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      The Main Causes and Mechanisms of Increase in Cardiac Troponin Concentrations Other Than Acute Myocardial Infarction (Part 1): Physical Exertion, Inflammatory Heart Disease, Pulmonary Embolism, Renal Failure, Sepsis

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          Abstract

          The causes and mechanisms of increased cardiac troponin T and I (cTnT and cTnI) concentrations are numerous and are not limited to acute myocardial infarction (AMI) (ischemic necrosis of cardiac myocytes). Any type of reversible or irreversible cardiomyocyte injury can result in elevated serum cTnT and cTnI levels. Researchers and practitioners involved in the diagnosis and treatment of cardiovascular disease, including AMI, should know the key causes and mechanisms of elevated serum cTnT and cTnI levels. This will allow to reduce or completely avoid diagnostic errors and help to choose the most correct tactics for further patient management. The purpose of this article is to discuss the main causes and mechanisms of increase in cardiac troponins concentrations in frequently occurring physiological (physical exertion, psycho-emotional stress) and pathological conditions (inflammatory heart disease, pulmonary embolism, chronic renal failure and sepsis (systemic inflammatory response)) not related to myocardial infarction.

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          Most cited references125

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          Fourth Universal Definition of Myocardial Infarction (2018).

          Kristian Thygesen, Joseph Alpert, Allan S. Jaffe … (2018)
          Article 0 comments Cited 811 times – based on 0 reviews     Review now
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            Cardiac metabolism and its interactions with contraction, growth, and survival of cardiomyocytes.

            Stephen Kolwicz, Suneet Purohit, Rong Tian (2013)
            The network for cardiac fuel metabolism contains intricate sets of interacting pathways that result in both ATP-producing and non-ATP-producing end points for each class of energy substrates. The most salient feature of the network is the metabolic flexibility demonstrated in response to various stimuli, including developmental changes and nutritional status. The heart is also capable of remodeling the metabolic pathways in chronic pathophysiological conditions, which results in modulations of myocardial energetics and contractile function. In a quest to understand the complexity of the cardiac metabolic network, pharmacological and genetic tools have been engaged to manipulate cardiac metabolism in a variety of research models. In concert, a host of therapeutic interventions have been tested clinically to target substrate preference, insulin sensitivity, and mitochondrial function. In addition, the contribution of cellular metabolism to growth, survival, and other signaling pathways through the production of metabolic intermediates has been increasingly noted. In this review, we provide an overview of the cardiac metabolic network and highlight alterations observed in cardiac pathologies as well as strategies used as metabolic therapies in heart failure. Lastly, the ability of metabolic derivatives to intersect growth and survival are also discussed.
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              Prognostic value of troponins in acute pulmonary embolism: a meta-analysis.

              Cecilia Becattini, Giancarlo Agnelli, M C Vedovati (2007)
              Whether elevated serum troponin levels identify patients with acute pulmonary embolism at high risk of short-term mortality or adverse outcome is undefined. We performed a meta-analysis of studies in patients with acute pulmonary embolism to assess the prognostic value of elevated troponin levels for short-term death and adverse outcome events (composite of death and any of the following: shock, need for thrombolysis, endotracheal intubation, catecholamine infusion, cardiopulmonary resuscitation, or recurrent pulmonary embolism). Unrestricted searches of MEDLINE and EMBASE bibliographic databases from January 1998 to November 2006 were performed using the terms "troponin" and "pulmonary embolism." Additionally, review articles and bibliographies were manually searched. Cohort studies were included if they had used cardiac-specific troponin assays and had reported on short-term death or adverse outcome events. A random-effects model was used to pool study results; funnel-plot inspection was done to evaluate publication bias; and I2 testing was used to test for heterogeneity. Data from 20 studies (1985 patients) were included in the analysis. Overall, 122 of 618 patients with elevated troponin levels died (19.7%; 95% confidence interval [CI], 16.6 to 22.8) compared with 51 of 1367 with normal troponin levels (3.7%; 95% CI, 2.7 to 4.7). Elevated troponin levels were significantly associated with short-term mortality (odds ratio [OR], 5.24; 95% CI, 3.28 to 8.38), with death resulting from pulmonary embolism (OR, 9.44; 95% CI, 4.14 to 21.49), and with adverse outcome events (OR, 7.03; 95% CI, 2.42 to 20.43). Elevated troponin levels were associated with a high mortality in the subgroup of hemodynamically stable patients (OR, 5.90; 95% CI, 2.68 to 12.95). Results were consistent for troponin I or T and prospective or retrospective studies. Elevated troponin levels identify patients with acute pulmonary embolism at high risk of short-term death and adverse outcome events.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Vasc Health Risk Manag
                Journal ID (iso-abbrev): Vasc Health Risk Manag
                Journal ID (publisher-id): vhrm
                Journal ID (pmc): vhriskman
                Title: Vascular Health and Risk Management
                Publisher: Dove
                ISSN (Print): 1176-6344
                ISSN (Electronic): 1178-2048
                Publication date (Electronic): 21 September 2021
                Publication date Collection: 2021
                Volume: 17
                Pages: 601-617
                Affiliations
                [1 ]Department of Cardiology and Cardiovascular Surgery, Samara State Medical University , Samara, 443099, Russia
                [2 ]Department of Histology and Embryology, Samara State Medical University , Samara, 443099, Russia
                Author notes
                Correspondence: Aleksey Chauin Department of Cardiology and Cardiovascular Surgery, Department of Histology and Embryology Samara State Medical University , 89 Chapaevskaya Street, Samara Region, Samara, 443099, RussiaTel +7 927 770-25-87 Email alekseymichailovich22976@gmail.com
                Author information
                http://orcid.org/0000-0002-2712-0227
                Article
                Publisher ID: 327661
                DOI: 10.2147/VHRM.S327661
                PMC ID: 8464585
                PubMed ID: 34584417
                SO-VID: 386b6d2f-5b44-4d9b-9e0b-c103efd37819
                Copyright © © 2021 Chauin.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 02 July 2021
                Date accepted : 31 August 2021
                Page count
                Figures: 1, References: 125, Pages: 17
                Categories
                Subject: Review

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: diagnostics,differential diagnosis,causes of increased concentration,mechanisms of increase,cardiac troponins,troponin t,troponin i,acute myocardial infarction,physical activity,psycho-emotional stress,myocarditis,endocarditis,pericarditis,sepsis,pulmonary embolism,chronic renal failure
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: diagnostics, differential diagnosis, causes of increased concentration, mechanisms of increase, cardiac troponins, troponin t, troponin i, acute myocardial infarction, physical activity, psycho-emotional stress, myocarditis, endocarditis, pericarditis, sepsis, pulmonary embolism, chronic renal failure

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