Case Report. A 74-year-old male diagnosed with NSTE acute coronary syndrome (non-Q wave myocardial infarction) in another hospital was transferred to our clinic due to residual angina. In 1996 the patient had a myocardial infarction (MI) and received three venous grafts via coronary artery bypass graft surgery (CABG) to relieve his unstable angina. The patient had significant cardiac risk factors including hypertension, hyperlipidemia and diabetes that had been diagnosed since 1996. At admission (October 2003), the patient experienced angina with mild exertion despite maximal anti-ischemic therapy, and showed ST-T changes on the lateral wall by ECG and an impaired ejection fraction of 38% by echocardiography. We decided to perform coronary angiography via the femoral approach, and placed the patient on clopidogrel 75 mg daily (with an initial dose of 300 mg) and aspirin 250 mg. The coronary angiography revealed 70% stenosis of the ostial left main artery, distal circumflex artery occlusion, left anterior descending artery (LAD) occlusion after the first diagonal branch and proximal occlusion of the right coronary artery (RCA). All of the venous grafts except the circumflex were patent; the circumflex was suboccluded with slow flow (Figure 1). We decided to open the suboccluded venous graft which was most likely the culprit lesion causing the unstable coronary syndrome. The patient was administered 10,000 U of heparin. Under a 310 s ACT control value, a JR 7 Fr guiding catheter was advanced in the graft ostium and an unsuccessful attempt was made to cross the lesion with an AngioGuard™ distal protection device (Cordis Corp., Miami, Florida). We finally crossed the stenosis with a PT Graphix™ balanced guidewire (Boston Scientific, Natick, Massachusetts) and delivered a 3.5 x 18 mm Multi-Link® Tetra™ Stent (Guidant Corp., Indianapolis, Indiana) at 10 atm at the stenosis level. No residual stenosis appeared, but severe no-reflow ensued (Figure 2). Verapamil (0.3 mg) was administered intracoronary without any changes, and eptifibatide infusion was started; the first bolus of 180 mg/kg was administrated intracoronary via a guiding catheter, followed by a second IV bolus, and then a continuous infusion of 2 mg/kg/minute. We previously reported (probably for the first time in the literature) a case of intracoronary infusion of eptifibatide (unpublished data). Under this therapy, no-reflow was persistent and the patient continued to complain of chest pain. ST-segment elevation in the lateral wall appeared on ECG. In this situation, we advanced the balloon catheter over the wire and gently advanced the guiding catheter on the balloon deeply into the venous graft. Having experience with thrombo-aspiration in femoral occlusions, we performed slow aspiration using a 50 ml syringe, with the guiding catheter deeply advanced in the graft. The aspiration was effective in this patient because the slugging contrast from the vein was removed into the catheter. We removed the catheter from the graft and washed the guiding catheter with saline and then performed angiography after recannulation of the vein graft ostium. The result was excellent, the no-reflow aspect disappeared and the ECG changes normalized, concomitant with pain dissolution (Figure 3). The eptifibatide infusion was maintained for 24 hours after the procedure, without significant CK-MB enzyme elevation, and the patient was asymptomatic at discharge. The patient has returned for 6-month follow-up without complaints, had a normal exercise stress test and showed an improved ejection fraction (EF) of 44%. Discussion. No-reflow is not a rare complication during vein graft percutaneous coronary intervention (PCI), and the exact cause of this is unknown. Some drugs and devices are effective, suggesting microembolic and vasospastic origin.6,7 It is easier to prevent the syndrome than to treat it. Preventive measures are efficacious when distal protection devices are used during PCI. In the SAFER trial, no-reflow occurred less frequently when distal protection devices were used (rates decreased from 9% to 3%). These rates are greater in cases of incorrect device placement or in unsuccessful procedures (from 2% to 13% in the SAFER trial and from 5% to 12.3% in a multicenter experience cited by Stone et al.2 Administration of vasodilators is one of the treatment options available once no-reflow has been diagnosed in a venous graft.1,5,8,9 In our experience, the intragraft administration of verapamil was inefficient or the was effect validated later (after graft aspiration). Although the administration of glycoprotein (GP) IIb/IIIa receptor inhibitors is controversial for the prevention and treatment of the no-reflow phenomenon,2,3,5 some new reports suggest that they might diminish no-reflow when administered via the intracoronary route, as these agents may achieve greater concentrations and reduce the thrombus that has already formed.2,5 GP IIb/IIIa inhibitors may also be effective even in the absence of thrombus in nonthrombotic mechanical experimental obstructions.4 All of these aspects suggest a platelet stabilizing effect and other possible effects.4,9 In our case, we administered intracoronary eptifibatide, though it is difficult to demonstrate its beneficial effect because of the graft aspiration performed soon after drug delivery. We were unable to find any data in the literature about the aspiration of a slugging graft (there are reports about prophylactic aspiration during balloon protection). The disappearance of no-reflow in the absence of an angiographically visible thrombus could be attributed to the aspiration of the vasoactive substances and to the combined effects of verapamil and eptifibatide. Acknowledgement. The authors wish to thank Ioana Bandila for assistance in preparing the manuscript and Maria Capusan, nurse technician.
1. Fischell TA, Maheshwari A. Current applications for nicardipine in invasive and interventional cardiology. J Invasive Cardiol 2004;16:428‚Äì432. 2. Stone GW, Rogers C, Ramee S. Distal filter protection during Saphenous vein graft stenting: Technical and clinical correlates of efficacy. J Am Coll Cardiol 2002;40:1882‚Äì1888. 3. D‚ÄôAgate DF, Patel S, Coppola JT. The evolving role of glycoprotein IIbIIIa receptor blockade during percutaneous coronary intervention of saphenous vein bypass grafts. J Invasive Cardiol 2004;16:500‚Äì503. 4. Kloner RA, Dai W. Glycoprotein IIbIIIa inhibitors and no-reflow. J Am Coll Cardiol 2004;40:284‚Äì286. 5. Kelly RV, Cohen MG, Stouffer GA. Incidence and management of no-reflow following percutaneous coronary interventions. Am J Med Sci 2005;329;78‚Äì85. 6. Galiuto L. Optimal therapeutic strategies in the setting of post-infarct no reflow: The need for a pathogenetic classification. Heart 2004;90;123‚Äì125. 7. Falk E, Thuesen L. Pathology of coronary microembolization and no reflow. Heart 2003;89:983‚Äì985. 8. Rezkalla SH, Kloner RA. No-reflow phenomenon. Circulation 2002;105:656. 9. Sanjiv K, Hiroshi I. Microvasculature in acute myocardial ischemia. Part II: Evolving concepts in pathophysiology, diagnosis and treatment. Circulation 2004;109;310‚Äì315.