Why the study?
Early predictors of late left ventricular remodelling post-myocardial infarction and their related molecular signatures needed to be identified.
Do early changes in regional myocardial strain predict late ventricular remodelling and correlate with specific molecular signatures in a porcine MI model?
Do early changes in regional myocardial strain predict late ventricular remodelling and correlate with specific molecular signatures in a porcine MI model?
Early changes in regional peak apical circumferential strain and specific protein markers (D-3PGDH, sFRP1) predict late left ventricular remodelling in a porcine MI model.
Early apical strain changes may flag late LVR risk in porcine MI; leaves open translation to human biomarkers and targets.
To identify early predictors of late left ventricular remodelling (LVR) post-myocardial infarction (MI) and related molecular signatures, a porcine model of closed-chest balloon MI was used. LVR was assessed by cardiac magnetic resonance imaging (CMRI) at baseline, 12–48 hours (acute), and 5–6 weeks (chronic) 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. LVR post-MI enhanced abundance of 39 proteins in infarcted LV territories,21 of which correlated with LV equatorial circumferential strain rate (ECSR). The strongest associations were observed for D-3-phosphoglycerate dehydrogenase (D-3PGDH), cysteine and glycine-rich protein-2 (CG-RP-2), and secreted frizzled-related protein 1 (sFRP1). Results indicate that early changes in regional peak ACS predict late LV remodelling and LVR post-MI is associated with augmented levels of D-3PGDH and sFRP1, which show the strongest association with peak ECSR. These findings might help to prevent LVR post-MI by influencing/directing LV unloading strategies or by pharmacological control of tissue levels of D-3PGDH and sFRP1.
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Mansell et al. (2021) studied this question.
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