Fig. 11.1
Intravascular images (a, b) and histologic sections (c, d) of a newly harvested saphenous vein in ex vivo study [5]. Intravascular ultrasound (a) shows single-layered appearance. Angioscopy (b) shows whitish and smooth surface. Corresponding histologic sections (c, d) demonstrate thin intima (I) and vessel wall (W) mainly consisting of smooth muscle cells and collagen fibers (elastic van Gieson stain)
11.2.2 Early Changes in Saphenous Vein Graft
Depending upon the harvesting technique, denudation of endothelial cells is frequent in freshly harvested veins before their insertion. The endothelium often appears disrupted and the intimal surface is usually covered, partially or completely, by fibrin. Endothelial injury exposes the thrombogenic subendothelium and media to circulating blood. Platelets become activated at the site of injury and play a central role in the initiation and progression of mural platelet thrombosis. Also, platelet activation leads to release enough platelet-derived growth factors to stimulate the slow and gradual process of primary intimal smooth muscle cell proliferation and secondary smooth muscle cell proliferation, the cell migrated from the media to the intima [7, 8]
Minimal medial edema and disruption of adventitia occur just after harvesting SVG. Mural edema becomes more pronounced, some medial smooth muscle cells become necrotic, and inflammatory infiltrates are present in the next 2 weeks. The smooth muscle fibers of the media gradually diminish in number and are replaced, in part or in whole, by fibrous tissue.
Fibrous tissue also increases in the adventitia, and its elastic fibers become severely disrupted or disappear completely. Organizing fibrin on the external surface of the SVG probably contributes to the adventitial fibrosis. Thus, the SVG becomes a fibrous-tissue conduit [6].
11.2.3 Late Changes in Saphenous Vein Graft
The principal changes of SVG body at more than 2 years after CABG are concentric circumferential fibrointimal proliferation and fibrotic-atrophied medial layer at angiographically normal sites (Fig. 11.2) [5].
Fig. 11.2
Intravascular images (a, b) and histologic sections (c, d) of the late stage saphenous vein graft in ex vivo study [5]. Intravascular ultrasound (a) shows triple-layered appearance. Angioscopy (b) shows whitish and smooth surface. Corresponding histologic sections (c, d) demonstrate concentric circumferential fibrointimal proliferation (I), fibrotic-atrophied media (M), and adventitia (Ad) (elastic van Gieson stain)
Further, atherosclerotic changes can be seen in SVG bodies with irregular luminal border, luminal narrowing, or occlusion in angiography. Lipid is present as intracellular lipid (foam cells, i.e., lipid-laden macrophages) located near the luminal surfaces of the intimal fibrous tissue, which does not narrow the lumen appreciably, and extracellular lipid deposits located deeper in the plaque, separated from the lumen by a layer of fibrous tissue, which significantly contribute to luminal narrowing. Hemorrhage into plaque is found into the lipid portion only and luminal narrowing is more common in SVGs with plaque hemorrhage than in those without. Luminal thrombus is sometimes present and small calcium deposit can be seen but it is not so often [6] (Fig. 11.3).
Fig. 11.3
Intravascular images (a, b) and histologic sections (c) of the late stage saphenous vein graft in ex vivo study. Intravascular ultrasound (a) shows eccentric plaque. Angioscopy (b) shows localized yellow plaque. Corresponding histologic section (c) demonstrates large atheromatous plaque (elastic van Gieson stain)
11.3 Angioscopic Findings of Saphenous Vein Graft
11.3.1 Early Stage
Angioscopy demonstrates whitish and smooth surface of lumen in a newly harvested SVG without fibrointimal proliferation (Fig. 11.1) and angiographically normal SVG within 1 year after CABG (Fig. 11.4). SVG has sometimes discrete or diffuse narrowing even in the early stage after CABG, where angioscopy shows whitish and smooth luminal narrowing indicating excessive fibrointimal proliferation in the SVG (Fig. 11.5) [5].
Fig. 11.4
An angiogram (a) and intravascular images (b–e) of the early stage saphenous vein graft [5]. Intravascular ultrasound (b, c) shows single-layered appearance at the sites in the angiogram (1, 2). Angioscopy (d, e) shows whitish and smooth wall
Fig. 11.5
An angiogram (a) and angioscopic images (b–e) of narrowed saphenous vein graft at the early stage. An angiogram shows stenosis (arrow) at proximal portion of the SVG. Angioscopy (b–e) demonstrates whitish and smooth luminal narrowing at the same site
11.3.2 Middle Stage
Angioscopy also reveals whitish and smooth surface of the lumen in angiographically normal SVG at 1–2 years after CABG and whitish and smooth tapered lumen at stenosis of the SVG, where histology of tissue resected by directional coronary atherectomy demonstrates fibrointimal proliferation containing elastic fibers (Fig. 11.6) [5].
Fig. 11.6
An angiogram (a–c), intravascular images (d–g) and corresponding histologic section (h) resected by directional coronary atherectomy in the middle-stage saphenous vein graft [5]. An angiogram (a) shows a discrete stenotic lesion (thick arrow). Angioscopy (g) shows whitish luminal narrowing. Intravascular ultrasound reveals triple-layered appearance (d, f) (small arrows) at site 1, 2 and residual plaque (e) with homogeneous dense echo at site 2 after directional coronary atherectomy (b, c). Histology of resected specimen (h) demonstrates thickened intima with elastic fibers (elastic van Gieson stain)
11.3.3 Late Stage
Angioscopy shows whitish and smooth luminal surface in angiographically normal SVG even at several years after CABG, where diffuse and circumferential intimal proliferation is revealed by ex vivo evaluation of the histology (Figs. 11.2 and 11.7) [5]. In angiographically irregular or narrowed sites in the SVGs, angioscopy reveals yellow atheromatous plaques with smooth surface or sometimes friable appearance corresponding to lipid-rich atheroma with necrosed tissue shown by histology (Figs. 11.2, 11.8 and 11.9) [5]. Friability is defined as the presence of fragmented and loosely adherent plaque lining the vessel wall corresponding to mass of foam cells or lipid debris with very thin or partially lacked fibrous cap (Figs. 11.10 and 11.11) [9]. This is a specific finding in the vein graft disease which is absent in the culprit lesion of native coronary artery in patients with unstable angina [10]. Also, ulceration with or without red thrombus and white thrombus or mass of fibrin floating in blood-flushing fluid can be seen by angioscopy (Fig. 11.12).
