The etiology of thrombocytosis can be classified into reactive and essential forms. The 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 after 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. This 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 cardiovascular 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 97.2？F. His cardiovascular examination revealed normal first and second heart sounds, with no jugular venous distention, murmurs, rubs, or gallops. The 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 fibrillation. Cardiopulmonary resuscitation (CPR) was performed for 40 minutes until the return of spontaneous circulation. The initial troponin T was 1.91？ng/mL (0.01–0.03) after 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 left anterior descending artery. Left circumflex coronary artery and right coronary artery were normal. Percutaneous transluminal coronary angioplasty was performed with a pressure of 8 atmospheres for 14 seconds,
References
[1]
W. Dameshek, “Some speculations on the myeloproliferative syndromes,” Blood, vol. 6, no. 4, pp. 372–375, 1951.
[2]
Gruppo Italiano Studio Policitemia, “Polycythemia vera: the natural history of 1213 patients followed for 20 years,” Annals of Internal Medicine, vol. 123, no. 9, pp. 656–664, 1995.
[3]
M. Griesshammer, M. Bangerter, T. Sauer, R. Wennauer, L. Bergmann, and H. Heimpel, “Aetiology and clinical significance of thrombocytosis: analysis of 732 patients with an elevated platelet count,” Journal of Internal Medicine, vol. 245, no. 3, pp. 295–300, 1999.
[4]
M. Bazzan, G. Tamponi, P. Schinco et al., “Thrombosis-free survival and life expectancy in 187 consecutive patients with essential thrombocythemia,” Annals of Hematology, vol. 78, no. 12, pp. 539–543, 1999.
[5]
K. Lata, N. Madiraju, and L. Levitt, “JAK2 mutations and coronary ischemia,” New England Journal of Medicine, vol. 363, no. 4, pp. 396–397, 2010.
[6]
F. Passamonti, E. Rumi, D. Pietra, M. Lazzarino, and M. Cazzola, “JAK2 (V617F) mutation in healthy individuals,” British Journal of Haematology, vol. 136, no. 4, pp. 678–679, 2007.
[7]
K. M. Stamou, K. G. Toutouzas, P. B. Kekis et al., “Prospective study of the incidence and risk factors of postsplenectomy thrombosis of the portal, mesenteric, and splenic veins,” Archives of Surgery, vol. 141, no. 7, pp. 663–669, 2006.
[8]
M. C. Cheung, L. K. Hicks, and J. Pendergrast, “Thrombocytosis,” The New England journal of medicine, vol. 350, no. 24, pp. 2524–2525, 2004.
[9]
Y. K. Keung and J. Owen, “Iron deficiency and thrombosis: literature review,” Clinical and Applied Thrombosis/Hemostasis, vol. 10, no. 4, pp. 387–391, 2004.
[10]
S. Ghaffari and L. Pourafkari, “Acute myocardial infarction in a patient with post-splenectomy thrombocytosis: a case report and review of literature,” Cardiology Journal, vol. 17, no. 1, pp. 79–82, 2010.
[11]
M. M. Hoeper, J. Niedermeyer, F. Hoffmeyer, P. Flemming, and H. Fabel, “Pulmonary hypertension after splenectomy?” Annals of Internal Medicine, vol. 130, no. 6, pp. 506–509, 1999.
[12]
P. N. Khan, R. J. Nair, J. Olivares, L. E. Tingle, and Z. Li, “Postsplenectomy reactive thrombocytosis,” Baylor University Medical Center Proceedings, vol. 22, no. 1, pp. 9–12, 2009.
[13]
B. wilkerson and S. Elkins, “Clinical significance of reactive thrombocytosis after acute myocardial infartction subsequent stent placement,” A Retrospective Chart Review, Soutnern Society for Clinical Investigation, New Orleans, La, USA, 2004.
[14]
A. Cortell, J. Sanchis, V. Bodí et al., “Non-ST-elevation acute myocardial infarction with normal coronary arteries: predictors and prognosis,” Revista Espanola de Cardiologia, vol. 62, no. 11, pp. 1260–1266, 2009.
[15]
R. Hall and C. D. Mazer, “Antiplatelet drugs: a review of their pharmacology and management in the perioperative period,” Anesthesia and Analgesia, vol. 112, no. 2, pp. 292–318, 2011.
