Efficacy and safety of colchicine in the treatment of acute myocardial infarction

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Abstract

Background:

There are no meta-analyses evaluating the efficacy and safety of colchicine in the treatment of acute myocardial infarction (AMI). Our protocol is conceived to evaluate the efficacy and safety of colchicine in comparison of placebo and test the hypothesis that a short course of treatment with colchicine could lead to reduced infarct size in patients presenting with AMI.

Methods:

We will follow the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) reporting guidelines and the recommendations of the Cochrane Collaboration to conduct this meta-analysis. Reviewers will search the PubMed, Cochrane Library, Web of Science, and EMBASE online databases for all English-language cohort studies published up to April, 2021. The cohort studies focusing on assess the efficacy and safety of colchicine in the treatment of AMI will be included in our meta-analysis. At least one of the following outcomes should have been measured: reduced infarct size, C-reactive protein (CRP) level, adverse events, death and major cardiovascular events. Review Manager software will be used for the meta-analysis. All outcomes are pooled on random-effect model. A P value of <.05 is considered to be statistically significant.

Results:

Our protocol is conceived to evaluate the efficacy and safety of colchicine in comparison of placebo and test the hypothesis that a short course of treatment with colchicine could lead to reduced infarct size in patients presenting with AMI.

Registration number:

10.17605/OSF.IO/NTU5F.

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Most cited references 12

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The inflammatory response in myocardial infarction.

Nikolaos G Frangogiannis, C. Smith, Mark L. Entman (2002)

One of the major therapeutic goals of modern cardiology is to design strategies aimed at minimizing myocardial necrosis and optimizing cardiac repair following myocardial infarction. However, a sound understanding of the biology is necessary before a specific intervention is pursued on a therapeutic basis. This review summarizes our current understanding of the cellular and molecular mechanisms regulating the inflammatory response following myocardial ischemia and reperfusion. Myocardial necrosis induces complement activation and free radical generation, triggering a cytokine cascade initiated by Tumor Necrosis Factor (TNF)-alpha release. If reperfusion of the infarcted area is initiated, it is attended by an intense inflammatory reaction. Interleukin (IL)-8 synthesis and C5a activation have a crucial role in recruiting neutrophils in the ischemic and reperfused myocardium. Neutrophil infiltration is regulated through a complex sequence of molecular steps involving the selectins and the integrins, which mediate leukocyte rolling and adhesion to the endothelium. Marginated neutrophils exert potent cytotoxic effects through the release of proteolytic enzymes and the adhesion with Intercellular Adhesion Molecule (ICAM)-1 expressing cardiomyocytes. Despite this potential injury, substantial evidence suggests that reperfusion enhances cardiac repair improving patient survival; this effect may be in part related to the inflammatory response. Monocyte Chemoattractant Protein (MCP)-1 is also markedly upregulated in the infarcted myocardium inducing recruitment of mononuclear cells in the injured areas. Monocyte-derived macrophages and mast cells may produce cytokines and growth factors necessary for fibroblast proliferation and neovascularization, leading to effective repair and scar formation. At this stage expression of inhibitory cytokines such as IL-10 may have a role in suppressing the acute inflammatory response and in regulating extracellular matrix metabolism. Fibroblasts in the healing scar undergo phenotypic changes expressing smooth muscle cell markers. Our previous review in this journal focused almost exclusively on reduction of the inflammatory injury. The current update is prompted by the potential therapeutic opportunity that the open vessel offers. By promoting more effective tissue repair, it may be possible to reduce the deleterious remodeling, that is the leading cause of heart failure and death. Elucidating the complex interactions and regulatory mechanisms responsible for cardiac repair may allow us to design effective inflammation-related interventions for the treatment of myocardial infarction.

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Colchicine alters the quantitative and qualitative display of selectins on endothelial cells and neutrophils.

B Cronstein, Y Molad, J Reibman … (1995)

Since colchicine-sensitive microtubules regulate the expression and topography of surface glycoproteins on a variety of cells, we sought evidence that colchicine interferes with neutrophil-endothelial interactions by altering the number and/or distribution of selectins on endothelial cells and neutrophils. Extremely low, prophylactic, concentrations of colchicine (IC50 = 3 nM) eliminated the E-selectin-mediated increment in endothelial adhesiveness for neutrophils in response to IL-1 (P < 0.001) or TNF alpha (P < 0.001) by changing the distribution, but not the number, of E-selectin molecules on the surface of the endothelial cells. Colchicine inhibited stimulated endothelial adhesiveness via its effects on microtubules since vinblastine, an agent which perturbs microtubule function by other mechanisms, diminished adhesiveness whereas the photoinactivated colchicine derivative gamma-lumicolchicine was inactive. Colchicine had no effect on cell viability. At higher, therapeutic, concentrations colchicine (IC50 = 300 nM, P < 0.001) also diminished the expression of L-selectin on the surface of neutrophils (but not lymphocytes) without affecting expression of the beta 2-integrin CD11b/CD18. In confirmation, L-selectin expression was strikingly reduced (relative to CD11b/CD18 expression) on neutrophils from two individuals who had ingested therapeutic doses of colchicine. These results suggest that colchicine may exert its prophylactic effects on cytokine-provoked inflammation by diminishing the qualitative expression of E-selectin on endothelium, and its therapeutic effects by diminishing the quantitative expression of L-selectin on neutrophils.

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Innate immune signaling in cardiac ischemia.

Fatih Arslan, Dominique de Kleijn, Gerard Pasterkamp (2011)

Despite advances in treatment of patients who suffer from ischemic heart disease, morbidity related to myocardial infarction is increasing in Western societies. Acute and chronic immune responses elicited by myocardial ischemia have an important role in the functional deterioration of the heart. Research on modulation of the inflammatory responses was focused on effector mediators such as leukocytes. However, increasing evidence indicates that various endogenous ligands that act as 'danger signals', also called danger-associated molecular patterns (DAMPs), are released upon injury and modulate inflammation. Originally described as part of the first-line defense against invading microorganisms, several Toll-like receptors (TLRs) on leukocytes and parenchymal cells have now been shown to respond to such signals and to have a pivotal role in noninfectious pathological cardiovascular conditions, such as ischemia-reperfusion injury and heart failure. From a therapeutic perspective, DAMPs are attractive targets owing to their specific induction after injury. In this Review, we will discuss innate immune activation through TLRs in cardiac ischemia mediated by DAMPs.

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Author and article information

Journal

Journal ID (nlm-ta): Medicine (Baltimore)

Journal ID (iso-abbrev): Medicine (Baltimore)

Journal ID (publisher-id): MEDI

Title: Medicine

Publisher: Lippincott Williams & Wilkins (Hagerstown, MD )

ISSN (Print): 0025-7974

ISSN (Electronic): 1536-5964

Publication date Collection: 09 April 2021

Publication date (Electronic): 09 April 2021

Volume: 100

Issue: 14

Electronic Location Identifier: e25429

Affiliations

[a ]Department of Cardiology, Wuhan Wuchang Hospital, Wuchang Hospital Affiliated to Wuhan University of Science and Technology

[b ]Department of Cardiology, Tianyou Hospital Affiliated to Wuhan University of Science and Technology, Hubei, China.

Author notes

[∗ ]Correspondence: Jinhe Zhao, Department of Cardiology, Tianyou Hospital Affiliated to Wuhan University of Science and Technology, Wuhan 430000, Hubei, China (e-mail: zhaojinheop@ 123456sina.com ).

Author information

Jinhe Zhao http://orcid.org/0000-0002-0270-9510

Article

Publisher ID: MD-D-21-02053 Accession ID: 25429

DOI: 10.1097/MD.0000000000025429

PMC ID: 8036066

PubMed ID: 33832144

SO-VID: acb277ab-050a-406d-852e-1509e2a5e548

License:

This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

History

Date received : 14 March 2021

Date accepted : 16 March 2021

Funding

Funded by: Wuhan Health Commission

Award ID: WX19D55

Award Recipient : Jinhe Zhao

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Keywords: acute myocardial infarction,colchicine,meta-analysis,protocol,review

Data availability:

Keywords: acute myocardial infarction, colchicine, meta-analysis, protocol, review

Efficacy and safety of colchicine in the treatment of acute myocardial infarction : A protocol for systematic review and meta-analysis

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Most cited references 12

The inflammatory response in myocardial infarction.

Colchicine alters the quantitative and qualitative display of selectins on endothelial cells and neutrophils.

Innate immune signaling in cardiac ischemia.

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