Differences in haemodynamic response to beta-blocking drugs between stable coronary artery disease and acute myocardial infarction

1986 ◽  
Vol 29 (6) ◽  
pp. 659-665 ◽  
Author(s):  
B. Silke ◽  
M. A. Frais ◽  
S. P. Verma ◽  
G. Reynolds ◽  
S. H. Taylor
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Stable Coronary Artery Disease ◽  
Haemodynamic Response ◽  
Beta Blocking ◽  
Artery Disease

scholarly journals High retinoic acid receptor-related orphan receptor A gene expression in peripheral blood leukocytes may be related to acute myocardial infarction

2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110196
Author(s):  
Heyu Meng ◽  
Jianjun Ruan ◽  
Xiaomin Tian ◽  
Lihong Li ◽  
Weiwei Chen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Peripheral Blood ◽  
Retinoic Acid Receptor ◽  
Stable Coronary Artery Disease ◽  
Orphan Receptor ◽  
Blood Leukocytes ◽  
Artery Disease

Objective This study aimed to investigate whether differential expression of the retinoic acid receptor-related orphan receptor A ( RORA) gene is related to occurrence of acute myocardial infarction (AMI). Methods This was a retrospective study. White blood cells of 93 patients with acute myocardial infarction and 74 patients with stable coronary artery disease were collected. Reverse transcription quantitative polymerase chain reaction and western blotting were used to measure RORA mRNA and protein expression, respectively. Results RORA mRNA expression levels in peripheral blood leukocytes in patients with AMI were 1.57 times higher than those in patients with stable coronary artery disease. Protein RORA levels in peripheral blood of patients with AMI were increased. Binary logistic regression analysis showed that high expression of RORA was an independent risk factor for AMI, and it increased the risk of AMI by 2.990 times. Conclusion RORA expression levels in patients with AMI is significantly higher than that in patients with stable coronary artery disease. High expression of RORA is related to AMI and it may be an independent risk factor for AMI.

scholarly journals Plasma EMMPRIN levels in acute myocardial infarction and stable coronary artery disease

2016 ◽  
Vol 39 (3) ◽  
pp. 79 ◽  
Author(s):  
Mehmet N Akkus ◽  
Adil Ormam ◽  
Sabri Seyis ◽  
Çagdas Baran ◽  
Aysegül Görür ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Plasma Levels ◽  
Stable Coronary Artery Disease ◽  
Healthy Controls ◽  
St Elevation ◽  
Artery Disease ◽  
Stable Cad

Purpose: The purpose of this study was to determine whether the plasma levels of soluble extracellular matrix metalloproteinase inducer (EMMPRIN) differed among the patients with ST-elevation myocardial infarction (STEMI), non-STEMI (NSTEMI) and stable coronary artery disease (CAD) and the healthy controls, and to identify the factors associated with the differences in plasma levels of this this protein among patients in these groups. Methods: Plasma EMMPRIN levels were compared among four age- and sex-matched groups of patients with STEMI, NSTEMI and stable CAD and healthy controls (n=44 per group), then logistic regression and correlation analyses were conducted for the whole acute myocardial infarction (AMI) patients group. Results: EMMPRIN levels were significantly higher in the STEMI (39.4±9.2ng/mL) and NSTEMI (37.1±10.5ng/mL) groups than in either the stable CAD (27.5±4.7ng/mL) or control (24.5±5.8ng/mL) groups (p

scholarly journals Bioactive Sphingolipids, Complement Cascade, and Free Hemoglobin Levels in Stable Coronary Artery Disease and Acute Myocardial Infarction

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
T. Jadczyk ◽  
K. Baranski ◽  
M. Syzdol ◽  
E. Nabialek ◽  
W. Wanha ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Acute Myocardial Infarction ◽  
Coronary Artery ◽  
Stable Coronary Artery Disease ◽  
Complement Cascade ◽  
Free Hemoglobin ◽  
Time Points ◽  
Bioactive Sphingolipids ◽  
Artery Disease

Background. Acute myocardial infarction (AMI) and coronary artery bypass graft (CABG) surgery are associated with a pathogen-free inflammatory response (sterile inflammation). Complement cascade (CC) and bioactive sphingolipids (BS) are postulated to be involved in this process.Aim. The aim of this study was to evaluate plasma levels of CC cleavage fragments (C3a, C5a, and C5b9), sphingosine (SP), sphingosine-1-phosphate (S1P), and free hemoglobin (fHb) in AMI patients treated with primary percutaneous coronary intervention (pPCI) and stable coronary artery disease (SCAD) undergoing CABG.Patients and Methods. The study enrolled 37 subjects (27 male) including 22 AMI patients, 7 CABG patients, and 8 healthy individuals as the control group (CTRL). In the AMI group, blood samples were collected at 5 time points (admission to hospital, 6, 12, 24, and 48 hours post pPCI) and 4 time points in the CABG group (6, 12, 24, and 48 hours post operation). SP and S1P concentrations were measured by high-performance liquid chromatography (HPLC). Analysis of C3a, C5a, and C5b9 levels was carried out using high-sensitivity ELISA and free hemoglobin by spectrophotometry.Results. The plasma levels of CC cleavage fragments (C3a and C5b9) were significantly higher, while those of SP and S1P were lower in patients undergoing CABG surgery in comparison to the AMI group. In both groups, levels of CC factors showed no significant changes within 48 hours of follow-up. Conversely, SP and S1P levels gradually decreased throughout 48 hours in the AMI group but remained stable after CABG. Moreover, the fHb concentration was significantly higher after 24 and 48 hours post pPCI compared to the corresponding postoperative time points. Additionally, the fHb concentrations increased between 12 and 48 hours after PCI in patients with AMI.Conclusions. Inflammatory response after AMI and CABG differed regarding the release of sphingolipids, free hemoglobin, and complement cascade cleavage fragments.

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