Search

Slow or no-reflow phenomenon (SNR) complicates 10%-15% of cases of percutaneous intervention (PCI) in aortocoronary saphenous vein grafts (SVG). At present, there are no uniform, effective strategies to predict or prevent this common and potentially serious complication. The purpose of our study was to characterize variables correlated with the risk of SNR in SVG PCI in the era of stenting and glycoprotein IIb/IIIa receptor inhibitors. We identified 2,898 consecutive patients who had PCI, of whom 163 underwent PCI of at least one SVG. The clinical and angiographic characteristics of patients who developed SNR (SNR group) were compared with those who did not (no-SNR group). A total of 23 patients experienced SNR and 140 did not. Using a stepwise multivariate logistic regression analysis, four independent predictors for SNR were detected: probable thrombus (OR 6.9; 95% CI, 2.1-23.9; P = 0.001), acute coronary syndromes (OR 6.4; 95% CI, 2.0-25.3; P = 0.003), degenerated vein graft (OR 5.2; 95% CI, 1.7-16.6; P = 0.003), and ulcer (OR 3.4; 95% CI, 0.99-11.6; P = 0.04). The risk of developing SNR could be estimated according to the number of predictors found: low-grade risk (1%-10%) if < or = one variable was present, moderate risk (20%-40%) if two variables were present, and high risk (60%-90%) if three or more variables were present. We identified and quantified current risk factors for SNR and concluded that the risk of developing SNR during PCI in SVG can be predicted by simple clinical and angiographic variables obtained before PCI. This information may be useful when the risk of PCI has to be balanced against alternative strategies such as medical therapy or redo-bypass surgery or in the selection of those patients that will most benefit from the use of protection devices during PCI., (Copyright 2001 Wiley-Liss, Inc.)

Slow or no reflow (SNR) complicates 10-15% of cases of percutaneous intervention (PI) in saphenous vein bypass graft (SVG). To date there have been limited options for the prevention and treatment of this common and potentially serious complication. We evaluated the procedural outcome of 143 consecutive SVG interventions. We compared patients who received pre-intervention intra-graft adenosine boluses with those who did not. In addition we examined the efficacy of adenosine boluses to reverse slow-no reflow events. Angiograms were reviewed and flow graded (TIMI grade) by film readers blinded to the use of any intraprocedural drug or clinical history. Seventy patients received intragraft adenosine boluses before percutaneous intervention (APPI), 73 received no preintervention adenosine (NoAPPI). There were no significant angiographic differences between the two groups at baseline. A total of 20 patients experienced SNR. The incidence of SNR was similar in the two groups (APPI = 14.2% vs. NoAPPI = 13.6%, P = 0.9). SNR was treated with repeated, rapid boluses (24 microg each) of intra-graft adenosine. Reversal of SNR was observed in 10 of 11 patients (91%) who received high doses of adenosine (>/=5 boluses, mean 7.7 +/- 2.6) and in 3 of 9 (33%) of those who received low doses (<5 boluses, mean 1.5 +/- 1.2). Final TIMI flow was significantly better in the high dose than in the low dose group (final TIMI 2.7 +/- 0.6 vs. 2 +/- 0.8, P = 0.04). No significant untoward complications were observed during adenosine infusion. These findings suggest that SNR after PI in SVG is not prevented by pre-intervention adenosine, but it can be safely and effectively reversed by delivery of multiple, rapid and repeated boluses of 24 microg of intra-graft adenosine.

Early bypass grafting following intracoronary thrombolysis with streptokinase may be indicated in patients with acute coronary artery thrombosis and severe coronary disease. To evaluate this approach, we prospectively studied 41 patients (32 men and nine women, mean age 53 years) with acute infarction. Emergency cardiac catheterization was performed within 18 hours after onset of chest pain and intracoronary streptokinase was given. All patients underwent bypass 3 to 10 days later (mean 7 days). Serial gated radionuclide left ventricular angiograms to determine ejection fraction were obtained on hospital admission, preoperatively, and 3 to 6 months later. Thirty-four patients had complete occlusion of the artery supplying the infarcted segment. In 30 patients (88%) reperfusion was not successful. In seven patients the artery was not totally thrombosed. Thirty-two patients (78%) had multivessel disease. An average of 2.8 grafts per patient were placed with an operative mortality of 2% (one patient). Serial measurements of ejection fraction were obtained in 23 patients in whom the admission ejection fraction was less than 50%. There was a significant increase in ejection fraction from admission (33% +/- 11%) to the preoperative measurement (41% +/- 9%, p less than 0.001), and this improvement persisted at follow-up (40% +/- 14%). Intracoronary streptokinase has been shown to restore blood flow to infarcting myocardium and to improve left ventricular performance. In patients with significant organic stenosis, the risk of bypass grafting 3 to 10 days after intracoronary streptokinase infusion appears to be no different from the risk of elective operation performed at a time remote from an acute infarction.

Intracoronary streptokinase infusion has been shown to improve left ventricular function and reduce hospital mortality in patients with acute myocardial infarction. Adjuvant coronary artery bypass surgery is of value in many of these patients who have recurrent angina, circulatory instability, severe coronary artery occlusive disease, or a high risk of reinfarction. There is little, if any, evidence that immediate coronary artery bypass surgery affects the results adversely--either because of recent myocardial infarction or recent streptokinase infusion, and early operation appears to be a safe and worthwhile modality of treatment in this group of patients with myocardial infarction.