994-99 Can Late Saphenous Vein Graft Closure Be Predicted by Quantitative Angiographic Analysis Before the Clinical Event?

Angiographic parameters predicting the likelihood of late occlusion of saphenous vein grafts (SVG) have been infrequently described. The Post-CABG Study, a 5-year trial aimed at reducing SVG closure in minimally symptomatic patients 1–11 years Post-CABG, offers a unique view into this event since this study requires an angiogram to document baseline graft patency. In this preliminary study we performed quantitative angiographic analysis (QAA Reiber) comparing the baseline Post-CABG study angiogram to an unscheduled “clinically driven” angiogram. Of 1253 enrolled patients with at least one patent SVG, 35 developed MI or unstable angina associated angiographically with a changed SVG lesion and either total or subtotal occlusion. Average patient age was 58±2 (SEM)years; 97% were male. Years since SVG placement to baseline angiogram averaged 6.5±0.4 (range 2–14). Time from the baseline to the unscheduled angiogram was 22±2 mo (range 3–47). In 28 patients the involved graft was single and in 7 sequential. The SVG insertion segments involved the LCX in 17, RCA in 15 and LAD in 10.ResultsThe initial lesion diameter at the site of the subsequent inciting lesion for all 35 patients averaged 2.58±0.17 mm, or 29.5±3.6% diam. stenosis. (This was defined as the most severe stenosis in any part of the graft in patients with subsequent total graft occlusion, and the exactly matched graft site in those with subtotal occlusion.) In 8 patients the baseline SVG was entirely normal. The initial lesion was >50% stenosis in only 4 patients. At the time of the clinical event, the lesion had progressed to 87±2.6% diam stenosis (N=35). In 16 patients the causal lesion was subtotal, while in 19 the SVG was totally occluded. The mean native vessel — responsible graft anastomotic diameter was 2.33±0.12mm.ConclusionQAA of SVG in asymptomatic patients may not predict subsequent graft closure associated with acute coronary syndromes. The initial site of the lesion is typically of mild-moderate severity, and only later exhibits rapid progression to occlusion

Coronary flow reserve in the newborn lamb: An intracoronary Doppler guide wire study

Recent studies indicate a severely reduced coronary flow reserve (CFR) in neonates with congenital heart disease. The significance of these studies remains debatable, as the ability of the anatomically normal neonatal heart to increase coronary flow is currently unknown. This study was designed to establish normal values for CFR in newborns after administration of adenosine [pharmacologic CFR (pCFR)] and as induced by acute hypoxemia (reactive CFR). Thirteen mechanically ventilated newborn lambs were studied. Coronary flow velocities were measured in the proximal left anterior descending coronary artery before and after adenosine injection (140 and 280 mug/kg i.v.) using an intracoronary 0.014-in Doppler flow-wire. Measurements were made at normal oxygen saturation (Sao(2)) and during progressive hypoxemia induced by lowering the fraction of inspired oxygen. CFR was defined as the ratio of hyperemic to basal average peak flow velocity. In a hemodynamically stable situation with normal Sao(2,) pCFR was 3.0 +/- 0.5. pCFR decreased with increasing hypoxemia. Regression analysis showed a linear relation between Sao(2) and pCFR (R = 0.86, p < 0.0001). Reactive CFR obtained at severe hypoxemia (Sao(2) <30%) was 4.2 +/- 0.8, and no significant further increase in coronary flow velocity occurred by administration of adenosine. Newborn lambs have a similar capacity to increase coronary flow in response to both pharmacologic and reactive stimuli as older subjects. Administration of adenosine does not reveal the full capacity of the newborn coronary circulation to increase flow, however, as the flow increase caused by severe hypoxemia is significantly more pronounced