Case Description. A 57-year-old male with no known coronary artery disease presented to an outside hospital with chest pain. He subsequently ruled in for a non-ST segment elevation myocardial infarction, with a peak CPK of 406 mg/mL, CPK-MB 4.6 ng/mL, and troponin T 1.66 ng/mL. Therapy with eptifibatide, aspirin, and unfractionated heparin was started, and the patient was transferred to our center. Diagnostic coronary angiography performed 24 hours later revealed insignificant disease in the left coronary system, a 95% proximal right coronary artery stenosis, a 95% distal stenosis, and extensive thrombus burden throughout the mid and distal vessel (Figure 1). The left ventricular ejection fraction was 45% with severe inferior hypokinesis. Patient management. Given the extensive thrombus burden, the patient was continued on eptifibatide for an additional 48 hours prior to elective intervention. Repeat angiography 2 days later showed no change from the diagnostic study. The patient was pre-treated with 325 mg of aspirin and 300 mg of clopidogrel, and unfractionated heparin was given to achieve an activated clotting time over 250 seconds. The proximal lesion was dilated with a 2.5 x 15 mm NC Raptor (Cordis Corporation, Miami Lakes, Florida) over a 0.014´´ x 300 cm Whisper wire (Guidant Corporation, Santa Clara, California). Prior to dilating the distal lesion, an Export Aspiration catheter, which comes packaged with the GuardWire Plus distal protection system (formerly PercuSurge, Medtronic AVE, Santa Rosa, California), was used to extract thrombus proximal to the distal lesion (Figure 2). The distal lesion was then dilated with a 3.5 x 15 mm NC Raptor (Cordis), followed by passage of the Export catheter (Medtronic AVE) into the distal vessel (Figure 3). The distal lesion was then stented with a 4.0 x 23 mm Hepacoat BxVelocity (Cordis) deployed at 14 ATM. Finally, the proximal lesion was stented with a 4.0 x 18 mm Hepacoat BxVelocity (Cordis) deployed at 10 ATM, followed by post-dilation with a 4.5 x 15 mm Raptorail (Cordis) to 6 ATM. Despite the extensive thrombus burden present, this strategy resulted in successful removal of thrombus, with no distal embolization (Figure 4). The patient was continued on eptifibatide for an additional 18 hours, clopidogrel 75 mg daily for 28 days, and daily aspirin 325 mg indefinitely. There was no peri-procedural increase in cardiac markers, and the patient was discharged the following day. How Would You Manage This Case? Stanley Bleich, MD Cardiology Associates of Jefferson Metairie, Louisiana The interventionalists who presented the above case should be commended for their work. The strategic pre-procedure planning, along with the obvious concern of clot-burden, was clearly the key to their success. The two lesions exhibited are of high grade, but do not present a difficult intervention. A successful approach is one that includes distal embolization protection as a primary goal. An excellent angiographic result with ischemic arterial occlusion would have been considered a failed clinical result. In reviewing the sequence of the angiographic studies, it is interesting to note that the repeat catherization performed 48 hours following the initial study showed persistent and complex thrombus. In fact, it actually appears as though the clot associated with the distal lesion was more organized. Although no absolute rule of time exists, initiation of the intervention might have been better 24 hours following the initiation of anti-thrombin/platelet therapy. The first day following the beginning of IIb/IIIa inhibition and heparin should be sufficient for clot lysis and prior to the time period of increased risk of re-thrombosis. Staggered angioplasty of the two lesions with clot extraction in between and subsequent stenting resulted in an excellent angiographic outcome. It is important to note that no obvious clinical or physical evidence of distal embolization occurred. I wholeheartedly agree with the use of unfractionated heparin in this situation. An anti-thrombin in this case is of paramount importance and should be one whose clinical effect can be monitored by laboratory analysis. Following discharge, this patient was given 75 mg of clopidogrel for a 28-day period. In view of the results of the CURE trial and the extreme clot-burden, I propose the question of a longer course of the drug. In summary, an aggressive, well-planned intervention with emphasis on the risk of ischemic distal embolization is best. The clinical and angiographic results were excellent. However, could this patient have benefited from earlier intervention and longer and more aggressive post-discharge anti-platelet therapy? George Dangas, MD, PhD Cardiology Research Foundation New York, New York This 57-year-old man was transferred from another hospital with a classic acute coronary syndrome on eptifibatide, aspirin and unfractionated heparin for high-risk PCI. On admission, I would add clopidogrel 300 mg, followed by 75 mg daily. PCI would be scheduled for the following morning, given the clinical acuity. On admission to the cath lab, careful optimization should be undertaken. Platelet aggregation monitoring should be measured; target value should be Robert D. Safian, MD Director, Cardiac and Vascular Intervention William Beaumont Hospital Royal Oak, Michigan The patient is a young man with an acute coronary syndrome and mild elevation of cardiac enzymes, consistent with non-Q wave myocardial infarction. He underwent coronary angiography, which revealed severe single vessel disease of the right coronary artery (RCA) and left ventricular dysfunction. The coronary angiogram demonstrated two high-grade stenoses in the proximal and distal RCA, with a large thrombus burden. Medical therapy included aspirin, clopidogrel, eptifibatide, and heparin. Percutaneous intervention was performed 48 hours after the diagnostic angiogram using angioplasty, mechanical aspiration of thrombus with an export catheter and stents, had a nice angiographic and clinical result. The approach to large native vessel coronary arteries with extensive thrombus might include intracoronary lytic infusion, intracoronary administration of glycoprotein IIb/IIIa antagonists, rheolytic thrombectomy (AngioJet, Hydrolyzer), and mechanical thrombectomy (X-sizer, TEC, catheter aspiration). Adjunctive medical therapy might include intravenous glycoprotein IIb/IIIa antagonists, “dual” oral antiplatelet therapy, and antithrombin therapy (unfractionated heparin, low-molecular weight heparins, or Angiomax). In general, percutaneous approaches to such lesions should involve an attempt at debulking thrombus as much as possible, since PTCA and/or stenting of such lesions is associated with a high risk of distal embolization, no-reflow, and poor outcomes. It is interesting, however, that although debulking such thrombotic lesions seems intuitively correct, this strategy has not been compared to standard therapies without debulking (in the native coronary circulation). While I think it was perfectly reasonable to try to debulk thrombus with a 48-hour course of antiplatelet and antithrombin therapy before intervention, I would have chosen a different strategy involving direct intervention at the time of the original diagnostic angiogram. I would place a prophylactic temporary transvenous pacemaker and utilize a 7 French (Fr) JR4 guiding catheter, a 0.014´´ guidewire (any flexible wire), and the AngioJet. After AngioJet, I would dilate and stent the vessel, as was done in this case. The other approach I would consider is using distal protection with the PercuSurge Guardwire system (using an 8 Fr system), with or without the AngioJet.