Pathology of Saphenous Vein Grafts

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Key points

  • Saphenous vein grafts (SVGs) are susceptible to accelerated atherosclerosis as compared with native coronary arteries, thus limiting the long-term benefits of coronary artery bypass graft surgery.

  • As early as the first year after surgery, thickening of the wall by neointimal growth and infiltration of foamy macrophages is observed.

  • SVG stenosis is associated with the development and expansion of necrotic cores and the occurrence of hemorrhage, leading to expansion and eventually rupture of the

Early changes

Within the first 72 hours after placement, a thin layer of platelets and fibrin is deposited along the vein graft intimal surface. During this period, acute inflammatory cells are often present in the walls of the grafts. Diffused intimal hyperplasia consisting of smooth muscle cells in a proteoglycan and collagen matrix is always observed in vein grafts in place for over 1 month.9, 10, 11, 12 The mechanism of this remodeling process11 is believed to involve responses to endothelial injury and

Vein graft thrombosis

Early graft failure due to thrombotic complications may occur secondary to damage to the vein itself during harvest and insertion, leading to excessive endothelial injury; poor run-off due to plaque present at the anastomosis and/or severe distal native coronary atherosclerosis; or technical factors (eg, graft twisting or kinking or distal arterial dissection during creation of the anastomosis).8, 11, 18, 19, 20 Vein graft occlusion rates within the first postoperative month range from 3% to

Chronic vein graft vasculopathy: fibrointimal hyperplasia and atherosclerosis

For most vein grafts, vasculopathy develops as an insidious lesion that is a major cause of morbidity and mortality. With the continued high volume of patients treated with CABG surgery and the aging of the population, the rates of repeat revascularization procedures (catheter-based and repeat CABG surgery) are increasing. During the first 6 years after CABG surgery, the rate of vein graft occlusion is 1% to 2% per year; from 6 to 10 years postoperatively, the occlusion rate increases to 4% per

SVG disease—risk factors

Risk factors for native coronary artery atherosclerosis, particularly abnormal serum lipids, have also been correlated with atherosclerosis of bypass vein grafts.17, 25, 26, 27, 28 From clinical studies of the known atherosclerotic risk factors, elevated serum total cholesterol, low-density lipoprotein (LDL) cholesterol and triglycerides, and low serum high-density lipoprotein (HDL) cholesterol levels appear to be important in the development of chronic vein graft atherosclerosis.29, 30, 31

SVG atherosclerosis: progression

To examine the progression of vein graft atherosclerotic lesions, the authors recently performed serial sectioning of morphological assessment of 31 SVGs from 16 patients in whom vein grafts were in place at least 2 years (mean age of vein graft 8.5 ± 5.9 years, range 2–22 years).35 There were 589 vein graft sections examined, of which 333 demonstrated fibrointimal thickening (FIT), and the remaining 256 showed atherosclerotic changes. Atherosclerotic lesions were classified as: intimal

SVG disease: comparison to coronary atherosclerosis

The histology of SVG atherosclerosis differs somewhat from native coronary atherosclerosis and may reflect the relatively rapid development of atherosclerotic disease in vein grafts less than 10 years. Typically, advanced atherosclerosis in vein grafts consists of a friable foam cell-rich lesion containing a large lipid (necrotic) core or several cores and a thin fibrous cap.6, 38, 39 Intraplaque hemorrhage within the large core is common (see Fig. 3), even in small plaques, but fibrocalcific

SVG failure: anastomosis

The proximal and distal sites of anastomosis (junction between graft and host vessel) are frequent sites of late graft failure, an effect that is partly related to adaptive responses to hemodynamic factors including wall shear stress.46, 47 Within the authors’ study at the aortic anastomosis, approximately 67% of sites showed only fibrointimal proliferation, and 33% of sites had atherosclerotic plaque (with or without lipid core formation). At the distal anastomosis of the SVG to the native

Summary

Compared with native coronary arteries, SVGs undergo more rapid atherosclerotic lesion development, thus limiting the long-term benefits of CABG surgery. As early as the first year after surgery, thickening of the wall by neointimal growth and infiltration of foamy macrophages are observed. SVG stenosis is associated with the development and expansion of necrotic cores and the occurrence of hemorrhage, leading to expansion and eventually rupture of the plaque. A thorough understanding of the

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  • Cited by (9)

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      According to a functional classification of arterial grafts, the ITA is a somatic artery with considerable amounts of elastic lamellae and with a lower tendency towards spasticity than other autologous conduits used for CABG (He, 2013). Other commonly used autologous grafts include radial artery (Gaudino et al., 2005), saphenous veins (Yazdani et al., 2013), the right gastroepiploic artery (Martínez-González et al., 2017) and some other rarely used alternative grafts used in patients with a complete lack of suitable conduits (Loskot et al., 2016). Blood vessel replacement with a small-diameter (<6 mm) graft represents the holy grail of peripheral vascular surgery (Kakisis et al., 2005).

    • Update on Cardiac Catheterization in Patients With Prior Coronary Artery Bypass Graft Surgery

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      Whereas atherosclerosis in coronary arteries takes decades to develop, accelerated atherosclerosis is observed in SVGs within months to years, often in a more concentric and diffuse pattern with less well-defined fibrous cap that likely responds differently to DES. Second, neoatherosclerosis occurs earlier in DES compared with BMS, which may lead to a catch-up phenomenon (61,62). Third, thin-strut BMS may have lower risk for restenosis in SVGs than thicker strut stents that were used in most prior studies.

    • Shedding Light Into Late Saphenous Vein Graft Failure

      2019, Cardiovascular Revascularization Medicine
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      Although the authors confirm the need for designated interventional strategies for late SVG failure, their report does not provide imaging insights of treated lesions following PCI, which leaves us with uncertainty of how those lesion characteristics impact on PCI results. Obstructive atherosclerotic lesions in native coronary arteries develop over decades, whereas accelerated atherosclerosis has previously been reported in SVGs within months to years in seminal autopsy studies [16,17]. Early changes can be observed within the first 72 hours after grafting, exhibiting a thin layer of platelets and fibrin deposited along the intimal surface of the vein graft [16].

    • The spectrum of clinical presentations and management options for the treatment of degenerative atherothrombotic disease of saphenous vein grafts

      2018, Cardiovascular Thrombus: From Pathology and Clinical Presentations to Imaging, Pharmacotherapy and Interventions
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    Dr Virmani is a consultant for Medtronic AVE, Abbott Vascular, W.L. Gore, Atrium Medical, Arsenal Medical, and Lutonix.

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