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Acute Profound Thrombocytopenia Following Angioplasty: the Dilemma in the Management and a Review of the Literature

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Acute Profound Thrombocytopenia Following Angioplasty: the Dilemma in the Management and a Review of the Literature Heart 2001;86:e18 (http://www.heartjnl.com/cgi/content/full/86/6/e18) 1of2 CASE REPORT Acute profound thrombocytopenia following angioplasty: the dilemma in the management and a review of the literature S N Makoni Abstract counts < 100 000, < 50 000, and < 20 000/ Abciximab, heparin, and clopidogrel are mm3, respectively. Among patients with often used together in the setting of coron- thrombocytopenia, the incidence of profound ary syndromes. These drugs are associated thrombocytopenia was 8.5%.3 Clopidogrel is a with thrombocytopenia and it is important thienopyridine derivative that irreversibly in- to quickly discriminate the cause of this hibits platelet aggregation by selectively bind- complication as it has implications for the ing adenylate cyclase coupled ADP receptors management of thrombocytopenia and the on the platelet surface. It has superior eYcacy coronary syndrome. This case highlights over aspirin in terms of prevention of myocar- some of the dilemmas that may arise as no dial infarction and vascular death.4 test can definitively identify the oVending drug, and stopping these drugs can aVect the outcome of the coronary event includ- Case report ing stent thrombosis. A 68 year old black man with a history of right (Heart 2001;86:e18) coronary artery stent one year before presenta- Keywords: profound thrombocytopenia; abciximab; tion was admitted after a positive exercise stress heparin; clopidogrel test. His medications were atorvastatin, meto- prolol, aspirin, clopidogrel, and amlodipine. Examination showed a normal blood pressure, Abciximab, a platelet glycoprotein IIb/IIIa weight of 95 kg and no signs of heart failure or inhibitor that blocks the final common pathway organomegaly. Haemoglobin was 13.9 g/dl, of platelet aggregation, thereby exerting a platelets 174 000, and coagulation profiles potent antiplatelet eVect, is used in the were normal. Cardiac catheterisation showed treatment of patients undergoing percutaneous 99% stenosis of the stent. He had balloon dila- coronary intervention.1 In the EPIC (evalua- tation and stent replacement. During the tion of IIb/IIIa platelet receptor antagonist 7E3 procedure he received heparin and abciximab in preventing ischemic complications) study infusions. After the procedure clopidogrel, there was a significant improvement in 30 day aspirin, and abciximab were continued. Seven and six month clinical outcomes when abcixi- hours after initiation of abciximab, the platelet mab was used in percutaneous coronary inter- count was 5000. Abciximab was stopped and vention compared with patients who had not complete blood count rechecked. A peripheral received abciximab. This benefit, however, smear confirmed thrombocytopenia without comes with potential complications of bleeding platelet clumping or schistocytosis. The patient and thrombocytopenia. The EPILOG (evalua- was noted to have mild haematuria and was tion in PTCA to improve long term outcome transfused with 12 units of pooled platelets. On with abciximab GP IIb/IIIa blockade) trial days 2 and 3 platelet counts were 124 000 and showed that abciximab administered with low 53 000, respectively. Mild haematoma was dose weight adjusted heparin diminished the noted at the site of a needle stick. Prothrombin risk of ischaemic complications within 30 days time was 11.4 seconds, partial thromboplastin Department of by 56% among patients undergoing percutane- time 22.7 seconds, FDP 8, fibrinogen 549, and Internal Medicine, ous transluminal coronary angioplasty blood cultures were negative. A serotonin Mercy Fitzgerald (PTCA) without increasing bleeding complica- release assay and enzyme linked immuno- Hospital, 1500 tions.2 Pooled data from three placebo control- sorbent assay (ELISA) for heparin dependent Lansdowne Avenue, led, randomised trials (EPIC, EPILOG, and antiplatelet factor 4 antibody were sent to a Darby, Pennsylvania 19023, USA EPISTENT (evaluation of platelet IIb/IIIa reference laboratory to exclude the possibility S N Makoni inhibitor for stenting)) of abciximab treatment of heparin induced thrombocytopenia (HIT) during percutaneous coronary intervention type II. On day 4 the platelet count was 40 000 Correspondence to: identified 178 patients (2.4% of 7290 patients) and the patient was started on danaparoid, Dr Makoni in whom thrombocytopenia developed after while HIT assay results were pending. On day [email protected] enrolment. Mild, severe, and profound 5 the platelet count was 45 000/mm3 and HIT Accepted 8 August 2001 thrombocytopenia were defined as platelet assays were negative. Danaparoid was stopped, www.heartjnl.com 2of2 Makoni no further drop in platelet count was noted, When heparin is stopped in suspected HIT, and the patient was discharged. another anticoagulant is required to prevent life threatening thromboembolic complications Discussion including skin necrosis, gangrene of the It is important to distinguish pseudothrombo- extremities, myocardial infarction, pulmonary cytopenia from true thrombocytopenia related embolism, and stroke. In the present case to abciximab, HIT, clopidogrel induced throm- danaparoid sodium was used. Enoxaparin may botic thrombocytopenic purpura (TTP), and cross react with heparin antibodies causing other causes because pseudothrombocytopenia thrombosis and therefore is contraindicated. involves no increased thrombotic or haemor- Clopidogrel may induce TTP, a disorder rhagic risk and has no clinical significance. characterised by diVuse microvascular occlu- Pseudothrombocytopenia is caused by EDTA sion of arterioles and capillaries resulting in dependent clumping of platelets in vitro. When ischaemic dysfunction of multiple organs. If the complete blood count is repeated using TTP is untreated, the mortality rate exceeds blood collected into citrate or heparin, pseudo- 90% and therefore constitutes a medical emer- thrombocytopenia is corrected. The incidence gency. Haemolytic uraemic syndrome, a vari- of pseudothrombocytopenia in the general ant of TTP, has been reported in a patient population was 0.1% compared with 1.1% in treated with clopidogrel.8 The absence of frag- patients on abciximab in the EPIC trial.5 Pseu- mented red blood cells and reticulocytes on dothrombocytopenia in the present patient was peripheral smear and a normal renal function excluded by absence of platelet clumping on made this unlikely. Normal haptoglobin, lac- peripheral smear. tate dehydrogenase, and bilirubin were used to There is a significant increase in thrombo- exclude a microangiopathic process. In this cytopenia when abciximab and heparin are patient, other potential causes of thrombocyto- used compared with placebo and heparin.6 A penia such as immune thrombocytopenia, and recent observation that incidence and severity rheumatological and bone marrow disorders of thrombocytopenia may be reduced by the were eliminated by a normal baseline platelet concomitant administration of low molecular count, absence of splenomegaly, and normal weight heparin (enoxaparin) instead of unfrac- prothrombin time, partial thromboplastin tionated heparin also suggests a possible inter- time, and FDP, and negative blood cultures. action between abciximab and the type of Thus, profound thrombocytopenia second- heparin.6 Thrombocytopenia related to abcixi- ary to abciximab and heparin was diagnosed in mab is frequently evident within the first 2–4 this patient by exclusion of other causes and hours, occurs rapidly, and may be reversed by the patient was safely managed with platelet platelet transfusion. Recovery starts after treat- transfusion. While the incidence of thrombo- ment is stopped and occurs at 20 000/mm3 cytopenia has been observed to increase when platelets per day, which reflects normal bone abciximab and unfractionated heparin are used marrow response. In one analysis thrombo- together, it is not clear whether clopidogrel cytopenia associated with abciximab treatment used in combination with abciximab and for PTCA was more frequent in patients who heparin increases the incidence of thrombo- were older (> 65 years) had a lighter weight cytopenia. Future trials should evaluate this. (< 90 kg), and had a lower baseline platelet 7 count (< 200 000), as was the case in this I am indebted to Whiton S Paine PhD and Peter Ennis MD for patient. their helpful comments and guidance, Tariro and Felistas for There are at least two discrete forms of HIT. their technical assistance and encouragement. The most clinically important is type II, a dis- 1 Ferguson JJ, Kereiakes DJ, Adgey JAA, et al. Safe use of order of delayed onset but persistent thrombo- platelet IIb/IIIa inhibitors. Am Heart J 1998;135:S77-89. cytopenia that begins 4–10 days after exposure 2 LincoV AM, Mark DB, Tcheng JE, et al. Economic assessment of platelet glycoprotein IIb/IIIa receptor block- to heparin and may be associated with venous ade with abciximab and low dose heparin during and arterial thromboses. Rarely are precipitous percutaneous coronary revascularization: results from the EPILOG randomized trial. Circulation 2000;102:2923–9. drops in platelet counts observed within 24 3 Keriakes DJ, Berkowitz SD, LincoV AM, et al. Clinical cor- hours unless the patient has received heparin relates and course of thrombocytopenia during percutane- 7 ous coronary intervention in the era of abciximab platelet within the previous two months. Type II is glycoprotein IIb/IIIa blockade. Am Heart J 2000;140:74– caused by IgG antibodies specific for a 80. 4 Coukell AJ, Markham A. Clopidogrel. Drugs 1997;54:745– complex of heparin and platelet
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