scholarly journals Galectin-3 in Acute Myocardial Infarction Patients with Atrial Fibrillation

2019 ◽  
Vol 28 (3) ◽  
pp. 284-290 ◽  
Author(s):  
Dragana Stanojevic ◽  
Svetlana Apostolovic ◽  
Dragana Stokanovic ◽  
Stefan Momčilović ◽  
Tatjana Jevtovic-Stoimenov ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Atrial Fibrillation ◽  
Acute Myocardial Infarction ◽  
Venous Blood ◽  
Control Group ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Galectin 3 ◽  
Predictive Role

Objective: Atrial fibrillation (AF) is common in acute myocardial infarction (AMI), and galectin-3 is possibly involved in its occurrence. Galectin-3 has been shown to play a central role in fibrosis and tissue remodeling and has a role in inflammatory and proliferative responses. The aim of our study was to measure galectin-3 levels in patients with myocardial infarction and to compare its levels in patients with or without AF, in order to investigate the potential predictive role of galectin-3 in this setting. Subjects and Methods: The study included 51 consecutive AMI patients with AF; 27 AMI patients (52.9%) had permanent/persistent AF, and 24 patients (47.1%) had paroxysmal AF. Thirty-eight consecutive AMI patients without AF were used as a control group. Blood samples were obtained from venous blood on the third day after reperfusion. Results: Patients with AF had higher levels of C-reactive protein (p < 0.01) and galectin-3 (p < 0.05) than those without AF. Patients with high galectin-3 had 4.4 times greater odds of having AF. Galectin-3 levels were lower in patients without AF (p < 0.01) than in those with permanent/persistent AF. Conclusion: AMI patients with AF had higher levels of galectin-3 than those without this arrhythmia. This biomarker of inflammation and fibrosis could be a potential target for treating AMI patients at high risk.

scholarly journals Plasma Level of High-Sensitive C-Reactive Protein in Patients with Acute Myocardial Infarction and Arterial Hypertension

2017 ◽  
Vol 23 (1) ◽  
Author(s):  
Wael Rumaneh
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasma Level ◽  
Arterial Hypertension ◽  
Ventricular Remodeling ◽  
Left Ventricular ◽  
Control Group ◽  
Blood Levels ◽  
C Reactive Protein ◽  
Reactive Protein

Arterial hypertension is an independent predictor of acute myocardial infarction. Nowadays, plasma level of high-sensitive C-reactive protein is a marker of cardiovascular risk. The objective of the research was to evaluate plasma level of high-sensitive C-reactive protein in patients with acute myocardial infarction and arterial hypertension depending on myocardial remodeling type. Materials and methods. 130 patients with myocardial infarction (63 individuals with concomitant arterial hypertension and 67 individuals without it) were observed. Transthoracic echocardiogram was used. To evaluate plasma level of high-sensitive C-reactive protein the ELISA method was applied. Results. Plasma level of high-sensitive C-reactive protein in patients with acute myocardial infarction increased by 5.11 times compared to the control group: (10.67 [5.43; 12.89]) mg/l and (2.09 [1.40; 4.60]) mg/l, respectively (p<0.001). In myocardial infarction and arterial hypertension, this parameter increased by 6.57 times (to (13.73 [7.05; 15.17]) mg/l) (p<0.001), and by 1.27 times (p<0.05) as compared to patients without arterial hypertension. No differences in plasma level of high-sensitive C-reactive protein were detected in patients with different types of left ventricular remodeling.Conclusions. Acute myocardial infarction caused by high plasma level of high-sensitive C-reactive protein is severer in co-existent arterial hypertension. There are no differences in blood levels of high-sensitive C-reactive protein depending on the type of left ventricular remodeling.

Serum Endothelial Cell–Specific Molecule 1 (Endocan) Levels in Patients With Acute Myocardial Infarction and Its Clinical Significance

Angiology ◽  
2016 ◽  
Vol 68 (4) ◽  
pp. 354-359 ◽  
Author(s):  
Chong-Rong Qiu ◽  
Qiang Fu ◽  
Jian Sui ◽  
Qian Zhang ◽  
Peng Wei ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
High Sensitivity ◽  
Control Group ◽  
C Reactive Protein ◽  
Protein Levels ◽  
Reactive Protein ◽  
The Relationship

Endothelial dysfunction is involved in the process of acute myocardial infarction (AMI), that is, the endothelial cell–specific molecule 1 (ESM-1; endocan) is a novel endothelial dysfunction marker. However, the relationship between patients with AMI and serum ESM-1 levels is not very clear. Patients with AMI (n = 216) and a control group (n = 60) without AMI were included in the study. High-sensitivity C-reactive protein (hsCRP) was measured, and the severity of AMI was assessed by a modified Gensini stenosis scoring system. Serum ESM-1 levels were significantly higher in the AMI group ( P < .05). High-sensitivity C-reactive protein levels were also significantly higher in the AMI group ( P < .05). In patients with AMI, serum ESM-1 levels were not significantly correlated with hsCRP levels. There was no significant correlation between serum ESM-1 level and Gensini score. Our findings suggest that serum ESM-1 levels may be a novel biomarker of endothelial dysfunction in patients with AMI.

scholarly journals C-Reactive Protein Apheresis as Anti-inflammatory Therapy in Acute Myocardial Infarction: Results of the CAMI-1 Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Wolfgang Ries ◽  
Jan Torzewski ◽  
Franz Heigl ◽  
Christian Pfluecke ◽  
Sebastian Kelle ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Clinical Trial ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Control Group ◽  
Lv Function ◽  
Myocardial Infarct Size ◽  
C Reactive Protein ◽  
Reactive Protein

Background: C-reactive protein (CRP) is a well-known marker of inflammation. It is less known that CRP mediates tissue damage in acute myocardial infarction (AMI) thus potentially worsening prognosis. A newly developed specific CRP adsorber allows efficient lowering of CRP levels and may improve survival.Objectives: Aim of this multi-center, controlled, non-randomized first-in-man CRP apheresis in Acute Myocardial Infarction study (CAMI-1) was to investigate the relationship between CRP levels (CRP gradient), myocardial infarct size and function as well as safety and efficacy of CRP apheresis in the setting of acute ST-segment Elevation Myocardial Infarction (STEMI) in humans.Methods: Eighty-three patients (45 apheresis, 38 controls) were recruited. CRP apheresis was performed 24 ± 12, 48 ± 12, and optionally 72 ± 12 h after onset of symptoms. First aphereses were performed at a median CRP concentration of 23.0 mg/L (range 9–279). In each apheresis session, 5,900 ± 400 mL plasma was processed via peripheral venous access. Primary study endpoint was a reduction in myocardial infarct size after STEMI as determined by cardiovascular magnetic resonance (CMR).Results: In controls, the CRP concentration significantly correlated with infarct size (p = 0.002) and decreased myocardial function (p ≤ 0.001). The CRP concentration in apheresis patients did not correlate with infarct size (p = 0.66) or left ventricular (LV) function (p = 0.79) and global strains and therefore significantly differed from controls (p = 0.03 and p = 0.002). Three major adverse cardiac events occurred in the control group after 12 months, none occurred in the apheresis group. Mean CRP depletion achieved over all apheresis procedures was 53.0 ± 15.1%. Apheresis sessions were well-tolerated. Reduced infarct size in the apheresis group compared to the control group (primary endpoint) was not achieved according to the original statistical analysis plan. Taking into account the individual CRP levels, however, revealed significant results. Modifications of the analysis plan were introduced in order to recruit a sufficient number of patients.Conclusions: This pilot study in humans reveals a correlation between CRP concentration and myocardial infarct size. CRP concentrations in STEMI can effectively be reduced by CRP apheresis without relevant side effects. CRP apheresis has the potential to interfere with deleterious aspects of STEMI. By lowering CRP levels, it resulted in the loss of correlation of CRP concentrations with myocardial infarct sizes as well as LV function. These results encourage a larger, randomized clinical trial.Clinical Trial Registration:https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&amp;TRIAL_ID=DRKS00008988, DRKS00008988.

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