Case presentation

An active 94-year-old retired psychiatrist with prior acute myocardial infarction 3 years earlier presented to the emergency department after awakening from sleep with severe chest pain. He was transported by ambulance where an electrocardiogram confirmed an acute anterior ST-segment elevation myocardial infarction. History obtained from his wife along with a quick review of the records revealed that, 3 years earlier, he presented with an acute anterior infarction complicated by cardiogenic shock and underwent emergent catheterization. That examination uncovered moderate disease in the right coronary artery, chronic occlusion of the proximal circumflex artery, and an acutely occluded, proximal left anterior descending artery. Reperfusion of the left anterior descending artery was successfully established by balloon angioplasty followed by placement of a 2.5 mm diameter by 16 mm long paclitaxel-eluting stent and he remained symptom-free until presentation.

Soon after arrival, his rhythm deteriorated to polymorphic ventricular tachycardia and he was successfully cardioverted to normal sinus rhythm. Two additional episodes of sustained ventricular tachycardia requiring cardioversion followed by progressive hypotension and diminished mental status led to endotracheal intubation and mechanical ventilation. He was administered intravenous infusions of amiodarone and dopamine and transported emergently to the cardiac catheterization laboratory.

Cardiac catheterization

Coronary angiography confirmed complete occlusion of the previously placed stent in the proximal left anterior descending artery and total occlusion of the left circumflex, as previously noted (Figure 26-1 and Video 26-1). There was moderate disease in the right coronary artery (Figure 26-2). After administration of a heparin bolus of 50 units/kg and an eptifibatide bolus (12.6 mg) followed by an infusion (2 mcg/kg/min), balloon angioplasty using a 2.5 mm diameter by 20 mm long balloon inflated to high pressures was performed. This restored TIMI-3 flow (Figure 26-3 and Video 26-2).

FIGURE 26-1 This angiogram of the left coronary artery shows the acute occlusion of the proximal left anterior descending artery stent and chronic occlusion of the left circumflex artery.

FIGURE 26-2 This is an angiogram of the right coronary artery. There is moderate nonobstructive disease noted in the proximal segment of the artery.

FIGURE 26-3 Angiogram obtained following balloon angioplasty of the occluded stent showing restoration of flow.

Postprocedural course

The patient was transported to the coronary care unit, requiring dopamine and dobutamine for blood pressure support. He remained intubated but was awake and responsive and denied chest pain. Routine admission blood analysis found normal renal function and a platelet count of 144 × 10⁹/L. However, the platelet count 2 hours later dropped to 65 × 10⁹/L and the eptifibatide infusion was discontinued. Five hours after receiving eptifibatide, the platelet count decreased to <10 × 10⁹/L. Hematology consultation recommended platelet transfusion. This raised the level to 35 × 10⁹/L. Fortunately, the patient had no mucosal, access site, or other evidence of bleeding and platelets recovered to 83 × 10⁹/L by the fourth day, and to 155 × 10⁹/L by the sixth day. Meanwhile, his hemodynamic status rapidly improved and the patient was removed from mechanical ventilation and inotropic support within 24 hours. Low dose beta-blocker, angiotensin-converting-enzyme inhibitor, statin, aspirin, and clopidogrel therapy were prescribed and the patient was ultimately discharged home.

Discussion

Although this case dramatically displays the potentially deadly consequences of late stent thrombosis after drug-eluting stent placement, more importantly, this case provides a classic example of the rare complication of acute, profound thrombocytopenia after glycoprotein IIb/IIIa inhibition.

Originally described with abciximab, thrombocytopenia has been associated with all three of the available glycoprotein IIb/IIIa receptor antagonists (abciximab, eptifibatide, and tirofiban). The mechanism is poorly understood but is believed to be an immune-mediated phenomenon.¹ For patients receiving abciximab, thrombocytopenia, defined as a platelet count of less than 100 × 10⁹/L, occurs in 2.7% of patients. Severe thrombocytopenia (platelet count less than 50 × 10⁹/L) occurs in 0.8% of patients receiving abciximab and profound thrombocytopenia (platelet count less than 20 × 10⁹/L) is observed in 0.3% of patients. ² Severe thrombocytopenia may be less frequent with infusions of eptifibatide and tirofiban than with abciximab, with platelet counts under 50 × 10⁹/L occurring in 0.2% to 0.5% of patients after receiving these agents.¹

It is important to distinguish true thrombocytopenia from “pseudothrombocytopenia”; the latter is due to artifactual clumping of platelets due to the anticoagulants used in the blood collection tubes and for the assay to measure platelets. Identification of platelet clumping on a blood smear and demonstration of a normal platelet count using a different anticoagulant confirms the diagnosis of pseudothrombocytopenia. It is also important to consider heparin-associated thrombocytopenia if this agent has been administered, although the clinical course and level of thrombocytopenia usually differ from that seen with glycoprotein IIb/IIIa receptor antagonists.

As observed in this case, most occurrences of severe and profound thrombocytopenia develop within the first few hours after administration of the drug bolus; for this reason, it is recommended that clinicians measure platelet counts 2 to 4 hours after the bolus is administered and again at 24 hours.¹ Risk factors for the development of thrombocytopenia have been studied and include advanced age, lower body weight, and lower baseline platelet count.^2,3

Patients developing severe thrombocytopenia are at increased risk of bleeding and have increased mortality compared to those without thrombocytopenia.^2,3 The management of severe thrombocytopenia includes maintaining platelet counts with platelet transfusions and close monitoring for bleeding complications. Immediate discontinuation of the glycoprotein IIb/IIIa receptor antagonist is obviously necessary. Adjunctive use of heparin or other anticoagulants should be avoided until platelet counts recover. The clinician is often faced with a dilemma regarding continued use of clopidogrel and aspirin. Although the cessation of these agents may result in stent thrombosis, continuation in the case of profound thrombocytopenia may lead to life-threatening bleeding and thus the risks and benefits of discontinuation of antiplatelet therapy should be carefully considered. Transfusion of platelets is recommended for platelet counts less than 20 × 10⁹/L. Platelet counts recover fairly rapidly with cessation of the agent. The case presented here is typical, with full recovery of the platelet count by 5 to 7 days after eptifibatide and 3 to 14 days for abciximab.¹