Y subjects were recruited from the Cardiology Service of Hospital Virgen de la Salud (Toledo, Spain). In case of ACS patients, the samples were obtained in the onset of the syndrome (t = 0 h) defined as the moment when the coronary event is diagnosed. Different pathologies and situations were considered as exclusion criteria. Tumour inflammatory diseases, alterations of coagulation, the existence of significant heart disease unrelated to the disease or its risk factors (valvular, pericardial affectations or cardiomyopathies), chronic treatments, except for ischemic heart disease and its riskTable 3 Baseline characteristics of healthy controls and ACS patients included in the studyHealthy controls (n = 30) Personal data Age (years) ?SD Sex (Male/Female) Risk factors Smokers Ex-smokers Diabetes mellitus Dyslipidemia
PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/21715270 Hypertension Renal disease Biochemical data Total cholesterol (mg/ LDL (mg/dL) HDL (mg/dL) Triglycerides (mg/dL) Background data Previous ACS Statins 0 0 8 17 4 10 182 ?37 103 ?36 50 ?12 123 ?50 165 ?27 99 ?28 49 ?8 144 ?59 172 ?28 109 ?31 47 ?9 161 ?43 3 3 1 6 14 0 10 8 5 23 22 3 9 7 7 17 22 3 64.2 ?11,5 17/18 68.3 ?9.8 27/8 67.1 ?8.7 21/6 NSTEACS patients (n = 30) STEACS patients (n = 30)Conclusions In the present study, our results from both 2D-DIGE analyses permitted us to suggest that NSTEACS patients had a characteristic plasma proteomic profile that differentiates them from those
PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/13867361 patients who have suffered a STEACS. Although in both 2D-DIGE experiments some patients had previously suffered ACS, as it was explained in detail in the Material and method section any previous disease or surgery should have occurred in a six months period before being included in the study. In our opinion, this period of time is broad enough to consider that the existence of a previous ACS in any patient would have no influence on the protein pattern found in our studies. Additionally, in spite of the large variety of biological processes of the identified proteins, based on our previous experience in secretome studies, the tissue is
4,4,5,5-Tetramethyl-2-(2-methylprop-1-en-1-yl)-1,3,2-dioxaborolane the origin of many of them [33,34]. As previously explained in the Background section, the wide number of biochemical disorders secondary to hypoxia suffered by the myocardium lead to tissue breakdown and the releasing of a large number of proteins of potential interest into the blood stream. In fact, among the proteins forming the characteristic plasma proteomic profile for STEACS patients appeared decreased expression levels of three proteins with antioxidant
3-(tert-Butyldimethylsilyloxy)propan-1-amine activity (1B-glycoprotein, peroxiredoxin-2 and haptoglobin) which will possible catalyze the damage caused by the plasma ROS in the endothelium. In spite ofLaborde et al. Proteome Science 2014, 12:43
http://www.proteomesci.com/content/12/1/Page 11 offactors, coronary angiograms normal ejection fractions less than 0.45, major trauma, thromboembolic events, revascularization or having undergone surgery within six months before the start of the study. The control group included 30 healthy volunteers with normal coronary arteries and up to two cardiovascular risk factors who attended the Department of Hemodynamic for various reasons. All healthy volunteers and patients had a sex and age distribution with no significant differences between them (Table 3).Depletion of high-abundant plasma proteinsIn order to increase the concentration of low-abundant proteins in plasma samples, the 14 most abundant plasma proteins were specifically removed by affinity chromato.