Abdominal aortic aneurysms (AAAs) are characterized by structural deterioration of aortic wall leading to progressive dilatation. The histopathological changes in AAAs are particularly evident within the elastic media, which is normally comprised mainly of vascular smooth muscle cells (SMCs). There are vascular myosin heavy chain (MHC) isoforms; SM2 is specifically expressed in differentiated SMCs and SMemb is a nonmuscle-type MHC abundantly expressed in SMCs of the fetal aorta with an immature phenotype. Although AAA altered expression of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), pathophysiological role of SMC phenotypic modulation in the AAA progression remains uncertain. To determine whether phenotypic modulation in vascular SMCs contributes to arterial medial degeneration, we examined MHC expression in SMCs of AAA. Aortic specimens were obtained from patients with slowly progressed AAA (n = 12) and rapidly progressed AAA (n = 5), and compared with normal aortic tissue (n = 3). Immunohistochemical staining was performed for detection of SMemb, SM2, MMP (types 2 and 9) and TIMP (types 1 and 2). Faint SMemb and abundant SM2 were observed in normal aorta, while the balance shifted to SMemb predominance in AAAs. Compared with slowly progressed AAA tissue, rapidly expanded AAA tissue demonstrated marked increases in SMemb expression with suppressed SM2. Predominant SMemb expression indicates presence of phenotypic modulated SMCs and enhanced MMP; while abundant TIMP was seen in mature SMCs expressing SM2. SMemb expression is markedly increased in AAA with MMP enhancement, and a significant imbalance between SMemb and SM2 results in rapid progression of AAA.

Aged↗

PubMedDate not supplied

Pathological study of implanted dacron grafts in surgery of thoracic aortic aneurysms.

We studied woven dacron grafts that had been implanted in 5 patients of thoracic aortic aneurysms. In addition to usual stains, immunocytochemical analysis was performed using monoclonal antibodies to the muscle actin (HHF35) and to the macrophage (HAM56). In the graft of 5 and 24 days implantation, thin thrombi containing red cells and fibrin covered the luminal surface in some places, and macrophages came into the thrombi. In the grafts of 12 and 38 months implantation, intimal hyperplasia of 0.2-1.0 mm thickness was seen at the anastomotic segments with the accumulation of smooth muscle cells. Except for the anastomotic segments, connective tissue matrix with collagen fibers covered the luminal surface, and in some hollows of the graft crimps, old and fresh thombi were seen in layers. Organizing thrombi of 1.0 mm thickness attached where the branched graft was anastomosed to the main graft. Anastomotic intimal hyperplasia in the graft of 148 month implantation was 0.4-1.0 mm in thickness and 5-10 mm in length, and aside from the intimal hyperplasia, an endothelial lining did not cover the luminal surface of the graft. In the thoracic aorta, woven dacron graft implantation did not cause a critical stenosis with the intimal hyperplasia. The mural thrombi formed at the branched graft, however, threatened to result in graft occlusion or embolization.

Aortic Aneurysm, Thoracic↗