Short-term intravenous eptifibatide infusion combined with reduced dose recombinant tissue plasminogen activator inhibits platelet recruitment at sites of coronary artery injury
Mark H. Rubenstein, MD*,
Aloke V. Finn, MD*,
Robert C. Leinbach, MD, FACC*,
Stanley Hollenbach, PhD ,
H. Thomas Aretz, MD*,
Renu Virmani, MD and
Herman K. Gold, MD, FACC*,*
* Cardiac Unit and the Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts, USA
Millennium Pharmaceuticals Inc., Boston, Massachusetts, USA
Armed Forces Institute of Pathology, Washington, D.C., USA
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Figure 1 A is a low-power view of the longitudinally cut proximal left anterior descending coronary artery from a dog assigned to receive eptifibatide alone (in Phase II) showing presence of thrombus at the site of the side branch catheter through which thrombin was infused. Just distal to the thrombus, the traumatized left anterior descending coronary artery is seen. B and E are high-power views of the thrombus, showing platelet aggregation with fibrin strands and an occasional red cell. (C and F are high-power views of an area of the vessel severely damaged from crush injury, demonstrating disrupted endothelium covered by a thick layer of aggregated platelets within a fibrin mesh. D and G are high-power views from a more distal, less severely injury vessel segment showing a fibrin mesh with platelet adherence to the underlying collagen at the site of vessel injury.
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Figure 2 A is a low-power view of the longitudinally cut proximal left anterior descending coronary artery from a dog assigned to receive eptifibatide + rt-PA in Phase II. There is virtually no visible thrombus in marked contrast to that seen in Figure 1. B and E are high-power views of the small thrombus (arrow) showing a few scattered platelets adhering to the minimal thrombus. C and F are high-power views of an area of the vessel severely damaged from crush injury with absence of endothelium and exposure of the underlying collagen with only an occasional platelet adhering to the collagen and rare red cells. D and G are high-power views from a more distal area of the vessel with focal loss of endothelium, demonstrating only rare platelets adhering to the underlying surface. Compared to Figure 1, high-power views F and G demonstrate a marked reduction in the number of platelets adhering to two different segments of comparable vessel wall injury.
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