The aim of the present study was to identify the mechanisms underlying the development of post-myocardial infarction (post-MI) heart failure. The left anterior descending coronary artery of rats was occluded to mimic human ischemic heart disease. Linear Trap Quadropole OrbiTrap mass spectrometry was used to profile the expressions of energy metabolism-associated and calcium-binding proteins in the post-MI and control groups. Using the online Protein Analysis Through Evolutionary Relationships classification system, 78 differentially expressed proteins were identified, including 50 downregulated proteins and 28 upregulated proteins in post-MI group when compared with the control group. The differentially expressed proteins were closely associated with energy metabolism, contractile function, calcium handling, pathological hypertrophy and cardiac remodeling. These results were further validated using western blotting. At different postoperative time points (1st and 14th day following surgery) during the progression of advanced heart failure post-MI, dynamic alterations in differential protein expression were identified. The expression of the vitamin D protein was significantly upregulated on the 1st day post-MI however, was then downregulated with progression of the disease on the 14th day post-MI. These results identified various target proteins associated with the disease, which may be used as diagnostic markers.

Previous studies have demonstrated that elevated admission and fasting glucose (FG) is associated with worse outcomes in patients with acute myocardial infarction (AMI). However, the quantitative relationship between FG levels and in-hospital mortality in patients with AMI remains unknown. The aim of the study is to assess the prevalence of elevated FG levels in hospitalized Chinese patients with AMI and diabetes mellitus and to determine the quantitative relationship between FG levels and the in-hospital mortality as well as the optimal level of FG in patients with AMI and diabetes mellitus.

S100 Ca2+-binding protein A1 (S100A1) is an important regulator of myocardial contractility. The aim of the present study was to identify the underlying mechanisms of S100A1 activity via profiling the protein expression in rats administered with an S100A1 adenovirus (Ad-S100A1-EGFP) following acute myocardial infarction (AMI). LTQ OrbiTrap mass spectrometry was used to profile the protein expression in the Ad-S100A1-EGFP and control groups post-AMI. Using Protein Analysis Through Evolutionary Relationships (PANTHER) analysis, 134 energy metabolism-associated proteins, which comprised 20 carbohydrate metabolism-associated and 27 lipid metabolism associated proteins, were identified as differentially expressed in the Ad-S100A1-EGFP hearts compared with controls. The majority of the differentially expressed proteins identified were important enzymes involved in energy metabolism. The present study identified 12 Ca2+-binding proteins and 22 cytoskeletal proteins. The majority of the proteins expressed in the Ad-S100A1-EGFP group were upregulated compared with the control group. These results were further validated using western blot analysis. Following AMI, Ca2+ is crucial for the recovery of myocardial function in S100A1 transgenic rats as indicated by the upregulation of proteins associated with energy metabolism and Ca2+-binding. Thus, the current study ascertained that energy production and contractile ability were enhanced after AMI in the ventricular myocardium of the Ad-S100A1-EGFP group.