Conclusion
Disparities in α-SMA expressions in the aortic tissues of the three groups represent the extent of SMC degenerations or a phenotypic switching between contractile and synthetic SMCs. The results imply severe SMC degenerations in patients with aortic aneurysm, which may be beneficial because of the production of extracellular matrix necessary for healing of the vascular wall, but severe disruptions in elastic fibers in patients with aortic dissection. Patients with coronary artery disease show slight SMC degeneration and phenotypic switching among the three groups. The possible apoptotic and genetic mechanisms of aortic structural impairments warrant further elaborations.
Methods
Forty-nine consecutive patients scheduled for surgical treatment for acute type A aortic dissection (20 patients), aortic aneurysm (9 patients), and coronary artery disease (20 patients) were included. Surgical specimens of the aorta were obtained and prepared for hematoxylin and eosin and immunohistochemical stainings.
Objective
The is to report immunohistochemical observations of aortic α-smooth muscle actin (SMA) expressions in patients with aortic aneurysm, acute aortic dissection, and coronary artery disease and to discuss phenotypic switching of smooth muscle cells (SMCs) of these lesions.
Results
A comparison of aortic structural changes between the three groups showed that patients with coronary artery disease had the least severe aorta degeneration with the most intense α-SMA positivity. Aortic structural impairment was the most severe in patients with aortic dissection, whereas α-SMA positivity was more intense in patients with aortic dissection than in those with aortic aneurysm.