ArticleJournal of the American Heart Association2015
Impact of left ventricular hypertrophy on troponin release during acute myocardial infarction: new insights from a comprehensive translational study.
Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- Impact of left ventricular hypertrophy on myocardial injury in patients with ST-segment elevation myocardial infarction.Clinical research in cardiology : official journal of the German Cardiac Society · 2018Trial
- Anthracycline cardiotoxicity: role of metabolic vulnerability induced by cardiac pressure overload.European heart journal · 2026Article
- Postoperative cardiac biomarker release is not associated with myocardial mass in computer tomography scans.Interdisciplinary cardiovascular and thoracic surgery · 2024Article
- Prognostic value of left ventricular hypertrophy in postoperative outcomes in type A acute aortic dissection.Journal of thoracic disease · 2022Article
- Generation and characterization of a novel knockin minipig model of Hutchinson-Gilford progeria syndrome.Cell discovery · 2019Article
- Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBiomarkers are frequently used to estimate infarct size (IS) as an endpoint in experimental and clinical studies. Here, we prospectively studied the impact of left ventricular (LV) hypertrophy (LVH) on biomarker release in clinical and experimental myocardial infarction (MI). METHODS AND
resultsST-segment elevation myocardial infarction (STEMI) patients (n=140) were monitored for total creatine kinase (CK) and cardiac troponin I (cTnI) over 72 hours postinfarction and were examined by cardiac magnetic resonance (CMR) at 1 week and 6 months postinfarction. MI was generated in pigs with induced LVH (n=10) and in sham-operated pigs (n=8), and serial total CK and cTnI measurements were performed and CMR scans conducted at 7 days postinfarction. Regression analysis was used to study the influence of LVH on total CK and cTnI release and IS estimated by CMR (gold standard). Receiver operating characteristic (ROC) curve analysis was performed to study the discriminatory capacity of the area under the curve (AUC) of cTnI and total CK in predicting LV dysfunction. Cardiomyocyte cTnI expression was quantified in myocardial sections from LVH and sham-operated pigs. In both the clinical and experimental studies, LVH was associated with significantly higher peak and AUC of cTnI, but not with differences in total CK. ROC curves showed that the discriminatory capacity of AUC of cTnI to predict LV dysfunction was significantly worse for patients with LVH. LVH did not affect the capacity of total CK to estimate IS or LV dysfunction. Immunofluorescence analysis revealed significantly higher cTnI content in hypertrophic cardiomyocytes.
conclusionsPeak and AUC of cTnI both significantly overestimate IS in the presence of LVH, owing to the higher troponin content per cardiomyocyte. In the setting of LVH, cTnI release during STEMI poorly predicts postinfarction LV dysfunction. LV mass should be taken into consideration when IS or LV function are estimated by troponin release.
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