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Background  Interleukin 6 concentration is associated with myocardial injury, heart failure, and mortality after myocardial infarction. In the Norwegian tocilizumab non–ST‐segment–elevation myocardial infarction trial, the first randomized trial of interleukin 6 blockade in  myocardial infarction , concentration of both C‐reactive protein and troponin T were reduced in the active treatment arm. In this follow‐up study, an aptamer‐based proteomic approach was employed to discover additional plasma proteins modulated by  tocilizumab  treatment to gain novel insights into the effects of this therapeutic approach.    Methods and Results  Plasma from  percutaneous coronary intervention– treated patients, 24 in the active intervention and 24 in the placebo‐control arm, drawn 48 hours postrandomization were randomly selected for analysis with the  SOMA scan assay. Employing slow off‐rate aptamers, the relative abundance of 1074 circulating proteins was measured. Proteins identified as being significantly different between groups were subsequently measured by enzyme immunoassay in the whole trial cohort (117 patients) at all time points (days 1–3 [7 time points] and 3 and 6 months). Five proteins identified by the  SOMA scan assay, and subsequently confirmed by  enzyme immunoassay , were significantly altered by  tocilizumab  administration. The acute‐phase proteins  lipopolysaccharide‐ binding protein, hepcidin, and insulin‐like growth factor‐binding protein 4 were all reduced during the hospitalization phase, as was the monocyte chemoattractant  C‐C  motif chemokine ligand 23. Proteinase 3, released primarily from neutrophils, was significantly elevated.    Conclusions  Employing the  SOMA scan aptamer‐based proteomics platform, 5 proteins were newly identified that are modulated by interleukin 6 antagonism and may mediate the therapeutic effects of  tocilizumab  in  non–ST‐segment–elevation myocardial infarction .

journal of the american heart association. cardiovascular and cerebrovascular disease

Novel Insights Into the Effects of Interleukin 6 Antagonism in Non–ST‐Segment–Elevation Myocardial Infarction Employing the SOMAscan Proteomics Platform