Acute regional changes in myocardial strain may predict ventricular remodelling after myocardial infarction in a large animal model

Doyin Odunmbaku-Mansell, V. D. Bruno, Eva Sammut, Amedeo Chiribiri, Thomas Johnson, I Khaliulin, Daniel Baz Lopez, H S Gill, Katharine Fraser, M Murphy, T Krieg, M. S. Suleiman, S George, Raimondo Ascione, Andrew Cookson

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To identify predictors of left ventricular remodelling (LVR) post-myocardial infarction (MI) and related molecular signatures, a porcine model of closed-chest balloon MI was used along with serial cardiac magnetic resonance imaging (CMRI) up to 5–6 weeks post-MI. Changes in myocardial strain and strain rates were derived from CMRI data. Tissue proteomics was compared between infarcted and non-infarcted territories. Peak values of left ventricular (LV) apical circumferential strain (ACS) changed over time together with peak global circumferential strain (GCS) while peak GLS epicardial strains or strain rates did not change over time. Early LVR post-MI enhanced abundance of 39 proteins in infarcted LV territories, 21 of which correlated with LV equatorial circumferential strain rate. The strongest associations were observed for D-3-phosphoglycerate dehydrogenase (D-3PGDH), cysteine and glycine-rich protein-2, and secreted frizzled-related protein 1 (sFRP1). This study shows that early changes in regional peak ACS persist at 5–6 weeks post-MI, when early LVR is observed along with increased tissue levels of D-3PGDH and sFRP1. More studies are needed to ascertain if the observed increase in tissue levels of D-3PGDH and sFRP1 might be casually involved in the pathogenesis of adverse LV remodelling.
Original languageEnglish
Article number18322
JournalScientific Reports
Issue number1
Publication statusPublished - 15 Sept 2021

Bibliographical note

Funding Information:
This work was supported by a Great West 4 (GW4) Initiator grant to Ascione (GW4-AF4-011) and partially by the University of Bath. In addition, this work was supported by the following grants to Ascione: Medical Research Council (MRC): MR/L012723/1; British Heart Foundation (BHF): IG/14/2/30991, PG/10/40/28369, PG/07/046/22772, and PG/16/104/32652) to Ascione, and by a Developmental Pathway Funding Scheme (DPFS) grant to Murphy, Krieg and Ascione (MR/M015769/1). Mansell was supported by an EPSRC DTP.

Funding Information:
The authors would like to thank the staff at the University of Bristol Translational Biomedical Research Centre, a national research facility for large animal co-funded by the British Heart Foundation and the Medical Research Council.

Publisher Copyright:
© 2021, The Author(s).

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