestion that coronary stenoses characterized angiographically by a "complex" morphology are prone to rapid progression and destabilization [26]. Another explanation for this finding is the low shear stress, which is prevalent at atherosclerosisprone sites, especially found in bifurcations [27,28].…”

Myocardial bridges are free from atherosclerosis: Overview of the underlying mechanisms

“…The absence of atherosclerosis within bridges and the increased susceptibility of the adjacent proximal segments can be further explained mechanistically (25). In atherosclerosis-prone regions proximal to a bridge, where low and oscillatory SS occur, the residence time of proatherogenic blood particles (eg, lipids, inflammatory cells) and their subsequent subendothelial accumulation increase, facilitating the atherosclerotic process, whereas the normal or high flow occurring within a bridge prevents blood stagnation, thereby protecting the endothelium from atherosclerosis (26).…”