Fig. 10.31 Angiosarcoma.(A)Angiosarcomaoftherightventricle.(B)Moderatelydifferentiatedangiosarcomawithdenseclumpsofatypicalcellsliningdistinctvascularlumina.(C)ImmunohistochemicalstainingofangiosarcomafortheendothelialcellmarkerCD31.
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The morphologic changes that occur in vessels following therapeutic intervention—balloon angioplasty, stenting, or bypass surgery—recapitulate many of the changes that occur in the setting of other forms of vascular injury. Local trauma (due to stenting), vascular thrombosis (after angioplasty), and abnormal mechanical forces (e.g., a saphenous vein inserted into the arterial circulation as a coronary artery bypass graft) all induce the same stereotypical healing responses—fibromuscular intimal hyperplastic lesions composed of SMCs and ECM. Thus, just as with atherosclerosis, interventions that injure the endothelium also tend to induce intimal thickening by recruiting SMCs and promoting ECM deposition.
Arterial stenoses (especially those in coronary and carotid arteries) can be dilated by transiently inflating a balloon catheter to pressures sufficient to rupture the occluding plaque (balloon angioplasty); in doing so, a limited arterial dissection also is induced. Angioplasty can be complicated by abrupt reclosure resulting from compression of the lumen by an extensive circumferential or longitudinal dissection, or by thrombosis. In view of this well over 90% of endovascular coronary procedures involve both angioplasty and concurrent coronary stent placement.
Coronary stents are expandable tubes of metallic mesh. They provide a larger and more regular lumen, “tack down” the intimal flaps and dissections that occur during angioplasty, and mechanically limit vascular spasm. Nevertheless, as a consequence of endothelial injury, thrombosis is an important immediate post-stenting complication; patients must receive potent anti-thrombotic agents (primarily platelet antagonists) to prevent acute catastrophic thrombotic occlusions until the stented region becomes endothelialized. The long-term success of angioplasty is limited by the development of proliferative in-stent restenosis. Such intimal thickening results in clinically significant luminal occlusion in up to one third of patients within 6 to 12 months of stenting (Fig. 10.32 ). The newest generation of drug-eluting stents is designed to avoid this complication by releasing anti-proliferative drugs (e.g., paclitaxel, sirolimus) into the adjacent vessel wall that block SMC activation. Use of such stents reduces the incidence of restenosis at 1 year by 50% to 80%.
Synthetic or autologous vascular grafts commonly are used to replace damaged vessels or bypass diseased arteries. Of the synthetic grafts, large-bore (12to 18-mm–diameter) conduits function well in high-flow locations such as the aorta, while small-bore artificial grafts (8 mm or less in diameter) generally fail as a result of acute thrombosis or late intimal hyperplasia, primarily at the junction of the graft and the native vasculature.