Evidence map›Paper›PMID 35559722›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2022

Myocardial injury, troponin release, and cardiomyocyte death in brief ischemia, failure, and ventricular remodeling.

John M Canty

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. StandardizedFrontiers in pharmacology · 2025
    Pooled it
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  8. Cardiotoxicity in breast cancer patients treated with chemoradiotherapy.Exploration of targeted anti-tumor therapy · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

John M CantyVeterans Affairs Western New York Health Care System, Departments of Medicine, of Physiology and Biophysics, and of Biomedical Engineering and The Clinical and Translational Research Center of the University at Buffalo, Buffalo, New York.ORCID 0000-0002-7959-6649
VA Western New York Healthcare System · US

Funding

University of Buffalo Clinical and Translational Science Institute - Supplement SchulyerUL1TR001412 · NCATS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI MURPHY, TIMOTHY F · 2015 to 2024
$33.8M
Metabolic Adaptation and Functional Recovery of Hibernating MyocardiumR01HL061610 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI CANTY, JOHN M · 2000 to 2018
$6.0M
CHRONIC ADAPTATIONS TO MYOCARDIAL ISCHEMIAR01HL055324 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI CANTY, JOHN M · 1996 to 2014
$4.2M
Preventing and Reversing Interstitial Fibrosis in HFpEFI01BX002659 · VA · VA WESTERN NEW YORK HEALTHCARE SYSTEM · PI Brian Raymond Weil · 2016 to 2026
–
BLRD VA I01 BX002659NCATS NIH HHS UL1 TR001412NHLBI NIH HHS R01 HL055324NHLBI NIH HHS R01 HL061610
6 · The paper itself

Abstract

Troponin released from irreversibly injured myocytes is the gold standard biomarker for the rapid identification of an acute coronary syndrome. In acute myocardial infarction, necrotic cell death is characterized by sarcolemmal disruption in response to a critical level of energy depletion after more than 15 min of ischemia. Although troponin I and T are highly specific for cardiomyocyte death, high-sensitivity assays have demonstrated that measurable circulating levels of troponin are present in many normal subjects. In addition, transient as well as chronic elevations have been demonstrated in many disease states not clearly associated with myocardial ischemia. The latter observations have given rise to the clinical concept of myocardial injury. This review will summarize evidence supporting the notion that circulating troponin levels parallel the extent of myocyte apoptosis in normal ventricular remodeling and in pathophysiological conditions not associated with infarction or necrosis. It will review the evidence that myocyte apoptosis can be accelerated by diastolic strain from elevated ventricular preload and systolic strain from dyskinesis after brief episodes of ischemia too short to cause a critical level of myocyte energy depletion. We then show how chronic, low rates of myocyte apoptosis from endogenous myocyte turnover, repetitive ischemia, or repetitive elevations in left ventricular diastolic pressure can lead to significant myocyte loss in the absence of neurohormonal stimulation. Finally, we posit that the differential response to strain-induced injury in heart failure may determine whether progressive myocyte loss and heart failure with reduced ejection fraction or interstitial fibrosis and heart failure with preserved ejection fraction become the heart failure phenotype.

Indexed as

Heart FailureMyocardial InfarctionHumansMyocytes, CardiacNecrosisTroponin IVentricular RemodelingTroponin IapoptosisHFpEFHFrEFischemiatroponin

Identifiers

PMID35559722
PMCPMC9169835
OpenAlexW4280500160

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.