Intimal Hypertrophy

However, small diameter arterial prostheses made of this nonthrombo-genic material occluded at the anostomosis within 4 to 10 days after implantation. We hypothesized that this failure was due to a difference in wall elasticity between the prosthesis and the artery which caused trauma to the arterial wall and stimulated intimal hypertrophy (23). Initial results using a more compliant form of the prosthesis showed improved patency giving support to this hypothesis. To investigate this hypothesis further and eliminate variables in the initial studies, we developed a technique to vary the elasticities of the prostheses made from this urethane polymer and yet maintain other properties more constant. 

Histological examination of specimens removed after one month demonstrated that some intimal hypertrophy had occurred in all arteries near each anostomosis. In the prostheses that failed, the hypertrophy had obliterated the lumen. At the time of this writing, prostheses whose compliances match the natural artery have been... 

The heart may be enlarged with left ventricular hypertrophy, particularly in cases which have exhibited hypertension during life. Metastatic calcification of the valves and of the myocardium may be present, explaining no doubt the cardiac murmurs which may have been detected clinically in such cases. Occasionally, medullary proliferation of large arteries and, in the smaller arteries, fragmentation of the intimal elastic lamina has been reported, in one case with impregnation with calcium salts. Local calcification of the media of the middle cerebral artery has been described. 

Overall, this volume provides a detailed analysis of a wide range of signal transduction systems that mediate hypertrophy, intimal hyperplasia, oxidative damage, contractility, cardiovascular protection, and remodeling. Many components of these signaling pathways are potential targets to develop new therapeutics to treat cardiovascular disorders. 

Biopsy specimens of PAH include constrictive lesions and complex lesions. Constrictive lesions comprise medial hypertrophy and intimal thickening. Medial hypertrophy is defined as the increase in both number and cross-sectional area of the SM cells lining the walls of the pre- and intra-acinar pulmonary arteries intimal thickening implies an increased number of fibroblasts in the thin layer between a SM cell and lamina propria of the blood vessel. These changes can be seen in both IPAH and pulmonary venous hypertension. In contrast, complex lesions are considered pathognomonic for PAH. The complex or plexiform lesion consists of focal proliferation of endothelial channels consisting of fibroblasts, SM cells, and connective tissue matrix. These lesions disrupt vascular vessel wall and serve as a nidus for in situ thrombosis. 

There was a minimal response to inhaled nitric oxide that was clinically unimportant in the patients with primary pulmonary hypertension and Eisen-menger s complex in whom intimal proliferation and hypertrophy obliterate small pulmonary vessels and reduce the pulmonary vascular cross-sectional area. The pulmonary arteriopathy of pulmonary venous hypertension resembles, in many ways, the pulmonary vascular changes of normal aging, in contrast to the vessel histology in pulmonary vascular obstructive disease. Therefore, the poor response to nitric oxide in the patients with advanced pulmonary vascular disease was not surprising. Indeed, the response to vasodilator therapy has been shown to be reduced in patients with an increased intimal area on lung biopsy. ... 

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