Unlike essential thrombocytosis, which is associated with thrombotic and hemorrhagic complications,
reactive thrombocytosis (RT) is usually considered a benign process without thrombotic
complications.
We describe a case of acute myocardial infarction in a young heavy smoker with RT following
splenectomy. Coronary angiography showed a linear filling defect at mid-part of left anterior
descending artery. We performed balloon angioplasty and stenting for this lesion. Aspirin and
clopidogrel were administered. His in-hospital course was uneventful and platelet count returned
to the normal range at four month follow-up. We concluded that RT may not be an
entirely benign process, especially in patients with a history of smoking. Regular monitoring of
platelet count, and possibly antithrombotic agents like aspirin prescription for high risk patients
with moderate thrombocytosis, may be useful. (Cardiol J 2010; 17, 1: 79-82

Ghaffari, Samad

Pourafkari, Leili

English

Via Medica Journals

www.cardiologyjournal.org 79CASE REPORTCardiology Journal2010, Vol. 17, No. 1, pp. 79–82Copyright © 2010 Via MedicaISSN 1897–5593Address for correspondence: Leili Pourafkari, MD, Cardiovascular Research, Department of Tabriz University of MedicalSciences, Madani Heart Hospital, Tabriz, Iran, tel./fax: +98 (411) 335 77 70, e-mail: leili.p@gmail.comReceived: 10.02.2009 Accepted: 15.04.2009Acute myocardial infarction in a patientwith post-splenectomy thrombocytosis:A case report and review of literatureSamad Ghaffari, Leili PourafkariCardiovascular Research Department of Tabriz University of Medical Sciences,Madani Heart Center, Tabriz, IranAbstractUnlike essential thrombocytosis, which is associated with thrombotic and hemorrhagic compli-cations, reactive thrombocytosis (RT) is usually considered a benign process without throm-botic complications.We describe a case of acute myocardial infarction in a young heavy smoker with RT followingsplenectomy. Coronary angiography showed a linear filling defect at mid-part of left anteriordescending artery. We performed balloon angioplasty and stenting for this lesion. Aspirin andclopidogrel were administered. His in-hospital course was uneventful and platelet count re-turned to the normal range at four month follow-up. We concluded that RT may not be anentirely benign process, especially in patients with a history of smoking. Regular monitoring ofplatelet count, and possibly antithrombotic agents like aspirin prescription for high risk pa-tients with moderate thrombocytosis, may be useful. (Cardiol J 2010; 17, 1: 79–82)Key words: myocardial infarction, thrombocytosis, angioplasty, splenectomyIntroductionThrombocytosis, often found incidentally, ismost commonly a reactive or secondary responseto chronic inflammation, iron deficiency, activemalignancy, infection, trauma, or splenectomy [1].In a small number of cases however, thrombocyto-sis may be attributable to a clonal process, such asone of the four well-described classic myeloprolif-erative disorders: chronic myelogenous leukemia,polycythemia vera (PV), agnogenic myeloid meta-plasia, and essential thrombocytosis (ET). Throm-bocytosis is a rare cause of myocardial infarction inpatients with intrinsically normal coronary arteries,and especially very rare in patients with reactivethrombocytosis [2].Case reportA 34 year-old male presented to the emergen-cy department with acute retrosternal chest painradiating to his left arm associated with cold sweatand nausea which woke him at 4 am, three hoursbefore his arrival at emergency department. He hadundergone distal pancreatectomy with splenecto-my, for chronic pancreatitis and pancreatic pseudo-cysts 12 days earlier. His past medical history alsoincluded migraine headaches. He had also beena heavy smoker. He didn’t have a family history ofcoronary artery disease. He had a blood pressureof 130/80 mm Hg, and  heart rate of 80/min. Hisphysical examination showed no pathological find-ings except for a recent laparatomy scar. His first80Cardiology Journal 2010, Vol. 17, No. 1www.cardiologyjournal.orgelectrocardiogram at the time of admission showedST segment elevation of 3–4 mm in precordial leads(Fig. 1). The patient received a loading dose of as-pirin 325 mg and clopidogrel 300 mg orally, heparin5000 IU bolus IV injection, metoprolol 50 mg, ator-vastatin 40 mg and was also placed on nitroglycer-in and heparin infusion. Thrombolytic therapy wasnot administered as it was contraindicated for hisrecent major surgery history. His laboratory testsshowed Hgb = 12.5 mg/dL, WBC = 11 000/mL,PLT = 792 000//mL, CK-MB = 110, cTNI = 8,ESR = 34, CRP: 1+ and the rest of routine labora-tory studies were within normal limits. Furtherwork-up for iron deficiency anemia was negative.Bedside echocardiography showed left ventricularejection fraction of 40% with hypokinesia of anteri-or wall and apical segments. He underwent coro-nary angiography which showed a linear filling de-fect at mid-portion of left anterior descending ar-tery (Fig. 2) which was treated with low pressureballoon inflation and then a 3 × 15 ProkinetikTM(Biotronik, Buelach, Switzerland) bare metal stentwas deployed. His hospital course was uneventfuland he was discharged in a stable condition on as-pirin 325 mg, clopidogrel 75 mg, metoprolol 100 mgand atorvastatin 40 mg daily on the fifth day follow-ing admission. At four month follow-up the patient’sgeneral condition was good, left ventricular ejectionfraction was about 50% and his platelet count was410 × 103/mL.DiscussionThrombosis represents the second highestcause of mortality in patients with PV or ET [3]. Inpublished series, the rate of cardiovascular compli-cations related to the presence of ET has rangedfrom 4% to 21%. Thrombosis, when it occurs, ismore common in the arterial vascular bed (75%)than in the venous circulation (25%) [4]. The overallrisk of thrombotic events in ET, which may includemyocardial infarction, stroke, pulmonary embolism,deep vein thrombosis, transient ischemic attack,retinal artery or venous occlusions, hepatic or por-tal vein thrombosis, and digital ischemia, has beenfound to be 6.6% per patient per year, in comparisonto 1.2% per patient per year in the control popula-tion. Paradoxically, patients with ET are prone tohemorrhagic complications. Bleeding tends to oc-cur spontaneously in superficial sites such as theskin and mucus membranes as well as the gastro-intestinal or respiratory tracts [5].Conversely, reactive thrombocytosis is a be-nign process and is not a risk factor for thromboem-bolic complications [6]. In the immediate post-op-erative period in uncomplicated splenectomy pa-tients, the platelet count rises steeply with a peakFigure 1. Electrocardiography shows ST segment ele-vations in leads V1–V5.Figure 2. Left anterior oblique view of left coronary sys-tem. Linear filling defect indicating thrombosis is seenwithin the left anterior descending (arrow).81Samad Ghaffari, Leili Pourafkari, AMI in a patient with post-splenectomy thrombocytosiswww.cardiologyjournal.orgvalue at seven to 12 days. It usually subsides overthe next two to three months. However in somepatients the thrombocytosis persists indefinitelyfollowing splenectomy [1].In a large retrospective study of 732 patientswith thrombocytosis, 87.7% had reactive thrombo-cytosis. Thromboembolic complications were re-ported in 12.4% of patients with primary thrombo-cytosis compared with 1.6% in patients with reac-tive thrombocytosis. All patients with secondarythrombocytosis developing thrombotic complica-tions had additional risk factors such as precedingsurgery or a co-existing malignancy [7]. In one largeretrospective study comprising 318 patients with-out myeloproliferative disorders who underwentsplenectomy, thrombocytosis developed in 75% ofthe patients without a substantial increase in theincidence of thromboembolic events [8]. On theother hand, in a retrospective study of 129 patientswith platelet counts of 1,000 × 109/L or more, Busset al. [9] reported an equal frequency of thromboticevents among patients with myeloproliferative dis-orders and those with reactive thrombocytosis. Ina retrospective study evaluating 80 splenectomizedpatients suffering from various types of hereditaryhemolytic anemia, sideroblastic anemia, hemoglob-inopathies, or thalassemia, Hirsh and Dacie foundthat 13% developed thromboembolic complicationsin association with persistent postsplenectomythrombocytosis, two of whom died from these com-plications a long time after splenectomy. Howev-er, the authors suggested that post-splenectomythrombocytosis should not be the only factor pre-disposing patients to thrombosis because manypatients from their own series have had compara-ble increases in the post-splenectomy platelet countthat have been maintained for many years and havenot developed signs of thromboembolism [10].To our knowledge, this is the third reportedcase of acute myocardial infarction in patients withreactive thrombocytosis [11, 12]. Our patient re-fused bone marrow biopsy. However, normal countof platelets at the time of surgery (256 × 103) witha dramatic rise to 792 × 103 on the twelfth post-operative day, together with the gradual decline tonormal range during the next four months favorreactive thrombocytosis. Also, studies to evaluatea hypercoagulable state and iron deficiency anemiaincluding factor V Leiden mutation, protein C and S,antithrombin activity and homocystein and fibrino-gen levels, together with lupus anticoagulant, anti-cardiolipin and anti beta II glycoprotein I antibod-ies were all negative. Coronary angiography showeda linear filling defect at mid-part of left anteriordescending artery consistent with a thrombosis.While coronary occlusion due to ET may occur asa result of thrombotic aggregation on the damagedendothelium in totally normal coronary arteries, italso could be due to the thrombotic material aggre-gation over the atherosclerotic lesions resulting instenosis of unimportance [13]. During angioplasty,the balloon was fully expanded at very low inflationpressure of about 1–2 atmospheres and in coronaryangiography images acquired just after this inflationthere was no residual stenosis. This may indicatelack of any atherosclerotic stenosis in our patient’scoronary tree. Our patient had a history of smok-ing which has been shown to be common in youngpatients with infarction and ET [14]. His past med-ical history also included migraine headaches whichare reported to be associated with vascular reactiv-ity and this may be an appropriate substrate for insitu thrombus formation [15].Our case demonstrates the potential for a ma-jor vascular event in the setting of reactive throm-bocytosis, especially in those with a history ofsmoking. While the preventive effect of anti-coa-gulant and anti-platelets drugs has not been well--established, regular monitoring of platelet count andpossibly antithrombotic agents like aspirin prescrip-tion for high risk patients with moderate thrombo-cytosis may be useful. Due to a very low event ratein this setting, large studies are needed to evaluatethis hypothesis.AcknowledgementsThe authors do not report any conflict of inter-est regarding this work.The authors would like to express their grati-tude to Dr. Nosratollah Paurafkari for his invalua-ble comments.References1. Lewis SM. The spleen. In: Hoffbrand AV, Catovsky D,Tuddenham EG eds. Postgraduate hematology. 5th Ed. Black-well Publishing, Oxford 2005: 364.2. Kelly SV, Burke RF, Lee KS et al. Acute myocardial infarction:An unusual presentation of essential thrombocytosis in a 17--year-old man. Clin Adv Hematol Oncol, 2008; 6: 133–136.3. Vannucchi AM, Barbui T. Thrombocytosis and thrombosis.Hematology Am Soc Hematol Educ Program, 2007; 2007:363–370.4. Scheffer MG, Michiels JJ, Simoons ML, Roelandt JRTC. Throm-bocythemia and coronary artery disease. Am Heart J, 1991; 122:573–576.5. Cheung B, Radia D, Pantelidis P, Yadegarfar G, Harrison C. Thepresence of the JAK2 V617F mutation is associated with a high-er haemoglobin and increased risk of thrombosis in essentialthrombocythaemia. Br J Haematol, 2006; 132: 244–245.82Cardiology Journal 2010, Vol. 17, No. 1www.cardiologyjournal.org6. Williams B, Morton C. Cerebral vascular accident in a patientwith reactive thrombocytosis: A rare cause of stroke. Am J MedSci, 2008; 336: 279–281.7. Griesshammer M, Bangerter M, Sauer T, Wennauer R,Bergmann L, Heimpel H. Aetiology and clinical significance ofthrombocytosis: Analysis of 732 patients with an elevatedplatelet count. J Intern Med, 1999; 245: 295–300.8. Boxer MA, Braun J, Ellmann L. Thromboembolic risk ofpostsplenectomy thrombocytosis. Arch Surg, 1978; 113:808–809.9. Buss DH, Stuart JJ, Lipscomb GE. The incidence of thromboticand hemorrhagic disorders in association with extreme throm-bocytosis: An analysis of 129 cases. Am J Hematol, 1985; 20:365–372.10. Cappellini MD, Grespi E, Cassinerio E, Bignamini D, Fiorelli G.Coagulation and splenectomy: An overview. Ann NY Acad Sci,2005; 1054: 317–324.11. Tai YT, Yu YL, Lau CP, Fong PC. Myocardial infarction compli-cating postsplenectomy thrombocytosis, with early left ventricu-lar mural thrombus formation and cerebral embolism: A casereport. Angiology, 1993; 44: 73–77.12. Nielsen H. Fatal acute myocardial infarction associated withpostsplenectomy thrombocytosis. Ugesker Laeger, 1988; 150:2125–2126.13. Ozben B, Ekmekci A, Bugra Z, Umman S, Meric M. Multiple coro-nary thrombosis and stent implantation to the subtotally occludedright renal artery in a patient with essential thrombocytosis: A casereport with review. J Thromb Thrombolysis, 2006; 22: 79–84.14. Pick RA, Glover MU, Nanfro JJ, Dubbs WF, Gibbons JA,Vieweg WR. Acute myocardial infarction with essential throm-bocythemia in a young man. Am Heart J, 1983; 106: 406–407.15. Tietjen GE. Migraine and ischaemic heart disease and stroke:Potential mechanisms and treatment implications. Cephalalgia,2007; 27: 981–987.

Acute myocardial infarction in a patient with post-splenectomy thrombocytosis: A case report and review of literature

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Acute myocardial infarction in a patient with post-splenectomy thrombocytosis: A case report and review of literature

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