Angiogenesis between coronary grafts through the aortic wall.

Following a total coronary occlusion, residual perfusion to the myocardium persists through native coronary collateral channels. Provided that they are of adequate size, collateral circulation may protect against myocardial infarction and death [1]. However, there is tremendous individual variability in the function of those neovascularizations among patients with chronic stenosis. Thus, the detailed mechanism of collateral artery growth is still unknown in the human adult. This report describes a case of a 61-year-old man that was admitted with progressive angina (CCS III on admission) for the last 3 months. He had a previous history of hypertension, dyslipidemia and insulindependent diabetes and two surgical myocardial revascularizations performed 14 and 8 years prior to admission. Medications taken on a daily basis included atenolol, amlodipine, trimetazidine, propatylnitrate, atorvastatin, metformin and insulin. Tc-Sestamibi Scintigraphy demonstrated irreversible defect of basal-inferior wall and moderate reversible defect of anterior-apical wall, along with reduced ventricular function during exercise. Coronary angiography showed occlusion of native vessels, pervious left internal mammary graft to a marginal branch and collateral circulation (CC) grade III to right coronary artery. Moreover, there was an ostial occlusion of a free right internal thoracic artery graft (RITA) to left anterior descending artery, which had a delayed filling through CC from a saphenous vein graft (SVG) to a