Coronary Stent Occlusion after Platelet Transfusion: A Case Series

The introduction of coronary artery stents in the early 1990s reduced the early and late reocclusion rates of symptomatic coronary artery stenoses after balloon angioplasty. Nevertheless, coronary stent occlusion by thrombosis may occur, even in patients on (dual) antiplatelet treatment, thereby increasing morbidity and mortality.^1-3 We report three cases of early coronary stent occlusion within 6–17 hours after transfusion of platelets for bleeding or anticipated bleeding, in order to draw attention to this important risk factor.

Case Reports

Patient A. a 53-year old male was admitted after an out-ofhospital cardiac arrest caused by ventricular fibrillation, and was successfully resuscitated. During emergency coronary angiography, a significant stenosis in the left anterior descending artery (LAD), just at the side branch of the first diagonal artery, was found (Figure 1A). A Lekton bare-metal stent (Biotronik, Berlin, Germany) was inserted after balloon dilatation (Figure 1B). After percutaneous coronary intervention (PCI), the patient was admitted to the intensive care unit (ICU) for treatment using hypothermia for 24 hours. Further treatment included clopidogrel (loading dose of 300 mg, followed by 75 mg daily) and acetylsalicylic acid (ASA, 80 mg daily). The patient’s platelet count on arrival was 424 x 109/L, his activated partial thromboplastin time (aPTT) was 181 seconds and his prothrombin time (PT) was 1.15 international normalized ratio (INR). After 24 hours of hypothermia, the patient was weaned from themechanical ventilator. Ten days after admission, before weaning had been completed, gastric bleeding developed, necessitating transfusion of red cell concentrates and 1 unit of donor platelets (at a platelet count of 180 x 109/L, an aPTT of 37 seconds, and a PT of 1.16 INR). Clopidogrel and ASA were discontinued. Seventeen hours after the administration of platelets and 31 hours after the last dose of clopidogrel and ASA, the patient developed congestiveheart failure with ST-segment elevation in the precordial leads of the electrocardiogram (ECG). Echocardiography showed akinesia of the anteroseptal, anterior, lateral and apical segments. Since thrombosis of the coronary artery stent was suspected, heparin (2500 unit bolus followed by 20,000 units/24 hours) and abciximab (10 μg/minute for 12 hours) were started. Coronary angiography revealed occlusion of the distal part of the stent in the LAD (Figure 2A). After wire passage (Figure 2B), the thrombus extended distally over a long course. A second baremetal stent was inserted (Figure 2C). Subsequently, antiplatelet therapy, consisting of clopidogrel (600 mg loading dose, 75 mg daily) and ASA (80 mg daily) was restarted. The patient’s further recovery was uneventful, and he was discharged from the hospital 21 days after admission. An echocardiogram 6 months later showed full recovery of his left ventricular function.

Patient B. While riding a bicycle, a 61-year-old female collapsed because of ventricular fibrillation. She was admitted after cardiopulmonary resuscitation. The ECG showed signs of anterolateral myocardial infarction (MI). The patient was transferred to the catheterization laboratory where coronary angiography revealed an occlusion of the LAD. A Lekton bare-metal stent was inserted after wire passage and predilatation, with good restoration of blood flow and normalization of the ECG. After the procedure, the patient was admitted to the intensive care unit (ICU) and treated with clopidogrel (300 mg loading dose, 75 mg daily) and ASA (80 mg daily). Her neurological condition remained poor. In order to promote weaning from the ventilator, a percutaneous tracheotomy was performed on day 7 after admission, after transfusion of donor platelets and discontinuation of clopidogrel and ASA. The platelet count before transfusion was 147 x 109/ L. The tracheotomy was uncomplicated, with only minimal blood loss during the procedure. Thirteen hours after the platelet transfusion, the ECG showed signs of recurrent ischemia of the anterolateral wall and ventricular fibrillation occurred. The platelet count was 200 x 109/ L, the aPTT was 42 seconds, and the PT was 1.1 INR. She was successfully resuscitated and the ECG changes quickly resolved after starting intravenous heparin (2500 IU bolus and 20,000 IU/24 hours) and nitroglycerin (2 mg/hour). Although stent thrombosis was suspected, angiography was not performed because of the rapidly resolving ECG changes. After a prolonged period in the ICU, she eventually died from neurological deficits.

Patient C. A 65-year-old male experienced cardiac arrest at home. After successful resuscitation, he was admitted. The electrocardiogram showed signs of acute anterolateral MI. Coronary angiography revealed triple-vessel disease, and during percutaneous coronary intervention, a Lekton bare-metal stent was inserted in the LAD. Although revascularization was incomplete, there was a significant reduction of the ST-segment elevation. The patient was treated intravenously with heparin (2500 IU bolus, 20,000 IU/24 hours), clopidogrel (loading dose 600 mg, 75 mg daily) and ASA (80 mg daily). On admission to the ICU, the patient’s platelet count was 167 x 109/ L, the aPTT was 119 seconds and the PT was 1.2 INR. A few hours after admission, the patient suffered from severe bleeding due to erosion in the pharynx that was causedby laryngeal intubation during resuscitation, which was stopped by applying tampons and discontinuing heparin. Ten days after admission, the patient started to bleed from the nasogastric tube as well as rectally, resulting in hypotension. The platelet count was 96 x 109/ L, the aPTT was 34 seconds and the PT was 1.32 INR after infusion of fresh frozen plasma. In a final attempt to stop the bleeding, 4 units of pooled donor platelets were administered. The platelet count rose to 149 x 109/ L. The antiplatelet therapy was not discontinued. Six hours after the start of platelet transfusion, the ECG showed signs of ischemia of the anterolateral wall, most likely due to stent occlusion. Refractory shock, of both hypovolemic and cardiogenic origin, resulted in the patient’s death.

Discussion

Although angiographic proof of stent thrombosis was only obtained in Patient A, the ECG changes in Patients B and C were highly suggestive of myocardial ischemia following stent occlusion by thrombosis. The stent thromboses occurred within 10 days after stent placement and within 6–17 hours after the administration of donor platelets. In Patient A, clopidogrel and aspirin had not been administered for 31 hours prior to the event, but antiplatelet activity must still have been adequate since both drugs irreversibly inhibit platelets and the lifetime of platelets is 7–10 days. In Patients B and C, antiplatelet therapy had not been discontinued. The observations thus strongly argue in favor of stent occlusion by thrombosis following donor platelet transfusion in our patients, in spite of adequate dual antiplatelet therapy.¹ One could argue that platelet transfusion was not necessary in the patient scheduled for emergency surgery, but dual antiplatelet therapy is a significant risk factor for severe surgical bleeding, and precautions are usually taken for elective surgery.^4,5

Stent thrombosis is a feared complication with a 70–90% risk of death or non-fatal MI.^2,3 The timeframe in which stent thrombosis occurs can be divided into 4 phases: (1) acute thrombosis (< 24 hours after placement); (2) subacute thrombosis (days 1–30); (3) late thrombosis (days 31 to 1 year); and (3) very late thrombosis (> 1 year).³ Acute and subacute thrombosis may occur in 0.5–0.9%.² The risk for stent thrombosis is highest in the first 14 days after insertion, particularly in the first 96 hours, and decreases thereafter.⁶ Stent thrombosis in the acute and subacute phases is probably initiated by platelet aggregation and adhesion to the surface, even after a neointima has formed.⁷ In the absence of effective endothelium-derived vasoregulation and fibrinolysis, the platelet clot will be stabilized by the deposition of a fibrin mesh. Moreover, circulating platelets can be activated after MI and PCI for at least 48 hours, and their ability to adhere may increase.^8,9 Risk factors for stent thrombosis further include: stenting across branch ostia, the presence of diabetes mellitus, a low ejection fraction, persistent coronary intimal dissection, increasing stent length, and bifurcation stenting in the setting of acute MI, but the strongest independent predictor of stent thrombosis is insufficient or prematurely discontinued antiplatelet therapy and, possibly, increased platelet reactivity.^1,2,9 We may now add transfusion of donor platelets as a risk factor for thrombotic stent occlusion. Indeed, donor thrombocytes may not be inhibited by antiplatelet drugs in the blood stream and administration is even recommended for emergency surgery in patients on dual antiplatelet regimens.¹⁰ The thrombogenic surface of a recently inserted stent may thus attract and activate donor platelets, resulting in thrombotic occlusion.⁷ There is a case report suggesting that essential thrombocythemia is a risk factor for stent thrombosis in spite of dual antiplatelet therapy.¹¹ Another report suggests that recovery from drug-induced thrombocytopenia may be a risk factor for stent thrombosis.¹² Our observations warn against platelet transfusion early after stent insertion, but it is unclear whether the same warning applies late after stent insertion. When stent thrombosis follows platelet transfusion, an emergency PCI may be indicated, when feasible, as it is highly effective (in > 90% of cases) in restoring vessel patency and flow.³

In conclusion, our observations emphasize the risks of platelet transfusion and we support withholding such treatment, unless vitally indicated, in patients with recent baremetal coronary artery stent implantation, even for those on dual antiplatelet therapy.

References

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11. Turgut T, Harjai KJ, Edupuganti R, et al. Acute coronary occlusion and in-stent thrombosis in a patient with essential thrombocythemia. Cathet Cardiovasc Diagn 1998;45:428–433.

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