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Angiographic Demonstration of Coronary Dethrombosis with Eptifibatide

Alessandro Colombo, MD, Framcesco Lavarra, MD, Paolo Danna, MD, Maurizio Viecca, MD
Alessandro Colombo, MD, Framcesco Lavarra, MD, Paolo Danna, MD, Maurizio Viecca, MD
Coronary thrombus dissolution after intracoronary1 or intravenous2,3 abciximab administration has been angiographically proven in previous clinical reports. The present report shows dissolution of coronary thrombi with eptifibatide, a pharmacologically different antagonist of the GPIIb/IIIa platelet receptor, in conjunction with alteplase (case #1) or alone (case #2). Case #1. The first case is that of a 55-year-old gentleman with no previous cardiovascular history. He was seen in the Emergency Room because of sudden chest pain with ST-segment elevation on the anterior ECG leads and no signs of heart failure. The therapeutic strategy was to administer intravenous nitrates and low-dose alteplase (50 mg bolus), followed by immediate coronary catheterization. The initial treatment made him recover from his symptoms in 15-30 minutes; the angiogram, obtained fifty minutes from initial treatment, showed a large thrombus into the proximal left anterior descending artery (LAD, Fig.1a) and unexpectedly a thrombus also into the proximal right coronary artery (RCA, Figure 1b). Since both vessels showed TIMI 3 flow and the ECG abnormalities had resolved, the choice was to defer a percutaneous intervention and to start pharmacologic platelet blockade. The patient was given intravenous eptifibatide (180 mg/kg single bolus plus 2 mg/kg/min. infusion) and heparin (5000 IU bolus plus 800 U/hour infusion), together with oral clopidogrel (300 mg) and aspirin (160 mg), and he was admitted to the CCU. CPK levels rose to a peak of 1350 U/l nine hours after symptoms onset. On the following day repeat coronary angiography showed complete resolution of the right coronary thrombus (Figure 2b) and marked reduction of the LAD thrombus (Figure 2a). The RCA had no underlying stenosis, while the LAD had a long 65% diameter lumen reduction. Direct stenting was performed on the LAD, which was followed by no residual stenosis and normal flow velocity. Eptifibatide and heparin were continued for further 24 hours and double antiplatelet treatment (clopidogrel 75 mg plus aspirin 160 mg) was scheduled for 30 days. Bivasal coronary thrombosis is an exceedingly rare clinical finding, and always raises the suspect of a prothrombotic state. Indeed, the patient was found to have a very high title of anti-phospholipid antibodies (IgG > 120 U/l, normal values Case #2. A 71-year-old lady was admitted to the CCU because of episodes of short-lived chest pain associated with transient ST-segment depression on the lateral ECG leads three months after surgical coronary revascularisation. After a 24-hour course of intravenous heparin, coronary angiography showed thrombotic occlusion of the venous graft connected to the right coronary artery (Figure 3). Multiple balloon inflations and thrombus aspiration with the ev3 X-Sizer device were only able to transiently restore blood flow through the graft, which was left occluded at the end of the procedure. Eptifibatide (two 180 mg/kg IV boluses plus 2 mg/kg/min infusion) was started and an angiogram repeated 4 hours later. The graft was now widely patent with TIMI 3 flow. A 23 x 3 mm. coronary stent was deployed into the distal part of the graft, where a 70% diameter reduction was present. The final angiographic result is shown in Figure 4. Intravenous heparin and eptifibatide were continued for further 24 hours, and oral clopidogrel was started and prescribed for 30 days, in conjunction with aspirin. CPK and troponin did not rise above the normal upper limits. Six months later the patient was asymptomatic and had a planned control coronary angiography. The graft was found to be patent with a modest stenotic pathology in the proximal tract and TIMI 3 flow velocity (Figure 5). Two years after the procedure, she fares well and is free from angina pectoris. Discussion. What we learned and retain firmly from these cases especially from the second one is that balloons and/or stents are not always the best initial approach to treat acute coronary syndromes. A careful and critical analysis of the angiographic picture is needed and powerful antiplatelet drugs may well be tried first. Moreover, in some cases catheter devices may be totally unable to open up a thrombosed artery, while GP IIb/IIIa integrin inhibitors can be quickly effective, as was the case of the second patient. In this respect, we contribute the angiographic documentation that eptifibatide may be quite as efficient as abciximab in dissolving intracoronary thrombus and so may represent a very good choice in the treatment of acute coronary thrombosis. Moreover, not only patients with thrombophilic syndromes may respond very well to antithrombotic drugs as shown in case 1 but also subjects with conventional ateromatous disease, as is the case of the second patient described. Acknowledgement. The authors express their gratitude to Mr. Renzo Pench for his support in the preparation of the pictures.
References
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