Plasma proteins and mechanisms involved in the evolvement of cardiac function after myocardial infarction.

Heart failure (HF) is a severe potential complication of myocardial infarction(MI). However precise mechanisms underlying progression from MI to HF are not yet fully understood. Exploring how plasma proteomic profiles of post-MI patients relate to cardiac function during follow-up can give insights into pathophysiological processes that contribute to HF development. We measured 4587 circulating proteins in 246 patients hospitalized for a first anterior Q-wave MI at 1, 3 and 12 months post-MI. Echocardiographic measurements of left-ventricular (LV) end-diastolic volume (EDV), LV ejection fraction (EF), and left atrial volume (AV), were assessed at hospital discharge, 3, and 12 months. Associations between protein and echocardiographic variables were assessed using pair-wise multivariate linear mixed-effects models. Median (IQR) age was 56 (46, 69) years, and 19% were women. Twenty-eight proteins were associated with LVEDV (linked to cardiac remodeling, vascular dysfunction, oxidative stress), twelve with AV (coronary artery disease, atherosclerosis, immune system), and eight with LVEF (cardiac hypertrophy, fibrosis, inflammation). Trajectories of all three echocardiographic variables were associated with NT-proBNP and BNP. Our results give an overview of the most important mechanisms related to the deterioration of cardiac function after MI, with cardiac stress, cardiac remodeling, vascular dysfunction, and inflammation emerging as central mechanisms.