Hindawi Publishing Corporation Case Reports in Cardiology Volume 2013, Article ID 707438, 3 pages http://dx.doi.org/10.1155/2013/707438 Case Report Reactive Thrombocytosis Associated with Acute Myocardial Infarction following STEMI with Percutaneous Coronary Intervention Nat Dumrongmongcolgul, Charoen Mankongpaisarnrung, Grerk Sutamtewagul, Nattamol Hosiriluck, Timothy Chen, Alexander Trujillo, Nicholas Dcunha, Kenneth Nugent, and Leigh Ann Jenkins Department of Internal Medicine, Texas Tech University Health Sciences Center, 3601 4th Street, Indiana Avenue, Lubbock, TX 79430, USA Correspondence should be addressed to Nat Dumrongmongcolgul; nat.dumrongmongcolgul@ttuhsc.edu Received 9 August 2013; Accepted 8 September 2013 Academic Editors: K. Shimada and C. Steinwender Copyright © 2013 Nat Dumrongmongcolgul et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. he etiology of thrombocytosis can be classiied into reactive and essential forms. he rate of thromboembolic events is higher in essential thrombocytosis, and these events include strokes, transient ischemic attacks, retinal artery or retinal vein occlusions, digital ischemia, and acute coronary syndrome. In a study of 732 medical and surgical patients with thrombocytosis, 88% had reactive thrombocytosis. Patients with reactive thrombocytosis do not require cytoreductive medications or antiplatelet treatment. We report a healthy 40-year-old man without any medical problems who developed a new episode of myocardial infarction associated with thrombocytosis ater an episode of myocardial infarction followed by percutaneous coronary intervention. He had thrombocytosis, and his platelet function test did not reveal adequate inhibition. To treat his acute coronary syndrome, therapeutic enoxaparin was added, and clopidrogel was substituted with ticagrelor. We decided to start hydroxyurea to reduce platelets counts. Enoxaparin and hydroxyurea were discontinued when platelet count returned to baseline. JAK-2 and BCR/ABL mutations were negative. his case report highlights a clinical dilemma (reactive thrombocytosis), which is challenging in terms of management and pathophysiology. 1. Main Document A 44-year-old man presented to the emergency department with shortness of breath and chest pain. His only cardiovas- cular risk factor was cigarette smoking. Physical examination revealed a blood pressure of 82/67 mmHg, heart rate of 132 beats per minutes, and body temperature of 97.2F. His cardiovascular examination revealed normal irst and second heart sounds, with no jugular venous distention, murmurs, rubs, or gallops. he remainder of his physical examination was unremarkable. Initial ECG was sinus tachycardia without ischemic ST-T changes. He developed an episode of witnessed cardiac arrest with ventricular ibrillation. Cardiopulmonary resuscitation (CPR) was performed for 40 minutes until the return of spontaneous circulation. he initial troponin T was 1.91 ng/mL (0.01–0.03) ater the rhythm was reestablished, the electrocardiogram showed sinus tachycardia with ST- segment elevation in I, aVL, V4, V5, and V6. CK-MB was 181.4 ng/mL (0.1–0.49), and creatine kinase was 4248 units/L (77–308). Emergency coronary angiogram showed only total occlusion of let anterior descending artery. Let circumlex coronary artery and right coronary artery were normal. Per- cutaneous transluminal coronary angioplasty was performed with a pressure of 8 atmospheres for 14 seconds, and then a bare metal stent (Vision 2.75 × 18 mm (diameter × length)) was implanted in the mid third of the let anterior descending artery. Aspirin, carvedilol, simvastatin, and clopidogrel were initiated. Ater percutaneous coronary intervention (PCI), he was placed on therapeutic hypothermia protocol for 24 hours. he hospital course was uneventful. He was extubated and