Acute myocardial infarction in myeloproliferative neoplasms

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Abstract

Myeloproliferative neoplasms (MPNs) are a heterogeneous group of hematologic malignancies characterized by an abnormal proliferation of cells of the myeloid lineage. Affected individuals are at increased risk for cardiovascular and thrombotic events. Myocardial infarction (MI) may be one of the earliest clinical manifestations of MPNs or may be a thrombotic complication that develops during the natural course of the disease. In the present review, we examine the epidemiology, pathogenesis, clinical presentation, and management of MI in MPNs based on the available literature. Moreover, we review potential biomarkers that could mediate the MI-MPNs crosstalk, from classical biochemical tests, e.g., lactate dehydrogenase, creatine kinase and troponins, to pro-inflammatory cytokines, oxidative stress markers, and clonal hematopoiesis.

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Clonal Hematopoiesis and Risk of Atherosclerotic Cardiovascular Disease

Olle Melander, Peter Libby, Sekar Kathiresan … (2017)

Background Clonal hematopoiesis of indeterminate potential (CHIP), defined by the presence of an expanded somatic blood cell clone in those without other hematologic abnormalities, is common in older individuals and associates with an increased risk of developing hematologic cancer. We previously found preliminary evidence for an association of CHIP with human atherosclerotic cardiovascular disease, but the nature of this association was unclear. Methods We used whole exome sequencing to detect the presence of CHIP in peripheral blood cells and associated this with coronary heart disease in four case-control studies together comprising 4,794 cases and 3,537 controls. To assess causality, we perturbed the function of Tet2, the second most commonly mutated gene linked to clonal hematopoiesis, in the hematopoietic cells of atherosclerosis-prone mice. Results In nested case-control analyses from two prospective cohorts, carriers of CHIP had a 1.9-fold (95% confidence interval 1.4–2.7) increased risk of coronary heart disease compared to non-carriers. In two retrospective case-control cohorts for early-onset myocardial infarction, those with CHIP had a 4.0-fold greater risk (95% confidence interval 2.4–6.7) of having myocardial infarction. Mutations in DNMT3A, TET2, ASXL1, and JAK2 were each individually associated with coronary heart disease. Those with clonal hematopoiesis also had increased coronary artery calcification, a marker of coronary atherosclerosis burden. Hyperlipidemic mice engrafted with Tet2−/− or Tet2+/− bone marrow developed larger atherosclerotic lesions in the aortic root and aorta than mice receiving control marrow. Analyses of Tet2−/− macrophages demonstrated elevated expression of several chemokine and cytokine genes that contribute to atherosclerosis. Conclusions Clonal hematopoiesis robustly associates with coronary heart disease in humans and causes accelerated atherosclerosis in mice.

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The NLRP3 inflammasome in acute myocardial infarction

Stefano Toldo, Antonio Abbate (2017)

The heart is extremely sensitive to ischaemic injury. During an acute myocardial infarction (AMI) event, the injury is initially caused by reduced blood supply to the tissues, which is then further exacerbated by an intense and highly specific inflammatory response that occurs during reperfusion. Numerous studies have highlighted the central role of the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in this process. The inflammasome, an integral part of the innate immune system, is a macromolecular protein complex that finely regulates the activation of caspase 1 and the production and secretion of powerful pro-inflammatory cytokines such as IL-1β and IL-18. In this Review, we summarize evidence supporting the therapeutic value of NLRP3 inflammasome-targeted strategies in experimental models, and the data supporting the role of the NLRP3 inflammasome in AMI and its consequences on adverse cardiac remodelling, cytokine-mediated systolic dysfunction, and heart failure.

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Philadelphia-negative classical myeloproliferative neoplasms: critical concepts and management recommendations from European LeukemiaNet.

Tiziano Barbui, Giovanni Barosi, Gunnar Birgegard … (2011)

We present a review of critical concepts and produce recommendations on the management of Philadelphia-negative classical myeloproliferative neoplasms, including monitoring, response definition, first- and second-line therapy, and therapy for special issues. Key questions were selected according the criterion of clinical relevance. Statements were produced using a Delphi process, and two consensus conferences involving a panel of 21 experts appointed by the European LeukemiaNet (ELN) were convened. Patients with polycythemia vera (PV) and essential thrombocythemia (ET) should be defined as high risk if age is greater than 60 years or there is a history of previous thrombosis. Risk stratification in primary myelofibrosis (PMF) should start with the International Prognostic Scoring System (IPSS) for newly diagnosed patients and dynamic IPSS for patients being seen during their disease course, with the addition of cytogenetics evaluation and transfusion status. High-risk patients with PV should be managed with phlebotomy, low-dose aspirin, and cytoreduction, with either hydroxyurea or interferon at any age. High-risk patients with ET should be managed with cytoreduction, using hydroxyurea at any age. Monitoring response in PV and ET should use the ELN clinicohematologic criteria. Corticosteroids, androgens, erythropoiesis-stimulating agents, and immunomodulators are recommended to treat anemia of PMF, whereas hydroxyurea is the first-line treatment of PMF-associated splenomegaly. Indications for splenectomy include symptomatic portal hypertension, drug-refractory painful splenomegaly, and frequent RBC transfusions. The risk of allogeneic stem-cell transplantation-related complications is justified in transplantation-eligible patients whose median survival time is expected to be less than 5 years.

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Author and article information

Contributors

Muhammad Romail Manan

Vincent Kipkorir

Iqra Nawaz

Maryann Wanjiku Waithaka

Bahadar Singh Srichawla

Amelia Maria Găman

Camelia Cristina Diaconu

Mihnea-Alexandru Găman

Journal

Journal ID (nlm-ta): World J Cardiol

Journal ID (publisher-id): WJC

Title: World Journal of Cardiology

Publisher: Baishideng Publishing Group Inc

ISSN (Electronic): 1949-8462

Publication date (Print): 26 November 2023

Publication date (Electronic): 26 November 2023

Volume: 15

Issue: 11

Pages: 571-581

Affiliations

Services Institute of Medical Sciences, Lahore 54000, Pakistan

Department of Human Anatomy and Physiology, University of Nairobi, Nairobi 00100, Kenya

Quaid-e-Azam Medical College, Bahawalpur 63100, Pakistan

Department of Human Anatomy and Physiology, University of Nairobi, Nairobi 00100, Kenya

Department of Neurology, University of Massachusetts Chan Medical School, Worcester, MA 01655, United States

Department of Pathophysiology, University of Medicine and Pharmacy of Craiova, Craiova 200143, Romania

Clinic of Hematology, Filantropia City Hospital, Craiova 200143, Romania

Department of Internal Medicine, Faculty of Medicine, “Carol Davila” University of Medicine and Pharmacy, Bucharest 050474, Romania

Internal Medicine Clinic, Clinical Emergency Hospital of Bucharest, Bucharest 105402, Romania

Faculty of Medicine, “Carol Davila” University of Medicine and Pharmacy, Bucharest 050474, Romania

Department of Hematology, Center of Hematology and Bone Marrow Transplantation, Fundeni Clinical Institute, Bucharest 022328, Romania

Department of Cellular and Molecular Pathology, Stefan S. Nicolau Institute of Virology, Romanian Academy, Bucharest 030304, Romania. mihneagaman@ 123456yahoo.com

Author notes

Co-corresponding authors: Camelia Cristina Diaconu and Mihnea-Alexandru Găman.

Author contributions: Manan MR, Kipkorir V, Nawaz I, Waithaka MW, Srichawla BS, and Găman MA reviewed the literature and drafted the manuscript; Găman AM, Diaconu CC, and Găman MA provided overall intellectual input, reviewed the literature, and edited the final version of the manuscript and contributed equally as senior/last authors; and all authors approved the final version to be published. Găman MA and Diaconu CC are co-corresponding authors for this manuscript due to their significant contribution to the conceptualization, methodology, supervision, writing, review and editing. Găman MA is the corresponding author responsible for the communication with the journal.

Supported by the grant funded by Competitiveness Operational Programme A1.1.4. ID: P_37_798 MYELOAL-EDIAPROT, Grant Agreement no. 149/26.10.2016 (MySMIS2014+: 106774).

Corresponding author: Mihnea-Alexandru Găman, Doctor, MD, PhD, Doctor, Research Fellow, Researcher, Faculty of Medicine, “Carol Davila” University of Medicine and Pharmacy, 8 Eroii Sanitari Boulevard, Bucharest 050474, Romania. mihneagaman@ 123456yahoo.com

Article

Other ID: jWJC.v15.i11.pg571 Publisher-manuscript ID: 87510

DOI: 10.4330/wjc.v15.i11.571

PMC ID: 10696206

PubMed ID: 38058401

SO-VID: 59a224e7-f359-47e0-a9d7-9bd6d93ceeca

License:

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

History

Date received : 14 August 2023

Date revision received : 21 October 2023

Date accepted : 13 November 2023

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Acute myocardial infarction in myeloproliferative neoplasms

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Karger: Cardiovascular System

Most cited references 80

Clonal Hematopoiesis and Risk of Atherosclerotic Cardiovascular Disease

The NLRP3 inflammasome in acute myocardial infarction

Philadelphia-negative classical myeloproliferative neoplasms: critical concepts and management recommendations from European LeukemiaNet.

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Cited by 3

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