Misguided Use of Multivariable Analysis to Study Primary Percutaneous Coronary Intervention in Patients With Prior Coronary Artery Bypass Graft.

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Coronary artery bypass graft (CABG) surgery has been a great advance in the treatment of coronary artery disease, but the treatment of saphenous vein bypass graft (SVBG) disease remains a frustrating challenge. Although the natural history of coronary artery disease occurs over decades, the natural history of SVBG disease occurs over years. Denudation of endothelial cells in freshly harvested saphenous veins at the time of CABG results in acute platelet and thrombin deposition that can lead to early SVBG thrombosis if there is poor flow in the graft because of surgical issues or disease in the microcirculation.1 Although the left internal mammary artery (LIMA) graft adapts well to the hemodynamic stress of coronary perfusion, the SVBG must adapt to high-pressure pulsatile arterial flow and that can contribute to chronic endothelial dysfunction. The resulting platelet and leukocyte activation can stimulate smooth muscle cell proliferation that narrows the SVBG lumen diameter. SVBG atherosclerosis, similar to coronary artery atherosclerosis, can develop later, and acute plaque rupture can cause late SVBG thrombosis. See Article by Iqbal et al Compared with native coronary artery atherosclerosis, SVBG atherosclerosis can be more diffuse, the fibrous cap can be weaker and thinner, and the plaque can be more fragile and friable, making it prone to distal embolization of atherosclerotic debris during percutaneous coronary intervention (PCI).1 In patients with acute SVBG thrombosis, the lack of side branches, the larger diameter of the vessel, and consequently, lower flow velocities promote excessive thrombus formation. The more distal the culprit lesion, the greater the thrombus burden in the proximal bypass conduit, and the more likely distal embolization will result in the microvascular no-reflow phenomenon with primary PCI. Early reports on fibrinolytic therapy in patients with ST-segment–elevation myocardial infarction demonstrated lower SVBG reperfusion rates than in native coronary arteries.2, …