Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 214

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