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Deaths Following Cardiac Surgery and Invasive Interventions
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
The most common is poor cardiac function which results from embolism and/or anoxia, hypoperfusion, exacerbation of pre-existing disease, iatrogenic factors and stress. This leads to multi-organ failure with cerebral anoxia, acute renal tubular necrosis, acute pancreatitis and adrenal cortical infarction. Systemic and coronary emboli may occur. Embolized material includes thrombi, fat, bone marrow, air, calcium, atheroma, talc, silicone, platelets and other debris from the perfusion apparatus. Hypoperfusion can lead to cerebral infarction or ischaemic damage to the bowel, without thrombosis or emboli present in these organs. Prolonged bypass can lead to consumption coagulopathy and haemorrhage from cannulation sites. Saphenous vein graft failure is most common within 30 days of operation and is dependent on several factors including vein size and excessive length, distal runoff and slow flow, and hypercoagulability and thrombosis. Alternatively, arterial grafts such as the LIMA and radial arterial grafts remain patent longer and have patency rates exceeding 90% at 10 years.
Pathophysiology and management of saphenous vein graft disease
Published in Expert Review of Cardiovascular Therapy, 2023
Elizabeth C. Ghandakly, Aaron E. Tipton, Faisal G. Bakaeen
Another cellular component of vein graft failure is thrombosis. During harvest and grafting, damage to the endothelium can occur. These areas of damage are prothrombic, resulting in the accumulation of fibrin and platelets. Tissue plasminogen activator production from the endothelium is also reduced resulting in further thrombus formation. Additionally, cardiopulmonary bypass results in the disruption of cellular homeostasis and causes a prothrombic state. This creates an even greater stimulus for thrombosis formation. Overall, the prothrombic state of vein grafts contributes to the development of intramural hyperplasia by accumulating platelets and fibrin and resulting in the formation of a neoendothelium. This progresses to become fibrotic tissue and ultimately contributes to graft failure [29].
Device profile of the VEST for external support of SVG Coronary artery bypass grafting: historical development, current status, and future directions
Published in Expert Review of Medical Devices, 2021
Pathophysiologic mechanisms underlying venous graft failure begin with the harvesting of the saphenous vein conduit and include endothelial cell loss, damage to medial smooth muscle cells and disruption of microperfusion to the vessel wall [4]. Subsequent interposition of the harvested conduit into the aorto-coronary arterial circulation leads to abrupt hemodynamic changes with increased blood pressure, shear stress, wall tension, and pulsatile flow [5]. This new environment induces circumfeggrential, longitudinal and radial stress that result in dilatation of the vein conduit. Additionally, activation of various intracellular signaling molecules occurs thereby stimulating smooth muscle cell proliferation and migration into the media and establishment of intimal hyperplasia [5–8]. Moreover, the arterialization of the vein graft results in disturbed and turbulent luminal flows patterns which promote atherogenesis. The geometric mismatch often seen (small artery – larger vein) also contributes to turbulent flow. A summary of factors implicated in the pathophysiology of vein graft failure are outlined in Table 1. The development of intimal hyperplasia and subsequent graft failure has important clinical implications in patient outcomes as they can presage the development of angina, myocardial infarction, ischemic heart failure and/or death and demand the need for additional percutaneous and/or surgical revascularization procedures with their attendant costs.
Intraoperative storage of saphenous vein grafts in coronary artery bypass grafting
Published in Expert Review of Medical Devices, 2019
Catherine J. Pachuk, Sophie K. Rushton-Smith, Maximilian Y. Emmert
Whereas the mechanisms of vein graft failure are not fully understood, a principal mediator of VGD following grafting in bypass surgeries is intraoperative damage, which occurs during vascular graft harvesting and handling [10–12]. Despite potential injury occurring to grafts during these procedures, VGD is considered a disease of IRI, and isolated conduits must be protected against ischemic injury to reduce the risk of VGD [7]. Solutions that interfere directly with the primary mechanisms of ischemic injury (i.e. oxidative damage and metabolic stress) are needed to avoid functional and structural damage to the graft endothelium. Subanalyses from the PREVENT IV study demonstrated that, compared with other factors, damage associated with the use of inappropriate graft storage solutions (e.g. saline and blood-based solutions) had the highest correlation with 12-month VGF (p < 0.001) [10,11], which is not surprising given that these solutions do not protect against IRI [6,7].