Mechanisms, Consequences, and Prevention of Coronary Graft Failure

Abstract

Graft failure occurs in a sizeable proportion of coronary artery bypass conduits. We herein review relevant current evidence to give an overview of the incidence, pathophysiology, and clinical consequences of this multifactorial phenomenon. Thrombosis, endothelial dysfunction, vasospasm, and oxidative stress are different mechanisms associated with graft failure. Intrinsic morphological and functional features of the bypass conduits play a role in determining failure. Similarly, characteristics of the target coronary vessel, such as the severity of stenosis, the diameter, the extent of atherosclerotic burden, and previous endovascular interventions, are important determinants of graft outcome and must be taken into consideration at the time of surgery. Technical factors, such as the method used to harvest the conduits, the vasodilatory protocol, the storage solution, and the anastomotic technique, also play a major role in determining graft success. Furthermore, systemic atherosclerotic risk factors, such as age, sex, diabetes mellitus, hypertension, and dyslipidemia, have been variably associated with graft failure. The failure of a coronary graft is not always correlated with adverse clinical events, which vary according to the type, location, and reason for failed graft. Intraoperative flow verification and secondary prevention using antiplatelet and lipid-lowering agents can help reducing the incidence of graft failure.

Minimally invasive multivessel coronary bypass surgery: Angiographic patency data

“…In addition to the above, it should be concluded that, in general, the ITA grafts demonstrated better patency rates over the SVG grafts, which is in agreement with the published rates of the postoperative graft patency for both the arterial and venous types of conduits 14 . In our experience, approximately every 4th graft to the diagonal branch was found occluded during the follow‐up.…”

Do storage solutions protect endothelial function of arterialized vein graft in an experimental rat model?

“…At mild term a graft failure can appear, and it is histologically characterized by an intimal hyperplasia (IH) which is a proliferation of smooth muscle cells (SMC) and a deposition of extracellular matrix (ECM) in the intima. An atherosclerosis mechanism is observed with a risk of vein graft thrombosis [4,5].…”

Hemostasis parameters in patients after coronary artery bypass surgery for stable angina

“…Одной из важнейших проблем коронарной хирургии является рецидив ишемии миокарда после КШ (возврат стенокардии, инфаркт миокарда (ИМ)), чем обусловлена потребность в повторных коронарных вмешательствах [2]. Морфологическим субстратом этих исходов, как правило, является недостаточность шунтов из-за их тромбоза, гиперплазии интимы, прогрессирования атеросклероза [3]. При этом пациенты с СД2 имеют худший прогноз после КШ в сравнении с лицами без нарушений углеводного обмена [4].…”