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Revista Española de Cardiología (English Edition) Revista Española de Cardiología (English Edition)
Rev Esp Cardiol. 2017;70:682 - Vol. 70 Num.08 DOI: 10.1016/j.rec.2017.04.026

Acute Coronary Syndrome in Patients With Thrombocytopenia

Francisco José Fernández-Fernández a,

a Servicio de Medicina Interna, Hospital Arquitecto Marcide, Complejo Hospitalario Universitario de Ferrol, A Coruña, Spain

Refers to

Article

To the Editor,

I read with great interest the article published in Revista Española de Cardiología by Bermejo et al.1 about eltrombopag therapy for primary immune thrombocytopenia (ITP) in a patient with a recent acute coronary syndrome (ACS). I would like to make some additional comments about other scenarios involving thrombocytopenia that may be seen in ACS patients. As Bermejo et al. point out,1 there is little published data on this subject. Some authors have proposed dual oral antiplatelet therapy in SCA patients with a platelet count of > 30 × 109/L, and choosing a type of stent that allows shortening the therapy duration with the smallest risk of stent thrombosis.2 The risk of bleeding in patients with thrombocytopenia depends not only on the platelet count, but also on the condition causing the thrombocytopenia.3 Patients with PIT and platelet counts between 20 to 30 and 50 × 109/L generally have a stable clinical course with no bleeding complications.4 The risk of severe bleeding in these patients is usually associated with platelet counts of < 10 to 30 × 109/L, and patients of advanced age have a higher risk.4 Therefore, the threshold of > 30 × 109/L proposed by some authors for ITP patients seems reasonable. Another scenario is thrombocytopenia associated with chronic liver disease. Because of the increased prevalence of metabolic syndrome and the relationship of this condition with both vascular disease and steatohepatitis, which can progress to cirrhosis, chronic liver disease may be a common cause of thrombocytopenia in the future. The perceived bleeding risk in cirrhotic patients with thrombocytopenia and a high international normalized ratio may be higher than the actual risk5 and lead to less intense antiplatelet therapy, thereby increasing the risk of thrombosis. Patients with liver cirrhosis have a balanced hemostatic status, in which the reduction in procoagulant factors is offset by a parallel decrease in anticoagulant factors. In addition, their increased concentration of von Willebrand factor, the main protein required for platelet adhesion, can compensate for the low platelet count and ensure primary hemostasis.5 As occurs in relation to ITP, the available data do not suffice to establish firm recommendations on the most appropriate antiplatelet therapy for patients with cirrhosis-associated thrombocytopenia and ACS. Hence, expert recommendations have added value in these cases. In this regard, I had the opportunity to consult Dr Donald Cutlip (Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts) about his recommendations for cirrhotic patients receiving metal stents. For these cases, he proposed dual antiplatelet therapy with aspirin and clopidogrel for 14 days in patients with a platelet count of < 20 × 109/L and for 14 to 30 days (according to the bleeding history) in those with counts of 20 to 50 × 109/L.

Two other scenarios to mention are chemotherapy-related thrombocytopenia in cancer patients and thrombocytopenia associated with myelodysplastic syndromes. Chemotherapy-related thrombocytopenia6 is transitory and has a predictable recovery period; there is a low risk of bleeding in patients with platelet counts of > 10 × 109/L. Patients with thrombocytopenia associated with myelodysplastic syndromes usually have a chronic course, and their bleeding risk is higher than in those with chemotherapy-induced thrombocytopenia.7 In myelodysplastic syndromes, platelets often express abnormally low concentrations of cell surface procoagulant markers or lack intracellular granules, and bleeding is common even in patients with platelet counts > 100 × 109/L.8 As is the case of the other conditions mentioned, there are no recommendations on the most appropriate antiplatelet therapy for patients with myelodysplastic syndrome-related thrombocytopenia who experience an ACS.

In conclusion, the bleeding risk associated with thrombocytopenia may differ depending on the origin of this condition. Over the next few years we will see more patients with thrombocytopenia who could develop an ACS, and these patients will require an appropriate antiplatelet strategy. It is important to develop the recommendations for this population in future clinical practice guidelines.

Bibliography

1. Bermejo N, Sigüenza R, Ibáñez F. Tratamiento de trombocitopenia inmune primaria con eltrombopag en un paciente con síndrome coronario agudo reciente. Rev Esp Cardiol. 2017;70:56-7.
2. Schulz-Schüpke S, Kastrati A. Duration of dual antiplatelet therapy after drug-eluting stents implantation: The jury is still out. Rev Esp Cardiol. 2015;68:827-9.
3. Rinder HM, Tracey JB, Recht M, et al. Differences in platelet alpha-granule release between normals and immune thrombocytopenic patients and between young and old platelets. Thromb Haemost. 1998;80:457-62.
4. Sanz MA, Vicente García V, Fernández A, et al. Diagnóstico, tratamiento y seguimiento de la trombocitopenia inmune primaria. Med Clin (Barc). 2012;138:. 261.e1-261.e17
5. Napolitano G, Iacobelis A, Merla A, et al. Bleeding after invasive procedures is rare and unpredicted by platelet counts in cirrhotic patients with thrombocytopenia. Eur J Intern Med. 2017;38:79-82.
6. Goldberg GI, Gibbon DG, Smith HO, DeVictoria C, Runowicz CD, Burns ER. Clinical impact of chemotherapy-induced thrombocytopenia in patients with gynecologic cancer. J Clin Oncol. 1994;12:2317-20.
7. Kantarjian H, Giles F, List A, et al. The incidence and impact of thrombocytopenia in myelodysplastic syndromes. Cancer. 2007;109:1705-14.
8. Manoharan A, Brighton T, Gemmell R, Lopez K, Moran S, Kyle P. Platelet dysfunction in myelodysplastic syndromes: a clinicopathological study. Int J Hematol. 2002;76:272-8.

1885-5857/© 2017 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved

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