This Is MS Multiple Sclerosis Community: Knowledge & Support

Although balloon angioplasty (percutaneous transluminal angioplasty, PTA) is a well-accepted method to reduce arterial stenosis, an important disadvantage of the method is the restenosis that develops in 30% to 50% of the patients.1 Although it has been accepted that intimal hyperplasia causes the restenosis,2 it recently became clear that restenosis after PTA is caused mainly by shrinkage of the vessel wall ("constrictive vascular remodeling").

Vascular remodeling has been observed in physiological conditions in response to changes in shear stress (SS), where it is aimed at restoring the original values of SS.3 Although it has been postulated that this mechanism is of importance in vascular remodeling after PTA, experimental data underlying this theory are currently lacking.1 This is of importance, because it has been shown that the endothelium plays an essential role in vascular remodeling.4 Immediately after PTA, the endothelium is disrupted and the regenerated endothelial layer is dysfunctional.5 Furthermore, because the vascular tissue is damaged after PTA, factors not involved in vascular remodeling during more physiological conditions might become of importance. Hence, the first question addressed in the present study was whether vascular remodeling after PTA is controlled by SS and if so, to which reference value the SS values will be restored during the remodeling process. To that end, we developed a method based on a combination of intravascular ultrasound (IVUS) and computational fluid dynamics that enables us to calculate regional SS over time.

The vessel wall responds to increments in blood pressure, at an unchanged flow, by increasing vessel wall thickness.6 The wall stresses (WS) calculated before and after these pressure elevations appear to be similar, implying that WS is normalized during these conditions. PTA increases local WS, and the constrictive vascular remodeling may be a consequence of WS normalization. Therefore, the second aim of the present study was to evaluate the existence of a WS feedback loop in constrictive vascular remodeling after PTA.

The positive results obtained with probucol suggest that the restenosis process is associated with oxidative stress. The powerful antioxidant effects of probucol18 may have prevented endothelial dysfunction,19 LDL oxidation,20 and macrophage and metalloproteinase21 activation. This could have limited smooth muscle cell activation, migration, and proliferation; matrix degradation; and deposition of new collagen fibers. By ultimately limiting smooth muscle cell contraction, collagen formation and cross-linking, and endothelial dysfunction, probucol may have modified vascular remodeling and allowed greater vessel enlargement. Specific inhibition by probucol of the secretion of interleukin-122 may also have decreased secretion of metalloproteinases23 and modified matrix remodeling.

An article on the effect of probucol, a powerful antioxidant, in reducing restenosis possibly due to vascular remodeling.
What I take from this, for something we can do as patients, is that an endothelial health program may be of especial importance in the months following angioplasty.

Cure, I am apparently going to disagree with you on every thread, but it is nothing personal.