~10% per year, with a dramatic reduction to 2% per year after CABG, the largest mortality benefit of CABG in any subgroup of patients.101,102
Appendix 1. Notes on various surgical grafts
A. SVG
1. General SVG outcomes
SVG grafts occlude at the following rates: ~10% in the first month, 15–25% in the first year, and 2–4% per year beyond the first year. Thus, the fastest occlusion rate occurs in the first year, and at 10 years, 50% of SVGs are occluded (Table 3.6). In addition, 20–40% of patients have native disease progression in non-grafted vessels or in grafted vessels distal to the anastomoses at 5–10 years of follow-up.
CABG patients who present with ACS often have an SVG culprit. However, < 50% of SVG occlusions lead to MI (STEMI or NSTEMI), the remainder being either silent or leading to stable angina;83 this depends on the status of the native vessel and the presence of collaterals. Overall, MI occurs at a rate of ~1–2% per year, and additional revascularization is required in ~15–20% of patients at 5 years (CASS, SYNTAX trials).84
Table 3.5 CAD mortality.
| Older data of medically treated CAD patients (CASS registry) 99,100 One- or two-vessel CAD: 1.5–2% mortality per yr Three-vessel CAD with normal EF: 4.5% mortality per yr Multivessel CAD with EF <35%: 10% morality per yr Contemporary data in non-extensive single or multivessel CAD, treated with PCI or medical therapy (COURAGE, BARI 2D PCI group) 1.5% mortality per yr 8-10% cardiovascular event rate in first yr, then 2% per yr Contemporary data in patients with multivessel CAD and normal EF undergoing CABG or PCI (SYNTAX, FREEDOM, BARI 2D CABG group) 2–3% mortality per yr (after a higher 1st-yr mortality of 3.5%) 12.5% overall death or cardiovascular event rate in first yr, then ~3% per yr (27% for CABG vs. ~37% for PCI at 5 years in complex patients) Contemporary data in multivessel CAD with EF <35% but no or mild HF (STICH) 6.5% mortality per yr with CABG, 8% mortality per yr with medical therapy (mortality would be higher with worse HF status) |
Mortality is higher in patients with ACS, low EF, symptomatic HF, or comorbidities.
Table 3.6 Causes and histology of SVG failure.
| < 1 month Graft thrombosis, often before hospital discharge, sometimes related to distal native disease past the anastomosis or to technical issues (anastomotic stenosis from the suture, SVG kinking or stretching) 1 month to 1–3 years Fibrointimal hyperplasia leads to peri-anastomotic or mid-graft stenosis: exposure of the vein to the arterial pressure leads to endothelial injury with formation of a hard neointima, called fibrointimal hyperplasia >1–3 years Atherosclerosis starts to develop at >1–3 years, with similar risk factors to native atherosclerosis As compared with native atherosclerosis, SVG atherosclerosis is more extensive, friable, with more foam cells and no fibrous cap, and may be mixed with thrombi. Aggressive lipid lowering slows down this process |
2. Factors determining SVG patency
Early and late SVG patency is dependent on a good flow through the graft and requires: (i) good distal runoff and good size of the recipient artery (>1.5–2.0 mm) without distal disease; (ii) significant proximal disease in the recipient artery (otherwise, the flow through the recipient artery prevents appropriate flow through the graft); (iii) well-matched size of the graft and recipient artery.103-105 This dependency on size and flow explains that SVG graft to LAD has higher patency than SVG to RCA or LCx, and that SVG to a diagonal or to a small vessel has the lowest patency. Of note, FFR-guided CABG, wherein only vessels with significant FFR are grafted, did not significantly improve clinical outcomes or graft failure compared to angiography-guided CABG (FARGO trial) (unlike the benefit of FFR-guided PCI);106 moreover, the disease progressed quickly after CABG, within 6 months, in vessels with insignificant FFR (from a mean of 0.89 to 0.81, with 40% of vessels progressing from insignificant to significant FFR). Also, in a patient who already needs CABG, adding a graft to a moderately obstructed territory may still protect it from infarcts.
3. Treatment of SVG failure
*In the first 30 days, ST elevation is often the result of venous graft thrombosis with distal embolization, which worsens the perfusion of a previously stable territory subtended by a stenotic artery or by collaterals. Since the main issue is distal embolization, routine PCI for every post-CABG ST elevation may not be helpful. If there is a clinical, arrhythmic (VT), or hemodynamic manifestation of ischemia, the patient often needs to be revascularized. Reoperation may need to be performed the first day after CABG; beyond the first day, angiography may be performed to identify the problem and potentially treat anastomotic SVG disease or native distal disease with PCI. If a thrombotic SVG occlusion is found, PCI of the native artery may be attempted if possible. A review of the preoperative anatomy is critical: e.g., an expected occlusion of a graft supplying a small distal RCA may not have any revascularization option when the native RCA has a CTO. ST elevation may also result from arterial graft spasm.
*Beyond the first 30 days, when SVG disease develops, it is best to treat the native artery if possible, as long-term patency of a percu-taneously treated SVG is low. If the native artery is not amenable to PCI (CTO), SVG PCI is performed, unless the SVG is also chronically occluded, in which case medical therapy is the best initial option. Location and timing of the disease determine long-term success. Distal SVG stenosis has the best long-term success rate with PCI, especially when it occurs within the first few years after CABG, in which case it is due to intimal hyperplasia without atherosclerosis (20% restenosis after plain angioplasty). Mid-shaft disease has intermediate long-term success rate, while proximal disease has the lowest success rate.
Regarding timing, disease occurring at <1–3 years without significant atherosclerosis has the best long-term success.107,108 In fact, the extent of atherosclerosis >1–3 years after CABG is a major determinant of long-term success. Treating the focal lesion, particularly a proximal lesion, does not prevent the eventual progression of the diffuse atherosclerotic disease and the eventual ~50% occlusion rate at 2 years. While DES may prevent the focal restenosis, it does not eliminate this aggressive disease progression outside the stented area and the long-term occlusion risk of diffusely diseased grafts. Degenerated SVGs with diffuse atherosclerosis have a high adverse event rate at 2 years (up to 45%), even if SVG stenosis is only moderate.109
Patients with multiple failing SVGs and no patent graft to the LAD have an indication for redo CABG, unless the operative risk is prohibitively high.
B. LIMA
LIMA graft is usually used as an in-situ graft: the distal part of the LIMA is connected directly to the LAD, while the proximal LIMA is not touched and remains connected to the subclavian artery. LIMA atherosclerosis is extremely uncommon, hence the excellent long-term patency of 90% at 10 years; a LIMA that is patent beyond the first few months post-CABG usually remains patent for life. LIMA has an intact internal elastic membrane that prevents smooth muscle migration and atherosclerosis. Early LIMA failure is possible, however, and is related to anastomotic fibrointimal hyperplasia or to poor LIMA development. LIMA may not develop or may regress because of a subclavian stenosis, poor distal LAD flow, or insignificant proximal LAD stenosis. Significant native proximal disease is necessary to allow SVG and, more particularly, LIMA and radial grafts to remain patent; a good native flow may impede SVG or LIMA flow, leading to thrombosis of the SVG or spasm of an arterial graft. In fact, bypassing a LAD that has <50–60% stenosis leads to disuse atrophy of the