Abstract
Introduction: Acute myocardial infarction (AMI) is a leading global cause of mortality. Following primary percutaneous coronary intervention (PCI), 25% require hospitalisation for symptomatic heart failure. Further understanding of the molecular pathogenesis and the temporal relationship of the protein profile associated with ischaemic insult and subsequent cardiac remodelling is required to improve risk stratification following AMI. Methods: 20 patients with AMI presenting to Royal Free Hospital in London were recruited for proteomic analysis (O link Proximity Extension Immunoassay) at presentation and at 24 and 72 hours following primary PCI. All underwent initial CMR on admission and at 6 month follow up to assess for myocardial oedema, left ventricular volumes and function and assessment of scar. Results: Proteomic biomarkers that increased on discharge following AMI were: IGFBP2 (8% increase, p=0.001), MMP-10 (5% increase, p=0.001), TIMP4 (14.4% increase, p<0.001), CSF-1 (3.4% increase, p<0.001), CHI3L1 (15% increase, p<0.001), ST2 (19% increase, p=0.001), TGF-alpha (17% increase, p=0.001), IL6 (38% increase, p<0.001), and NT-proBNP (93% increase, p<0.001). The only biomarker that significantly decreased was IGFBP-1 (24% decrease, p=0.003). Notably, increased post-PCI biomarkers correlated with reduced infarct size at follow-up, including CCL23 (R=-0.6, p=0.016), IL6 (R=-0.051, p=0.04), NT-proBNP (R=-0.72, p=0.002). High biomarkers at initial presentation associated with reduced left ventricular end diastolic volume (LVEDV) were CSF-1 (R=-0.64, p=0.03) and CCL23 (R=-0.76, p=0.006). Discussion: Following AMI, we observed increase in proteins implicated in inflammation, angiogenesis and tissue repair. IGFBP1 as a stress hormone significantly decreased after PCI. Markers that showed linear association with reduced cardiac preload measured by LVEDV were linked with angiogenesis promotion and resolution of inflammation.
Published Version
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