The Roles of Vascular Smooth Muscle Cells in the Aortic Wall Thinness under Prolonged Continuous Flow Left Heart Bypass

Abstract

Aortic wall thinness was one of the most characteristic changes observed in experimental animals under prolonged continuous flow left heart bypass. The goal of this study was to determine the roles of smooth muscle cells in the vascular remodeling process in cases demonstrating aortic wall thinness under prolonged continuous flow left heart bypass. The aortic samples from three goats in which continuous flow left heart bypass was performed were subjected to histological and immunohistochemical analyses. After 4 weeks of observation, the pulse pressure in the goats under the continuous flow left heart bypass was clearly lower than that in the normal healthy goats. The aortic walls of these goats became thinner, an effect caused by the dilation of their internal diameter. These aortic smooth muscle cells maintained contractile formation due to the fact that they contained abundant alpha-smooth muscle actin (SMA) and smooth muscle myosin heavy chain (SMMS). These cells also synthesized redundant matrix metalloproteinase-2 and -9, and the ratio of the SMMS-positive to the SMA-positive area was significantly lower (0.76) than that observed in the control goat (1.00; P < 0.05). The smooth muscle cells demonstrated synthetic-dedifferentiated formation, which is one of the phenotypes of smooth muscle cell function. In conclusion, aortic wall thinness under prolonged continuous flow left heart bypass is caused by over-synthesis of matrix metalloproteinase in smooth muscle cells, and this refers the vascular remodeling process of the extracellular matrix.

Rapid Speed Modulation of a Rotary Total Artificial Heart Impeller

“…In the clinical setting a limited fluid volume is available in the atrial remnants and inflow cuffs of the RBP, which can result in a high risk of atrial suction, especially at high pulse amplitudes or due to mismatched vascular resistances. Furthermore, a potentially increased risk of damage to the remodeled arterial tree due to excessively high flow rates and pressure gradients should be evaluated and weighed against the risk of vascular malformations due to perfusion with diminished pulsatility . These factors warrant the requirement of a wide range of preclinical studies and careful application of pulsatile operation modes, where generating the maximum achievable pulsatile output may not be the favorable operation strategy.…”

“…Rotary VAD support with diminished pulsatility is a well‐established therapy, and its clinical outcomes are comparable with or superior to those of positive‐displacement VADs . However, multiple studies indicate that pulsatile perfusion may improve patient quality of life by potentially enhancing the baroreceptor reflex, reducing the occurrence of arteriovenous malformations, improving microcirculatory perfusion, and reducing the risk of thrombus formation in potential stagnant flow areas. In contrast, rapid acceleration during pulsatile speed modulation is associated with increased blood shear stress, which may increase the patient's risk of developing acquired von Willebrand syndrome .…”

Artificial Organs 2003: A Year in Review

“…Toshihide Mizuno et al of the National Cardiovascular Center Research Institute investigated the role of vascular smooth muscle cells in the vascular remodeling process in cases demonstrating aortic wall thinness under prolonged continuous flow left heart bypass (35). Aortic wall thinness is caused by over‐synthesis of matrix metalloproteinase, and this refers to the vascular remodeling process of the extracellular matrix.…”