IMR Press / RCM / Volume 22 / Issue 1 / DOI: 10.31083/j.rcm.2021.01.256
Open Access Review
Platelet reactivity in dyslipidemia: atherothrombotic signaling and therapeutic implications
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1 Division of Hemostasis and Thrombosis, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, USA
2 Versiti Blood Research Institute, Milwaukee, WI 53226, USA

Academic Editor: Peter A. McCullough

Rev. Cardiovasc. Med. 2021, 22(1), 67–81;
Submitted: 23 November 2020 | Revised: 5 January 2021 | Accepted: 6 January 2021 | Published: 30 March 2021
(This article belongs to the Special Issue Thrombosis: Clinical Diagnosis and Treatment)

The risks for adverse thrombotic events, including myocardial infarction, stroke, and deep vein thrombosis, are markedly increased in dyslipidemia and other metabolic disorders and are the major cause of death worldwide. Recent evidence points out that increased thrombotic risk in dyslipidemia is mediated by platelets circulating in a pre-activated state. The mechanisms of platelet reactivity in this setting are multifaceted including platelet activation by classic agonist receptor signaling as well as platelet sensitization by pattern recognition receptors. Elevated platelet counts in dyslipidemia due to dysregulation in hematopoiesis also contribute to the overall thrombotic phenotype. Despite recent advancements in antiplatelet and anticoagulation therapies, recurrences of adverse thrombotic events remain to be a large clinical burden. In the light of new knowledge, understanding mechanisms that drive pathologic thrombosis in dyslipidemia, the antithrombotic approach shall be revisited. Here, we discuss potential therapeutic avenues based on the overview of platelet signaling mechanisms that contribute to a prothrombotic phenotype in dyslipidemia.

Antiplatelet therapy
Fig. 1.
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